Diabetic Type 2 Informations

The Study report

Of

Diabetic Type 2

 

 

Created by

Dr Iwan suwandy,MHA

copyright@2013

This Study  dedicated

To my wife, sons and  my brother ,ls for all Diabetic Type 2 community in all over the world,specially( khususnya) Indonesia.

Introductions

Indonesian version

Seseorang dengan diabetes tipe 2 dapat menggunakan latihan untuk membantu mengendalikan kadar gula darah mereka dan memberikan energi otot mereka perlu untuk berfungsi sepanjang hari.
Dengan mempertahankan diet sehat dan olahraga yang cukup, seseorang dengan
diabetes tipe 2
NON Insulin dependend diabetes melittus (NIDDM)
  mungkin dapat menjaga gula darah mereka dalam

rentang non-diabetes normal tanpa pengobatan.

 

Original info

 

A person with type 2 diabetes can use exercise to help control their blood sugar levels and provide energy their muscles need to function throughout the day.

By maintaining a healthy diet and sufficient exercise, a person with

type 2 diabetes

NON Insulin Dependend diabetes melittus(NIDDM)

 may be able to keep their blood sugar in the normal non-diabetic range without medication.

 

STUDI KEPUSTAKAAN

 

Diabetes tipe 2


Definisi
Diabetes tipe 2 adalah penyakit (kronis) seumur hidup di mana ada gula tingkat tinggi (glukosa) dalam darah. Diabetes tipe 2 adalah bentuk paling umum diabetes.

Alternatif Nama
Noninsulin-dependent diabetes; Diabetes – tipe 2;

 

Diabetes onset(Timbul) saat  dewasa

Penyebab, kejadian, dan faktor risiko
Diabetes disebabkan oleh masalah dalam cara tubuh Anda membuat atau menggunakan insulin. Insulin dibutuhkan untuk memindahkan gula darah (glukosa) ke dalam sel, di mana disimpan dan kemudian digunakan untuk energi.

 

Pathogenesis
Pada  diabetes tipe 2, lemak, hati, dan sel-sel otot tidak merespon dengan benar terhadap insulin.

Hal ini disebut resistensi insulin.

 Akibatnya, gula darah tidak masuk ke sel-sel ini untuk disimpan untuk energi.

Bila gula tidak dapat memasuki sel, gula tingkat tinggi membangun dalam darah. Hal ini disebut hiperglikemia.

Diabetes tipe 2 biasanya terjadi perlahan-lahan dari waktu ke waktu.

 

Kebanyakan orang dengan penyakit kelebihan berat badan ketika mereka didiagnosis.

 

Peningkatan lemak membuat lebih sulit bagi tubuh Anda untuk menggunakan insulin cara yang benar.

Diabetes tipe 2 juga dapat mengembangkan pada orang yang tipis. Ini lebih umum pada orang tua.

Riwayat keluarga dan gen memainkan peran besar pada diabetes tipe 2. 

Kegiatan tingkat rendah, pola makan yang buruk, dan berat badan berlebih di sekitar pinggang meningkatkan risiko Anda.

Lihat juga: diabetes tipe 2 untuk daftar faktor risiko.

Gejala
Sering kali, orang dengan diabetes tipe 2 tidak menunjukkan gejala pada awalnya. Mereka mungkin tidak memiliki gejala selama bertahun-tahun.

Gejala-gejala awal diabetes meliputi:
• Kandung kemih, ginjal, kulit, atau infeksi lain yang lebih sering atau menyembuhkan perlahan
• Kelelahan
• Kelaparan
• Meningkatnya rasa haus
• Peningkatan buang air kecil
Gejala pertama mungkin juga:
• kabur visi
• Disfungsi ereksi
• Nyeri atau mati rasa pada kaki atau tangan

Tanda dan tes
Dokter mungkin menduga bahwa Anda memiliki diabetes jika kadar
gula darah Anda lebih tinggi dari 200 mg / dL.

Untuk memastikan diagnosa, satu atau lebih dari tes berikut harus dilakukan.

 Tes darah Diabetes :
kadar glukosa darah puasa

diabetes didiagnosis jika lebih tinggi dari 126 mg / dL dua kali
 Uji Hemoglobin A1c
o Normal: Kurang dari 5,7%
o Pra-diabetes: 5,7% – 6,4%
o Diabetes: 6,5% atau lebih tinggi

Sedamg 6,5-9

Buruk lebih dari 9

Fakta Uji

Hemoglobin A1c 
The A1c Accu
Base Kit Test adalah tes yang sangat akurat (kurang dari 1,0% CV) mampu mendeteksi varian hemoglobin abnormal dan / atau diam seperti S hemoglobin, dan C dan F dan lebih dari 850 lainnya.

Setiap sampel disaring lebih dulu karena keberadaan hemoglobin abnormal dan / atau kinetika eritrosit terganggu (usia normal atau volume sel darah merah) Contoh, anemia (yang palsu dapat menurunkan nilai A1C).
 
Individu dengan diabetes yang berlangsung lama dapat hadir dengan kondisi yang disebut
kekurangan  eritropoeitin (EPO) .

Kekurangan  EPO dan / atanemia dianggap kondisi serius yang memerlukan intervensi medis yang tepat.

 DEK dapat mempengaruhi jawaban A1c dan setiap sampel harus diskrining untuk kehadiran DEK.

Perkiraan melaporkan bahwa lebih dari 650.000 orang Amerika Hitam dengan diabetes yang tahu untuk memiliki Trait Sickle Cell (Hb “S, C atau F”) “Jangan tertipu oleh klaim akurasi ketika metode A1c dan / atau perangkat monitoring pakai memiliki CV ( koefisien variasi) lebih besar dari 2,0% atau tidak dapat mendeteksi hemoglobin abnormal “.


“Sebuah metode A1c dan / atau perangkat monitoring dengan CV sebesar 7,0% bisa berarti bahwa jika tingkat A1C Anda yang sebenarnya adalah 6,5% itu bisa dilaporkan di mana saja dari 5,0% menjadi 8,0% memberikan informasi palsu terapi dan / atau menyesatkan,”
 

 belum lagi dampak dari hemoglobin abnormal pada nilai A1c bahwa metode tertentu atau perangkat tidak mampu mendeteksi.
Setiap sampel A1c AccuBase dianalisis dengan prosedur HPLC-IE dengan hasil Kromatogram dicetak seperti yang ditunjukkan di bawah ini.

 Staf laboratorium tersedia untuk membahas kromatogram individu dengan dokter Anda dan / atau tenaga medis.

 

The A1c AccuBase Test Kit adalah non-puasa, tongkat jari, mail-in test, dianggap tes A1C yang paling akurat dan tepat yang tersedia.

Tes ini dianggap sensitif dan cukup spesifik untuk mendeteksi diabetes (kurang dari 2,0% CV). CV berada di bawah 1,0%. CV menunjukkan tingkat akurasi diulang dibandingkan dengan nilai laboratorium diketahui A1c. CV rendah adalah tes yang lebih akurat A1c.


The A1c AccuBase Metode pengujian Kit adalah NGSP bersertifikat (nilai direferensikan ke DCCT). The A1c AccuBase Kit Uji tidak memerlukan waktu pengeringan, sampel dapat dikumpulkan dan dikirimkan dalam beberapa menit. Kit ini dilengkapi dengan pasien botol ID positif dan tabung kapiler plastik / perangkat.


Metode analisis gangguan gratis. Sampel yang stabil selama 30 hari un-didinginkan. Setiap hasil tes dilengkapi dengan perhitungan Glukosa Darah mean berdasarkan Persamaan MBG DCCT:% A1c X 31,7-66,1 = MBG di mg / dl. Hasil tes biasanya tersedia dalam 5 sampai 7 hari mailing bentuk.

 

Penanganan khusus dapat diatur untuk menyediakan, hari berikutnya, hasil sehari dua hari atau tiga. Ideal untuk diabetes rahasia (rata-rata glukosa darah) skrining, program penjangkauan dan jalur klinis

 .
Grafik pertama menunjukkan kromatogram normal dengan tidak hadir hemoglobin varian dan tingkat A1C yang normal.

 
The Kromatogram pada grafik kedua menunjukkan tingkat yang sangat tinggi dari F hemoglobin (25,6%). Tingkat peningkatan Hb F menghasilkan nilai A1c sub-normal 3,2%. Normal berkisar dari uji A1C (4,2% – 6,0%).


Kecuali Anda telah disaring untuk varian hemoglobin Anda tidak akan tahu Anda membawa varian persisten turun-temurun, atau menyadari dampaknya terkait pada tingkat A1C Anda.


Peningkatan kadar Hemoglobin F dapat mewakili peningkatan risiko SIDS pada bayi, dan dapat mewakili sebagai asosiasi dalam berbagai jenis leukemia dan / atau tumor padat. Ibu yang merokok atau telah terkena pencemaran lingkungan selama kehamilan mungkin memiliki tingkat yang jauh lebih tinggi dari Hb F pada bayi yang dapat meningkatkan risiko SIDS pada bayi baru lahir.


AccuBase A1c Kit Uji Diselesaikan untuk digunakan OTC oleh FDA (tidak ada resep yang diperlukan di sebagian besar negara). Pasien dapat menerima salinan hasil tes. Pelaporan elektronik kepada organisasi managed care kesehatan / penyedia tersedia.


The AccuBase A1cTest Kit menggunakan “standar emas” HPLC-IE atau BA metodologi untuk mengumpulkan dan menganalisis sampel A1c di lokasi situs alternatif seperti rumah, kantor dokter dan / atau klinik

• tes toleransi glukosa oral – diabetes didiagnosis jika kadar glukosa lebih tinggi dari 200 mg / dL setelah 2 jam

Skrining diabetes dianjurkan untuk:
• Kegemukan anak yang memiliki faktor risiko lain untuk diabetes, dimulai pada usia 10 dan diulang setiap 2 tahun
• Kegemukan dewasa (BMI lebih besar dari 25) yang memiliki faktor risiko lain

Dewasa di atas usia 45 setiap 3 tahun

Anda harus melihat dokter anda setiap 3 bulan.

Pada kunjungan ini, Anda dapat mengharapkan dokter untuk:
• Periksa tekanan darah Anda
• Periksa kulit dan tulang pada kaki dan kaki
• Periksa apakah kaki menjadi mati rasa
• Periksa bagian belakang mata dengan alat khusus yang disebut terang ophthalmoscope

Tes berikut akan membantu Anda dan dokter Anda memantau diabetes Anda dan mencegah masalah:
• Apakah tekanan darah Anda diperiksa setidaknya setiap tahun (darah tujuan tekanan harus 130/80 mm / Hg atau lebih rendah).

• Memiliki hemoglobin A1c Anda uji (HbA1c) setiap 6 bulan jika diabetes Anda terkontrol dengan baik, jika tidak setiap 3 bulan.

Apakah kolesterol dan trigliserida diperiksa tahunan (mencapai tingkat LDL di bawah 70-100 mg / dL).


• Dapatkan tes tahunan untuk memastikan ginjal Anda bekerja dengan baik (mikroalbuminuria dan serum kreatinin).
• Kunjungi dokter mata Anda setidaknya sekali setahun, atau lebih sering jika Anda memiliki tanda-tanda penyakit mata diabetes.


• Lihat dokter gigi setiap 6 bulan untuk membersihkan gigi menyeluruh dan ujian. Pastikan dokter gigi dan ahli kesehatan tahu bahwa Anda memiliki diabetes.

Pengobatan

Tujuan pengobatan pada awalnya adalah untuk menurunkan kadar glukosa darah tinggi. Jangka panjang Tujuan pengobatan adalah untuk mencegah masalah dari diabetes.

Pengobatan utama untuk diabetes tipe 2 adalah olahraga dan diet.
 tes baru adalah 

Aggregasi Thrombosit(hemostasis tes untuk menentukan apakah anda hiper atau normal aggresasi):  ADP 1 normal 0-15, ADP 2 normal  11-35, ADP 5 normal 25- 68 dan ADP 10 normal 49-84 (tes ini agak mahal sekitar Rp 300.000)


Platelet Function Testing: Light Transmission Aggregometry [LTA]


Introduction

Platelet function testing is difficult, time consuming and prone to a wide-variety of problems due to pre-analytical variables.

Before undertaking any tests of platelet function – consider:

Variable

Interpretation

Clinical History & examination. Some syndromes [e.g. Hermansky Pudlak syndrome, Cheddiak Higashi syndrome, Wiskott-Aldrich syndrome, Velocardiofacial Syndrome (VCFS), Noonan syndrome, MYH9-related disorders] are associated with abnormal platelet function and you may get some idea of the diagnosis from the clinical history and examination.
Drug History There are a large number of drugs and especially food substances that can interfere with platelet function.
Full Blood Count (FBC) and Blood Film 1. Consider pseudothrombocytopenia often due to cold reacting platelet agglutinins or to platelet satellitism.  Approximately 0.1% of the healthy population show EDTA-induced pseudothrombocytopenia and it is important to exclude this before undertaking more extensive tests of platelet function.  Similar findings have also been reported with the use of both citrate and heparin as anticoagulants.  A blood film may identify platelet clumps and provide a clue to the diagnosis.2. Mean Platelet Volume [MPV – reference range 7-10fL]: the MPV is an often ignored parameter of the FBC but can provide important insights into the causes of a low platelet count. 
  – It can also in some cases give a clue to the diagnosis e.g. the hereditary macrothrombocytopenias, Bernard Soulier Syndrome [BSS]
  – In individuals with an elevated MPV, an immunological-based platelet count may provide a more accurate and often significantly higher platelet count.
  – The MPV can be an indication of platelet turnover – an increased MPV indicating accelerated platelet clearance as in ITP or gestational thrombocytopenia.
  – The MPV may be reduced in cases of Wiskott-Aldrich Syndrome and in some cases of bone marrow failure.3. An examination of the blood film and platelet morphology can be useful in both establishing a diagnosis of pseudothrombocytopenia but also in establishing a primary platelet problem e.g. Gray Platelet Syndrome.  In some cases of thrombocytopenia e.g. May Hegglin anomaly – the blood film may show the presence of Döhle bodies [light blue-gray, oval, basophilic, leukocyte inclusions located in the peripheral cytoplasm of neutrophils.]

 

 Pengujian Fungsi Trombosit : Cahaya Transmisi Aggregometry [LTA]
________________________________________

Pengantar
Pengujian fungsi platelet(thrombosit)  sulit, memakan waktu dan rentan terhadap berbagai-masalah akibat pra-analitis variabel.

Sebelum melakukan apapun tes fungsi platelet – dipertimbangkan:

Variabel Interpretasi

 

Klinis Sejarah & pemeriksaan.

Beberapa sindrom [misalnya Hermansky Pudlak sindrom, Cheddiak Higashi sindrom, Wiskott-Aldrich syndrome, Syndrome Velocardiofacial (VCFs), sindrom Noonan, MYH9 yang berhubungan dengan gangguan] yang berhubungan dengan fungsi trombosit yang abnormal dan Anda mungkin mendapatkan beberapa ide diagnosis dari sejarah klinis dan pemeriksaan.


Sejarah Obat

Ada sejumlah besar obat dan terutama zat makanan yang dapat mengganggu fungsi trombosit.
Darah penuh Count (FBC) dan Film Darah

  1. 1.    Pertimbangkan pseudothrombocytopenia sering karena dingin agglutinins platelet bereaksi atau satellitism trombosit.

Sekitar 0,1% dari populasi menunjukkan pseudothrombocytopenia sehat EDTA-diinduksi dan penting untuk mengecualikan ini sebelum melakukan tes lebih luas dari fungsi platelet. Temuan serupa juga telah dilaporkan dengan penggunaan kedua sitrat dan heparin sebagai antikoagulan. Sebuah film darah dapat mengidentifikasi gumpalan trombosit dan memberikan petunjuk untuk diagnosis.

2. Volume rata-rata trombosit [MPV – referensi kisaran 7-10fL]: MPV adalah parameter sering diabaikan dari FBC tetapi dapat memberikan wawasan ke dalam penyebab dari jumlah platelet yang rendah.
  – Hal ini dapat juga dalam beberapa kasus memberikan petunjuk untuk diagnosis misalnya yang turun-temurun macrothrombocytopenias, Bernard Soulier Syndrome [BSS]
  – Pada individu dengan MPV ditinggikan, hitungan imunologi berbasis trombosit dapat memberikan jumlah trombosit lebih akurat dan sering lebih tinggi secara signifikan.
  – The MPV bisa menjadi indikasi omset platelet – sebuah MPV meningkat menunjukkan izin trombosit dipercepat seperti di ITP atau trombositopenia kehamilan.
  – The MPV dapat dikurangi dalam kasus Wiskott-Aldrich Syndrome dan dalam beberapa kasus kegagalan sumsum tulang.

3. Pemeriksaan film darah dan morfologi trombosit dapat berguna di kedua membangun diagnosis pseudothrombocytopenia tetapi juga dalam membangun misalnya masalah utama platelet Gray trombosit Syndrome.

 

Dalam beberapa kasus trombositopenia misalnya Mei Hegglin anomali – film darah dapat menunjukkan adanya badan DOHLE [. Cahaya biru-abu-abu, oval, basofilik, inklusi leukosit terletak di sitoplasma perifer neutrofil]

Principles of Light Transmission [Born] Aggregometry

Platelet aggregation testing measures the ability of various agonists to platelets to induce in vitro activation and platelet-to-platelet activation. Classically Born aggregometry uses platelet rich plasma [PRP] but whole blood aggregometry can be also used.
In the Born aggregometer, PRP is stirred in a cuvette at 37°C and the cuvette sits between a light course and a photocell. When an agonist is added the platelets aggregate and absorb less light and so the transmission increases and this is detected by the photocell.

You can also see the principles of Born aggregometry as an animation on this site [http://www.platelet-research.org/3/aggregometry.htm]

Light Transmission Aggregometry: Variable

Variable

Explanation

Pre-Analytical Variables Drugs which can interfere with platelet function include aspirin and anti-inflammatory drugs, specific anti-platelet drugs including clopidogrel and imidazole.  However, there are numerous other drugs whose primary role is not to inhibit platelet function but nevertheless can do so e.g. antibiotics, anti-depressants, beta-blockers etc – Click HERE for a list of drugs etc that may affect platelet function tests.Food stuffs
– A high fat diet can lead to the presence of chylomicra in the plasma and interfere with light transmission in aggregation testing.
– Others include garlic, turmeric and caffeine.Platelet count: In individuals with very high or low platelet counts, it may be necessary to adjust the platelet count to achieve a count in the region of 200-400 x 109/L.  For very high counts the count can be adjusted with PPP.  Platelet counts below 200 x 109/L can give rise to diminished aggregation responses.  Although it seems logical to undertake additional centrifugation in such cases to increase the platelet count, in practice this can lead to activation of platelets and is not recommended.

Temperature: Blood samples for platelet aggregation testing should be stored at room temperature.

pH: Platelet aggregation should be carried out at physiological pH.

Fibrinogen Concentration: Platelets will only aggregate (although they may agglutinate) if fibrinogen is present and so it is important to check fibrinogen levels before undertaking platelet aggregation testing.

Anticoagulant: Current guidelines suggest that samples for platelet aggregation testing should be collected into citrate. However, more recent data suggests that heparin , but not citrate, preserves platelet responses for up to 24 h as determined by a range of techniques

Preparation of Platelet Rich Plasma [PRP] Platelets are very sensitive and can be readily activated during the preparation of PRP.Anticoagulant: Venous blood with minimal venous occlusion, is collected into 3.2%/0.109M citrate in a ratio of 1:9 [1 part anticoagulant to 9 parts blood.] Whole blood samples should be processed within 4 hours of collection.

Blood samples for platelet aggregation testing should be stored at room temperature – cooling platelets can lead to activation.

Transport samples to the laboratory at room temperature. PRP is prepared by centrifugation at 20°C for 10-15 minutes at 150-200

g. The PRP is carefully removed and placed into a stoppered plastic tube. PRP should be stored at room temperature. PPP can be prepared by further centrifugation of the remaining plasma at 2700g for 15 minutes.

Agonists Addition of a platelet agonist to the PRP leads to platelet activation, a change in their shape from discoid to spiny spheres which is associated with a transient increase in optical density. The only exceptions to this are epinephrine in which there is no shape change and ristocetin which causes platelet agglutination rather than aggregation i.e. there is no binding of fibrinogen. There are two types of agonists:Strong Agonists e.g. Collagen, thrombin, TxA2: These directly induce platelet aggregation, TxA2 synthesis and platelet granule secretion.

Weak Agonists e.g. ADP & epinephrine: These induce platelet aggregation without inducing secretion. 

Platelet secretion can sometimes follow aggregation induced by a weak agonist, when the synthesis of endogenous TxA2 is triggered by the close platelet-to-platelet contact that occurs during platelet aggregation.

Strong agonists, when used at low concentrations, may act like weak agonists, but weak agonists even at high concentrations will not act as strong agonists.

With some weak agonists [ADP and adrenaline] at critical concentrations, the platelet aggregation curve has a biphasic appearance: an initial wave of aggregation (primary wave), followed by a secondary wave of aggregation, which is usually irreversible [see illustration below.] Secondary wave aggregation may not occur and the primary wave may disaggregate. At higher agonist concentrations (except with epinephrine) the two waves of aggregation combine and only a single wave is seen and the biphasic waveform is absent.

The aggregation response to an agonist is amplified by the production of TxA2 from membrane phospholipids and by the secretion of ADP from the dense granules.  ADP and TxA2 are agonists, which, by interacting with their specific receptors, amplify the aggregation response of the platelet.

Top of Form

Transmisi cahaya Aggregometry:

 

Variable
Variabel Penjelasan
Pra-Analytical Variabel Obat yang dapat mengganggu fungsi trombosit meliputi obat aspirin dan anti-inflamasi, spesifik obat anti-platelet termasuk clopidogrel dan imidazol. Namun, ada banyak obat lain peran utamanya adalah bukan untuk menghambat fungsi trombosit namun demikian dapat melakukannya misalnya antibiotik, anti-depressants, beta-blocker dll – Klik DI SINI untuk daftar dll obat yang dapat mempengaruhi tes fungsi platelet.

Bahan makanan
– Diet tinggi lemak dapat menyebabkan kehadiran chylomicra dalam plasma dan mengganggu transmisi cahaya dalam pengujian agregasi.
– Lainnya termasuk bawang putih, kunyit dan kafein.

Platelet count: (perhitungan Thrombosit)

 

Pada individu dengan jumlah trombosit yang sangat tinggi atau rendah, mungkin perlu untuk menyesuaikan jumlah trombosit untuk mencapai hitungan di wilayah 200-400 x 109 / L.

 

 Untuk jumlah yang sangat tinggi menghitung dapat disesuaikan dengan PPP. Jumlah trombosit di bawah 200 109 L x / dapat menimbulkan respon agregasi berkurang.

 

 Meskipun tampaknya logis untuk melakukan sentrifugasi tambahan dalam kasus tersebut untuk meningkatkan jumlah trombosit, dalam praktek ini dapat menyebabkan aktivasi trombosit dan tidak dianjurkan.

Suhu: Sampel darah untuk pengujian agregasi platelet harus disimpan pada suhu kamar.

pH: agregasi trombosit harus dilakukan pada pH fisiologis.

Konsentrasi fibrinogen:

 

Trombosit hanya akan agregat (meskipun mereka mungkin mengaglutinasi) jika fibrinogen hadir dan sehingga sangat penting untuk memeriksa tingkat fibrinogen sebelum melakukan pengujian agregasi platelet.

 

 

 

 

Antikoagulan:

 

Pedoman saat ini menunjukkan bahwa sampel untuk pengujian agregasi platelet harus dikumpulkan ke sitrat.

 

Namun, data yang lebih baru menunjukkan bahwa heparin, tetapi tidak sitrat, menjaga respon trombosit sampai 24 jam sebagaimana ditentukan oleh berbagai teknik

Persiapan Plasma Kaya trombosit [PRP] Trombosit sangat sensitif dan dapat dengan mudah diaktifkan selama persiapan PRP.

Antikoagulan: vena darah dengan oklusi vena minimal, yang dikumpulkan ke 3,2% / sitrat 0.109M dalam rasio 1:9 [1 bagian antikoagulan untuk 9 bagian darah.]

Seluruh sampel darah harus diproses dalam waktu 4 jam dari koleksi.

Sampel darah untuk pengujian agregasi platelet harus disimpan pada suhu kamar – trombosit pendinginan dapat menyebabkan aktivasi.

Transportasi sampel ke laboratorium pada suhu kamar. PRP disiapkan oleh sentrifugasi pada 20 ° C selama 10-15 menit pada 150-200g.

 

PRP ini dengan hati-hati dihapus dan ditempatkan dalam tabung plastik tutup. PRP harus disimpan pada suhu kamar.

 

PPP dapat dibuat dengan sentrifugasi lebih lanjut dari plasma yang tersisa pada 2700g selama 15 menit.


Agonis

 

Penambahan suatu agonis trombosit untuk PRP mengarah ke aktivasi trombosit, perubahan dalam bentuk mereka dari diskoid ke bola berduri yang dikaitkan dengan peningkatan transien dalam densitas optik.

 

Satu-satunya pengecualian untuk ini adalah epinephrine yang tidak ada perubahan bentuk dan ristocetin yang menyebabkan aglutinasi platelet daripada agregasi yaitu tidak ada pengikatan fibrinogen.

Ada dua jenis agonis:

Kuat Agonis mis Kolagen, trombin, TXA2: Ini secara langsung menginduksi agregasi platelet, TXA2 sintesis dan sekresi granul trombosit.

Lemah Agonis mis ADP & epinefrin: Ini menginduksi agregasi platelet tanpa mendorong sekresi.

Sekresi platelet(thrombosit) terkadang dapat mengikuti agregasi disebabkan oleh agonis lemah, ketika sintesis TXA2 endogen dipicu oleh kontak platelet-to-platelet dekat yang terjadi selama agregasi platelet.

Agonis yang kuat, bila digunakan pada konsentrasi rendah, dapat bertindak seperti agonis lemah, tetapi agonis lemah bahkan pada konsentrasi tinggi tidak akan bertindak sebagai agonis yang kuat.

Dengan beberapa agonis lemah [ADP dan adrenalin] pada konsentrasi kritis, kurva agregasi platelet memiliki penampilan biphasic:

 

[. Lihat ilustrasi di bawah ini]

 

gelombang awal agregasi (gelombang primer), diikuti oleh gelombang sekunder agregasi, yang biasanya ireversibel agregasi gelombang sekunder tidak mungkin terjadi dan gelombang primer mungkin memisahkan. Pada konsentrasi agonis yang lebih tinggi (kecuali dengan epinefrin) dua gelombang agregasi menggabungkan dan hanya gelombang tunggal terlihat dan gelombang biphasic tidak ada.

Tanggapan agregasi untuk agonis yang diperkuat oleh produksi TXA2 dari fosfolipid membran dan oleh sekresi ADP dari butiran padat. ADP dan TXA2 adalah agonis, yang, dengan berinteraksi dengan reseptor khusus mereka, memperkuat respon agregasi platelet.

Commonly used Agonists in Light Transmission Aggregometry

Commonly used agonists, their working concentration and mode of action are listed below. In practice many laboratories use a number of agonists and various dilutions but vary the actual agonists or agonist concentration depending upon the results of initial tests and the suspected abnormality. Not all laboratories necessarily use the concentrations shown below e.g. some labs may use collagen at 5μg/mL rather than 4μg/mL.
It is useful to consider the role of these various agonists by looking at an image of a platelet and the various receptors that are activated by the agonists discussed below and how these interact with the platelet.
This
LINK takes you to an image that you may find useful to consider with the table below and this REFERENCE is to a paper that summarises the traces seen with various agonists.

 

 

 

 

Umumnya digunakan Agonis di Aggregometry Transmisi Cahaya


Agonis umum digunakan, konsentrasi kerja dan cara kerja yang tercantum di bawah ini.

 

Dalam prakteknya banyak laboratorium menggunakan sejumlah agonis dan pengenceran berbagai tapi bervariasi agonis aktual atau konsentrasi agonis tergantung pada hasil tes awal dan kelainan yang dicurigai.

 

Tidak semua laboratorium tentu menggunakan konsentrasi yang ditunjukkan di bawah misalnya beberapa laboratorium dapat menggunakan kolagen di 5μg/mL daripada 4μg/mL.


Hal ini berguna untuk mempertimbangkan peran tersebut agonis berbagai dengan melihat gambar trombosit dan reseptor berbagai yang diaktifkan oleh agonis dibahas di bawah ini dan bagaimana berinteraksi dengan platelet ini.

LINK ini akan membawa Anda ke gambar yang Anda mungkin menemukan berguna untuk mempertimbangkan dengan tabel di bawah ini dan REFERENSI ini adalah sebuah makalah yang merangkum jejak dilihat dengan berbagai agonis.

 

Agonist

Working Concentration

Comment

ADP Low dose: 1, 2.5, 5μMHigh dose: 10μM 

 

 

 

 

 

 

 

Dosis rendah: 1, 2,5, 5μM

Dosis tinggi: 10ìm

ADP binds to the ADP receptor on the surface of platelets.  Initial binding results in the release of intracellular calcium and a change in the shape of the platelet leading to the primary wave of aggregation.  The secondary wave reflects the release of ADP from platelet storage granules.
Low dose ADP induces only primary aggregation and the effect is reversible. ADP and arachadonic acid are considered mild platelet agonists.
ADP binds to two G-protein coupled receptors: P2Y1 and P2Y12. Binding of ADP to the P2Y1 receptor induces shape change and initiates primary wave platelet aggregation through calcium mobilisation. The P2Y12 receptor is considered to be the major ADP receptor and responsible for full platelet aggregation through the inhibition of adenyl cyclase.
The P2Y12 receptor is also the target for clopidogrel. With both ADP and Arachadonic acid – this second wave of aggregation is inhibited by aspirin and NSAID’s.
ADP mengikat ke reseptor ADP pada permukaan trombosit. Awal mengikat hasil dalam pelepasan kalsium intraseluler dan perubahan dalam bentuk platelet (thrombosit) menyebabkan gelombang utama agregasi.  

Gelombang sekunder mencerminkan pelepasan ADP dari butiran penyimpanan trombosit.

ADP dosis rendah hanya menginduksi agregasi primer dan efeknya reversibel. ADP dan asam arachadonic dianggap agonis trombosit ringan.

ADP mengikat dua G-protein reseptor coupled: P2Y1 dan P2Y12. Pengikatan ADP ke reseptor P2Y1 menginduksi perubahan bentuk dan memulai agregasi platelet gelombang primer melalui mobilisasi kalsium. Reseptor P2Y12 dianggap reseptor ADP utama dan bertanggung jawab atas agregasi platelet penuh melalui penghambatan adenilat adenyl.
Reseptor P2Y12 juga merupakan target untuk clopidogrel. Dengan kedua ADP dan asam arachadonic – ini gelombang kedua agregasi dihambat oleh aspirin dan NSAID

Collagen 1, 4μg/mL Collagen binds to the GpVI and GpIa/IIa receptors inducing granule release, TXA2 generation and then sustained GPIIb-IIIa activation.
The GpIa/IIa receptor is involved in platelet adhesion. The GpVI receptor is involved in platelet signalling and TXA2 generation.
A lag phase is seen with collagen following addition of the agonist to the PRP and usually <1 minute.
Kolagen mengikat merangsang reseptor rilis GpVI dan GPIA / IIa granul, TXA2 generasi dan kemudian berkelanjutan GPIIb-IIIa aktivasi.
Reseptor GPIA / IIa terlibat dalam adhesi platelet. Reseptor GpVI terlibat dalam signaling platelet dan TXA2 generasi.
Sebuah fase lag terlihat dengan penambahan kolagen berikut agonist untuk PRP dan biasanya <1 menit
Ristocetin Low dose: 0.5mg/mLHigh dose: 1.5, 5mg/mL Ristocetin (but not generally in low dose i.e. 0.5 mg/mL) causes platelet agglutination (and not aggregation) through the VWF and GPIb-IX-V complex. [Platelet aggregation requires the binding of fibrinogen to the platelet via the GpIIb-IIIa complex.]Ristocetin (tapi tidak umumnya dalam dosis rendah yaitu 0,5 mg / mL) menyebabkan aglutinasi platelet (dan tidak agregasi) melalui VWF dan GPIB-IX-V kompleks. [Agregasi trombosit membutuhkan pengikatan fibrinogen ke platelet melalui kompleks GpIIb-IIIa.]
Adrenaline 5, 10μM Adrenaline binds to the á2-adrenergic receptor on the surface of platelets leading to inhibition of adenyl cyclase and the release of calcium ions. Aggregation of platelets with Adrenaline is similar to that of ADP with an initial primary wave of aggregation, the release of stored ADP from the platelet dense bodies and second wave sustained aggregation. As with ADP, this second wave of aggregation is inhibited by aspirin and NSAIDs. Adrenaline is considered [as is ADP] to be a weak agonist. However, defects in signalling through the á2-adrenergic have been associated with a bleeding disorder.A small proportion of the population may not always show full aggregation to adrenaline due to natural variations in adrenoreceptor numbers. Such individuals have not related platelet defect. 

 

Adrenalin mengikat reseptor 2-adrenergik á pada permukaan platelet menyebabkan penghambatan adenyl cyclase dan pelepasan ion kalsium. Agregasi trombosit dengan Adrenalin adalah mirip dengan ADP dengan gelombang primer awal agregasi, pelepasan ADP disimpan dari tubuh padat platelet dan gelombang kedua agregasi berkelanjutan. Seperti ADP, ini gelombang kedua agregasi dihambat oleh aspirin dan NSAID. Adrenalin dianggap [seperti ADP] menjadi agonis lemah. Namun, cacat pada sinyal melalui adrenergik 2-á telah dikaitkan dengan gangguan perdarahan.

Sebagian kecil dari populasi mungkin tidak selalu menunjukkan agregasi penuh untuk adrenalin karena variasi alami dalam jumlah adrenoreseptor. Orang-orang seperti tidak terkait cacat platelet

Arachadonic Acid 500μg/mL Arachadonic Acid is the precursor of thromboxane A2 [TXA2] within platelets. Arachadonic Acid is converted to TXA2 by cyclooxygenase and thromboxane synthase. TXA2 is a potent inducer of platelet aggregation causing granule release, more TXA2 generation and then sustained GpIIb-IIIa activationAsam arachadonic adalah prekursor tromboksan A2 [TXA2] dalam trombosit. Asam arachadonic diubah menjadi TXA2 oleh siklooksigenase dan tromboksan sintase. TXA2 merupakan inducer kuat dari agregasi platelet menyebabkan pelepasan granul, generasi yang lebih TXA2 dan kemudian berkelanjutan GpIIb-IIIa aktivasi
Thrombin Low dose: 50nmol/LHigh dose: 100nmol/L Thrombin is the most potent physiological activator of platelets and protease-activated receptors 1 (PAR1) and 4 (PAR4) are activated by thrombin. PAR1 and PAR4 are members of a 7-transmembrane group of G-protein coupled receptors that are activated by a single cleavage within the N-terminal domain to generate a new N-terminus which activates the G-subunits and intracellular signalling.Thrombin induces platelet aggregation at low concentration [50nmol/L] but at this dose it is insufficient to induce full aggregation but binds to platelets and induces a shape change. At a higher concentration (100nmol/L), thrombin induces full aggregation.Trombin adalah aktivator fisiologis paling ampuh trombosit dan protease-diaktifkan reseptor 1 (par1) dan 4 (PAR4) yang diaktifkan oleh trombin. Par1 dan PAR4 adalah anggota dari kelompok 7-transmembran G-protein reseptor yang digabungkan diaktifkan oleh pembelahan tunggal dalam domain N-terminal untuk menghasilkan N-terminus baru yang mengaktifkan G-subunit dan sinyal intraseluler.

Trombin menginduksi agregasi platelet pada konsentrasi rendah [50nmol / L] tetapi pada dosis ini tidak cukup untuk menginduksi agregasi penuh tetapi mengikat platelet dan menginduksi perubahan bentuk. Pada konsentrasi yang lebih tinggi (100nmol / L), trombin menginduksi agregasi penuh.

Platelet hyperaggregation and increased plasma level of von Willebrand factor in diabetics with retinopathy

Look Inside Get Access

Summary

In 18 insulin-dependent diabetics (6 without retinopathy, 6 with proliferative retinopathy and 6 with proliferative retinopathy treated by hypophysectomy) matched for age and duration of diabetes, in vitro haemostasis was studied using ADP induced platelet aggregation, ristocetin induced platelet aggregation which allows von Willebrand factor (VIII VWF) assay, and determination of antihemophilic factor procoagulant activity (VIII AHF). Using gel filtration-isolated platelets, the ADP induced hyperaggregation previously reported in diabetics with severe retinopathy untreated by hypophysectomy appeared to be related to a platelet and not a plasma factor; the normal results of thrombin induced aggregation suggests that the presumed abnormal platelet factor is related to the platelet plasma membrane. High level of plasma VIII VWF was observed in diabetics with proliferative retinopathy while the VIII AHF level was within normal limits.

Supported by a grant from the Institut National de la Santé et de la Recherche Médicale (I.N.S.E.R.M.)

Presented in part at the EASD 10th Annual Meeting, Jerusalem, 1974

Chargée de Recherche au C.N.R.

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Platelet hiperagregasi dan tingkat plasma peningkatan faktor von Willebrand pada penderita diabetes dengan retinopati
• D. Bensoussan,
• S. Levy-Toledano,
• P. Passa,
• J. Caen,
• J. Canivet


Terlihat dalam Dapatkan Akses
ringkasan


Pada 18 insulin-dependent diabetes (6 tanpa retinopati, 6 dengan retinopati proliferatif dan 6 dengan retinopati proliferatif dirawat oleh hypophysectomy) cocok untuk usia dan durasi diabetes, dalam hemostasis vitro dipelajari dengan ADP agregasi platelet diinduksi, ristocetin diinduksi agregasi platelet yang memungkinkan von Willebrand factor (VWF VIII) assay, dan penentuan aktivitas prokoagulan faktor antihemophilic (VIII AHF).

 

Menggunakan gel filtrasi-terisolasi trombosit, ADP diinduksi hiperagregasi sebelumnya dilaporkan pada penderita diabetes dengan retinopati parah diobati dengan hypophysectomy tampaknya berkaitan dengan faktor trombosit dan plasma tidak, hasil normal trombin diinduksi agregasi menunjukkan bahwa faktor trombosit dianggap abnormal terkait ke membran plasma platelet.

 

Tinggi tingkat plasma VIII VWF diamati pada penderita diabetes dengan retinopati proliferatif sementara tingkat VIII AHF adalah dalam batas normal.


Didukung oleh hibah dari Institut National de la Sante et de la Recherche Médicale (INSERM)

Disajikan dalam bagian pada Pertemuan Tahunan ke-10 EASD, Yerusalem, 1974
Chargée de Recherche au C.N.R

Fenomena Sindroma Kekentalan Darah (Sindroma Hughes)

OPINI | 30 April 2011 | 16:06 Dibaca: 4895   Komentar: 10   4 aktual

 

Dari Stroke hingga Keguguran

Definisi Sindroma Darah Kental ini adalah keadaan dimana darah lebih mudah menggumpal, mudah membeku dan mengental dibanding darah normal, sehingga mengakibatkan aliran darah terputus sehingga suplai zat nutrisi pada jaringan yang di lewatinya menjadi terhenti dan mengakibatkan kematian pada jaringan tersebut.

Karena terjadi di dalam darah dan bisa menganggu sirkulasinya, maka gejala yang ditimbulkan sindroma darah kental cukup luas.

Semua organ dapat terkena dan akan menunjukkan gejala sesuai dengan organ yang bersangkutan.

 

Di mata, misalnya, bisa mengakibatkan penglihatan menjadi kabur sampai kebutaan akibat sumbatan total.

 Di telinga, gejalanya bisa berdengung/berdenging (tinitus), vertigo, gangguan pendengaran dan ketulian.

Kekentalan darah juga bisa mengenai sistem saraf. 

Gejala kekentalan darah yang paling sering ditemukan adalah sakit kepala, nyeri kepala migrain, kejang, gangguan kognitif dan bahkan stroke.

 Yang khas , tidak seperti umumnya, penderita stroke akibat kekentalan darah biasanya berusia muda.

Kekentalan darah sangat ditakuti jika menyebabkan sumbatan pada pembuluh darah jantung. Karena bisa menyebabkan serangan jantung tiba-tiba.

Disamping itu dapat menyebabkan nyeri dada (angina pectoris) dan kerusakan katup jantung (insufisiensi mitral).

Pada organ reproduksi wanita, sindroma ini bisa menimbulkan gejala berupa keguguran yang berulang, infertilitas, eklamsia-preeklamsia, dan kelahiran prematur. Bila kekentalan darah menyebabkan sumbatan di kaki atau tangan, maka keluhan yang timbul pun beragam.

Sumbatan yang ringan hanya menimbulkan gejala pegal-pegal, sedangkan sumbatan yang besar bisa mengakibatkan rasa nyeri dan pembengkakan sering dikelirukan dengan penyakit rematik.

 

Pada dasarnya keadaan hiperkoagulasi dan hiperagregasi trombosit pada sindroma darah kental (sindroma hughes) bisa ditemukan di semua pembuluh darah dalam tubuh.

Yang perlu dicatat, lokasi penyumbatan pada pasien dengan sindrom ini bahkan bisa terjadi pada tempat-tempat yang tidak biasa.

 Antara lain pembuluh darah yang bertanggung jawab memberi suplai pada organ ginjal, paru, hati dan saluran cerna lainnya.

Pengobatan Sederhana

             Walau diagnosis sindroma darah kental sulit ditegakkan, sebenarnya pengobatannya cukup sederhana.

Ada dua jenis obat untuk sindroma darah kental ini, yaitu antikoagulasi (anti pembekuan darah) misalnya heparin dan warfarin, dan anti agregasi trombosit (antiplatelet) contohnya aspirin.

 Keduanya bertugas membuat darah menjadi encer, dengan mempengaruhi proses koagulasi dan trombosit.

            Pengobatannya yang sederhana bukan berarti mudah dan tanpa efek samping.

 Efek samping.

 Efek samping berupa pendarahan perlu terus dipantau. Selama menggunakan obat-obatan ini keadaan darah penderita harus selalu dikontrol dengan melakukan pemeriksaan laboratorium dalam periode tertentu.

Pemeriksaan laboratorium

            Biasanya point pemeriksaan darah di laboratorium disamping darah rutin (hemoglobin, hematokrit, lekosit, trombosit, hitung jenis darah) juga faal hemostasis seperti Waktu Pembekuan (CT), Retraksi Bekuan, APTT, Waktu Protrombin (PT), Agregasi Trombosit, Waktu Protrombin, D-Dimer, Fibrinogen, ACA IgG, ACA IgM, AT III, Waktu Trombin (TT), Von Willebrand Faktor (vWF) dan Viskositas Darah

http://kesehatan.kompasiana.com/medis/2011/04/30/fenomena-sindroma-kekentalan-darah-sindroma-hughes/

 

The 6th Congress of Asia Pacific Society on Thrombosis and Haemostatis (APSTH Bali 2010)
Terapi Antikoagulan pada
Fetal Loss Syndrom Terkait APS
 
SIMPOSIA Edisi Desember 2010 (Vol.10 No.5)


Sindroma Antifosfolipd atau Antiphospholipid syndrome (APS) adalah satu dari dua penyakit baru yang ditemukan di abad ke-20 selain AIDS. Penyakit ini ditandai dengan adanya antibodi antifosfolipid (APL) yang merusak protein-protein yang terlibat dalam koagulasi dan antikoagulasi seperti protrombin, protein C, protein S, dan antitrombin III. 

 Hingga saat ini, atau lebih dari 100 tahun setelah ditemukan pertama kali,

 

APL masih belum sepenuhnya dipahami.  Dalam penelitian in vitro, antibodi ini termasuk ke dalam kelas heterogenus antibodi autoreaktif yang memiliki waktu beku panjang. Namun dalam penelitian in vivo, ia berkaitan dengan tromboemboli arteri maupun vena.

 

APL dalam manifestasi klinis, selain merupakan faktor risiko terjadinya trombosis vena maupun arteri, dari sisi ilmu kebidanan menjadi penyebab fetal loss syndrom atau keguguran berulang.

APL juga berkaitan dengan penyakit jantung valvular,

mikroangiopati ginjal, trombositopenia, dan gangguan kognitif.

 

APS katastropik adalah salah satu bentuk APS yang jarang ditemukan, yakni kegagalan multiorgan akibat trombosis (terutama mikrovaskular) yang menyebar. Tingkat kematian pada APS katastropik amat tinggi.

 

 

 

 

“Untuk mendiagosa APS, tidak terbatas pada kondisi klinis, namun tantangan utama adalah menemukan antibodi-antobodi yang signifikan tidak terbatas pada beta2-glikoprotein (GPI) yang menandakan APL positif,” jelas Dr. Christopher Ward dari Departemen Hematologi dan Kedokteran Transfusi, Royal North Shore Hospital, Australia. Ward berbicara dalam The 6th Congress of Asia Pacific Society on Thrombosis and Haemostatis (APSTH) di Bali, pertengahan Oktober tahun ini.

 

Kriteria diagnosis terkini untuk APS, tambah Ward, adalah adanya tromboemboli pada arteri, vena, dan mikrovaskular serta kejadian obstetrik yang menunjukkan adanya APL persisten. APL  yang bersifat sementara bisa juga patogenik, namun dibutuhkan bukti lain yang memperkuat diagosis.

 

Penyakit-penyakit autoimun yang juga menghadirkan tromboemboli, menurut beberapa studi cohort, harus dibedakan meskipun pada pasien tromboemboli seringkali disertai juga dengan penyakit autoimun. APL yang asimptomatik bukan menjadi indikasi dilakukan profilaksis.

 

Terapi untuk tromboemboli vena terkait ditemukannya APL adalah antikoagulan yang efektif, seperti vitamin K-antagonis dan heparin.

 

Namun penelitian terbaru menunjukkan terapi warfarin dengan intensitas tinggi (INR >3) tidak dibutuhkan oleh mayoritas pasien.

APL merupakan faktor risiko yang spesifik untuk kegagalan terapi warfarin, sehingga INR terapetik pasien harus dipertahankan. “Ada bukti peningkatan risiko APS rekuren, oleh karena itu pemberian warfarin yang tidak perlu atau dalam jangka waktu lama harus dipertimbangkan kembali, terutama setelah tromboemboli vena (VTE) pertama” jelas Ward.

 

 

 

Terapi Low molecular weight-heparin (LMVH) bisa diberikan dan terbukti bermanfaat untuk pasien APS yang gagal dengan warfarin.

 

 Sedangkan antikoagulan oral atau penghambat trombin belum diketahui efikasinya.

 

Pada intinya, manajemen tromboemboli arteri pada APS yang terbaik belum ditemukan. Namun di awal terapi bisa diberikan kombinasi antikoagulan dan antiplatelet.

 

Untuk mencegah keguguran berulang atau masalah obstetrik lainnya pada wanita dengan APL, bisa diberikan profilaksis heparin plus aspirin secara rutin, namun dasar ilmiahnya juga masih terbatas. 

 

Dipaparkan Lee Lai Heng dari Departemen Hematologi, Singapore General Hospital,   LMVH dikombinasikan dengan aspirin cukup efektif seperti halnya UFH plus aspirin dalam mencegah keguguran berulang akibat APS.

 

Pasien yang tidak tengah menjalani terapi antikoagulan, harus diberi aspirin sebelum konsepsi, dilanjutkan pemberian LMWH atau heparin ketika terjadi kehamilan.

 

 Pasien yang menjalani terapi warfarin dalam waktu lama untuk trombosis yang dialami sebelumnya, harus dipertimbangkan dengan serius sebelum di-switch ke LMWH sebelum konsepsi untuk melihat efek teratogenik warfarin. Jika pasien akan mulai terapi dengan LMWH setelah konsepsi, sebaiknya dilakukan di usia kehamilan 6 minggu. 

“Selama terapi harus dilakukan monitoring untuk mendeteksi masalah yang mungkin timbul seperti komplikasi pendarahan akibat trombositopenia terkait penggunaan heparin,” jelas Lee.

 

 

Untuk memastikan kelahiran yang aman, terapi antikoagula harus dihentikann 24 jam sebelum kelahiran dengan operasi. Setelah kelahiran, baik warfarin maupun LMWH dikonjugasi dengan stoking kompresi elastis harus dilanjutkan sebagai profilkasis VTE maternal pada periode post-partum.

Profilaksi Fetal Loss Syndrome dengan kalsium nadroparin

Dijelaskan DR. dr. Djumhana Atmakusuma, dari Divisi Hematologi dan Trombosis, Departemen Penyakit Dalam FKUI/RSCM, gangguan koagulasi , sebagai konsekuensi penyakit autoimun, menjadi penyebab utama keguguran berulang. Angkanya mencapai 50-60% jika dibandingkan penyebab lain seperti abnormalitas kromosom (10%), gangguan anatomi (10%), dan masalah hormon (15-20%).

Gangguan koagulasi atau pembekuan darah yang menyebabkan keguguran, amat luas. Bisa disebabkan APS, trombositopenia, trombofilia, defisiensi antitrombin III (AT III), protein C dan Protein S, atau karena hipofibrinolisis, resistensi APC, dan faktor V leiden.

The American College of Chest Physician  (APCC) tahun 2001 merekomendasikan terapi LMWH seperti enoxaparin, sebagai profilaksis antikoagulan dalam mencegah risiko keguguran berulang.

 

Alternatif lain adalah pemberian kalsium nadroparin yang merupakan kelompok antikoagulan parenteral. Kalsium nadroparin selama ini digunakan untuk mencegah dan menangani VTE. Apakah ia cukup efektif dan aman untuk fetal loss syndrome?

Penelitian pernah dilakukan dengan melihat data pemberian kalsium nadroparin pada perempuan hamil di salah satu rumah sakit di Jakarta, antara tahun 2000-2004. Ada 648 (dari 731) subyek penelitian, yang mendapat terapi dan bisa dievaluasi. 77, 32% subyek memiliki gejala gangguan sirkulasi dan penyakit autoimun.

 

Dari seluruh subyek, 49% memiliki riwayat aborsi spontan, 6% memiliki riwayat IUFD, 2% memilki riwayat kematian perinatal dan lainnya. Dari 648 pasien, 239 (73%) tangah hamil saat kunjungan pertama, 126 (20%) hamil setelah beberapa kali kunjungan, dan 283 (45%) dalam kondisi masih hamil.

 

Hasil tes laboratorium menujukkan pasien-pasien ini mengalami trombositosis (1,8%), hiperagregasi platelet (45,5%), hiperkoagulasi (56%), hiperfibrinogenemia (19,3%), defisiensi protein C (14,7%), defisiensi protein S (36,5%), dan defisiensi AT III (18,6%). Uji antibodi antifosfolipid (APL) menunjukkan ACA IgG moderat pada 2,7% (tes 1), tinggi pada 0,3% (tes 1), ACA IgM moderat pada 5,6% (tes 1), 5,9% (tes 2), dan 4% (tes 3). Sedangkan ACA IgG tinggi ditemukan pada 2,4% (tes 1),  2,2% (tes 2), dan 4% (tes 3).

 

Ada 234 subyek yang menerima profilaksis suntikan kalsium nadroparin, kebanyakan dikombinasi dengan aspirin dosis rendah. 181 bisa di-follow up dan sebanyak 166 subyek bisa melahirkan bayi dan 14 orang mengalami keguguran.

 

Efek samping selama terapi adalah gatal di seluruh tubuh (10 orang), gatal di bekas suntikann (43 orang) dan purpura (1 orang)

. Di luar pemberia kalsium nadroparin, ada 12 pasien yang menerima enoxapoarin dan 6 orang riteraoi dengan UFH.

APS katastropik

Di awal sempat disinggung tentang APS katastropik (CAPS) yang bisa berdampak kematian. Dijelaskan Dr. Inho Kim dari Seoul National University Hospital, Korea Selatan,

 

APS katastropik dilaporkan kurang dari 1% dari prevalensi APS.  CAPS didefinisikan sebagai kondisi yang dikarakteristikkan dengan kejadian penyumbatan vaskular yang multipel, biasanya menyerang pembuluh-pembuluh darah mikro dan hasil uji lab menunjukkan adanya antibodi antifosfolipid.

 

Dulu tingkat kematian akibat CAPS mencapai 50%, meskipu saat ini sudah turun hingga “hanya” 20%.

Turunnya angka kematian akibat CAPS disebabkan peningkatan terapi dengan antikoagulan, kortikosteroid, dan pergantian plasma.

 

Salah satu studi tentang CAPS menunjukkan bahwa tingkat kesembuhan tertinggi (77,8%) diperoleh melalui terapi kombinasi antikoagulan, kortikosterpid, dan peragntian plasma ini.  Konsensus internasional pun merekpomendasikan kombinasi 3 terapi ini sebagai terapi lini pertama CAPS.

 

Saat ini penggunaan imunoglobulin intravena (IVIG) belum banyak dipraktikkan untuk CAPS.

 

Terapi kombinasi antikoagulan+ kortikosteroid+ IVIG tidak menunjukkan tambahan manfaat (recovery 69%) dibandingkan kombinasi antikoagulan, kortikosterpid, dan peragntian plasma (77,8%).

 

Namun penggunaan IVIG bisa digunakan jika tidak ada terapi penggantian plasma.

 

Hanya penggunaannya harus hati-hati pada pasien usia lanjut yang komorbid dengan diabetes, hipertensi atau hiperkolesterolemia.(Ana/Bali)

 

Method

Platelet aggregometry is performed as follows:

metode
Aggregometry trombosit dilakukan sebagai berikut

Step

 

1 Platelet aggregometry is performed at 37°C.
2 The aggregometer is calibrated by:
– A cuvette containing PRP which equates to 0% light transmission
– A second cuvette containing PPP which equates to 100% light transmission.
3 Platelets will only aggregate if they are activated (with an agonist) and in contact with each other – so they must be stirred whilst testing is taking place. Absence of stirring will lead to an absence of, at least a significant reduction in, aggregation.A check for spontaneous platelet aggregation [SPT] is made.SPA is rare in healthy individuals but seen in some cases of VWD, in some patients with diabetes, in some lipid disorders and in a variety of other disorders] should be made in all patients by placing undiluted PRP in the aggregometer and stirring for 15 minutes.  In cases of SPA, dilution of the PRP may abolish this and if the platelet count remains >200 x 109/L then aggregation testing can proceed.

Trombosit hanya akan agregat jika mereka diaktifkan (dengan agonis an) dan kontak dengan satu sama lain – sehingga mereka harus diaduk sementara pengujian berlangsung. Tidak adanya pengadukan akan mengakibatkan tidak adanya, setidaknya penurunan yang signifikan dalam, agregasi.

Sebuah cek untuk agregasi platelet spontan [SPT] dibuat.

SPA jarang terjadi pada orang sehat, tetapi dilihat dalam beberapa kasus VWD, pada beberapa pasien dengan diabetes, dalam beberapa gangguan lipid dan berbagai gangguan lain harus] dibuat pada semua pasien dengan menempatkan PRP murni di aggregometer dan diaduk selama 15 menit . Dalam kasus SPA, cairan PRP dapat menghapus ini dan jika jumlah trombosit tetap> 200 x 109 / L maka pengujian agregasi dapat melanjutkan

4 In general – 270μL of PRP is added to the aggregometry cuvette and warmed at 37°C until a steady baseline is achieved. 30μL of the agonist is added the response recorded.The tests are repeated using a panel of agonists.

Secara umum – 270μL dari PRP ditambahkan ke kuvet aggregometry dan dihangatkan pada 37 ° C sampai dasar stabil tercapai.

30μL agonis tersebut akan ditambahkan respon direkam.

Tes diulang dengan menggunakan sebuah panel agonis

 

 

 

 

 

The following aggregation trace shows the events in classic biphasic aggregation:

Jejak agregasi berikut menunjukkan peristiwa di agregasi biphasic klasik

 


1. Baseline
2. Addition of agonist – this results in a change in platelet change and hence a drop in the baseline absorbance
3. Primary wave aggregation
4. Release of nucleotides
5. Secondary wave aggregation

dasar
2. Penambahan agonis – ini menghasilkan perubahan dalam perubahan trombosit dan karenanya penurunan absorbansi dasar
3. Primer gelombang agregasi
4. Pelepasan nukleotida
5. Sekunder gelombang agregasi


Adrenaline and low dose ADP classically give a biphasic aggregation curve whereas with a number of other agonists only a single wave is seen and it is not possible to distinguish the primary wave from the secondary wave.

Adrenalin dan dosis rendah ADP klasik memberikan kurva agregasi biphasic sedangkan dengan sejumlah agonis lain hanya gelombang tunggal terlihat dan tidak mungkin untuk membedakan gelombang primer dari gelombang sekunder.

 

Interpretation

Calculating the slope or the rate of aggregation

Look at the image below:

interpretasi
Menghitung kemiringan atau tingkat agregasi
Lihatlah gambar di bawah ini

Historically, percentage [%] maximal aggregation has been reported when analysing aggregation curves. To calculate the % maximal aggregation, the distance between the baseline [0% aggregation – platelet rich plasma] and platelet poor plasma [100% aggregation] [Y] is divided by the maximal aggregation [X]. So in the example above if the Y = 100mm and X = 87mm then percentage maximal aggregation = X/Y = 87%.

Secara historis, persentase [%] agregasi maksimal telah dilaporkan ketika menganalisis kurva agregasi. Untuk menghitung agregasi% maksimal, jarak antara baseline [agregasi 0% – plasma kaya platelet] dan plasma miskin trombosit [100% agregasi] [Y] dibagi oleh agregasi maksimal [X]. Jadi, dalam contoh di atas jika Y = 100mm dan X = 87mm maka persentase agregasi maksimal = X / Y = 87%

To calculate the slope [and this forms the basis of the VWF:RCo functional assay]:
1. Draw a line at a tangent to the aggregation curve.
2. Determine how many millimetres [mm] the chart recorder records in 1 minute.
3. Measure in mm from the point where the tangent intersects the baseline to the distance equal to 1 minute.
4. Draw a line perpendicular to the baseline from the ‘1 minute’ point to the intersect point of the tangent.
5. Measure the distance [in mm] covered from the baseline to the intersect point [X].


6. Derive the maximal height of the aggregation [100% aggregation or maximal aggregation] from the y-axis [Y].
Divide X/Y to calculate the slope or rate of aggregation.

In the example above, if X = 23mm and Y = 97mm, the slope is X/Y = 0.24

 Untuk menghitung lereng [dan ini membentuk dasar dari VWF: RCo uji fungsional]:
1. Menarik garis di bersinggungan dengan kurva agregasi.
2. Tentukan berapa banyak milimeter [mm] catatan perekam grafik dalam 1 menit.
3. Mengukur dalam mm dari titik di mana garis singgungnya memotong baseline untuk jarak yang sama dengan 1 menit.
4. Gambarkan garis tegak lurus ke baseline dari titik menit ‘1 ‘ke titik berpotongan garis singgungnya.
5. Ukur jarak [di mm] tertutup dari baseline ke titik berpotongan [X].

6. Turunkan ketinggian maksimal agregasi [agregasi 100% atau agregasi maksimal] dari sumbu y [Y].
Bagilah X / Y untuk menghitung kemiringan atau tingkat agregasi.

Dalam contoh di atas, jika X = 23mm dan 97mm Y =, kemiringan adalah X / Y = 0,24

Interpretation of Platelet Aggregation Traces

The interpretation of platelet aggregation traces can be difficult. The attached file [click HERE] provides a summary of the abnormalities that may be identified by platelet aggregation testing.
Common aggregation traces that you are likely to encounter in an an exam-type setting are:
       – Glanzmann’s Thrombasthenia [or afibrinogenaemia]
       – Bernard-Soulier Syndrome [or Von Willebrand Disease]
       – Storage Pool Disorder [or release defect]
       – The effects of Aspirin [or an aspirin-like defect]
       – The effects of Aspirin Clopidogrel

Representative traces for some disorders and shown below and others are covered in the data interpretation section. In each case the control is shown in blue and the patient in red.

  1. 1.    In the patient shown below, the only abnormality is a lack of agglutination with ristocetin. Possible diagnoses are therefore, Von Willebrand Disease or Bernard Soulier Syndrome.

 

Interpretasi Jejak Agregasi trombosit


Penafsiran jejak agregasi platelet bisa sulit. File terlampir [klik DI SINI] menyediakan ringkasan dari kelainan-kelainan yang dapat diidentifikasi dengan tes agregasi trombosit.
Jejak agregasi umum bahwa Anda mungkin menghadapi dalam suasana ujian-jenis adalah:
        – Glanzmann ini Thrombasthenia [atau afibrinogenaemia]
        – Bernard-Soulier Syndrome [atau Von Willebrand Penyakit]
        – Penyimpanan Renang Disorder [atau cacat release]
        – Efek Aspirin [atau cacat aspirin-seperti]
        – Efek dari Clopidogrel Aspirin
Perwakilan jejak untuk beberapa gangguan dan ditampilkan di bawah ini dan lain-lain akan dibahas dalam bagian interpretasi data. Dalam setiap kasus kontrol ditampilkan dalam warna biru dan pasien dalam merah.

1. Pada pasien yang ditunjukkan di bawah, kelainan satunya adalah kurangnya aglutinasi dengan ristocetin. Kemungkinan diagnosis karena itu, Von Willebrand Penyakit atau Bernard Soulier Syndrome


2. This is the converse of the patient shown above and the only agglutination [and this is not complete] is seen with the ristocetin. There is no aggregation with ADP, adrenaline or collagen.
Possible diagnoses include Glanzmann’s thrombasthenia or afibrinogenaemia. Remember, platelet agglutination with ristocetin occurs independently of fibrinogen.
In the traces shown below it is clear that only partial agglutination is seen with ristocetin emphasising that for aggregation to occur, binding of fibrinogen to the GpIIb/IIIa receptor is necessary.

  1. 2.    Ini adalah kebalikan dari pasien yang ditunjukkan di atas dan aglutinasi satunya [dan ini tidak lengkap] terlihat dengan ristocetin tersebut. Tidak ada agregasi dengan ADP, adrenalin atau kolagen.  

Diagnosis mungkin termasuk Glanzmann ini thrombasthenia atau afibrinogenaemia. Ingat, aglutinasi platelet dengan ristocetin terjadi secara independen dari fibrinogen.
Dalam jejak ditunjukkan di bawah ini jelas bahwa hanya aglutinasi parsial terlihat dengan ristocetin menekankan bahwa untuk agregasi terjadi, pengikatan fibrinogen ke reseptor GpIIb / IIIa diperlukan.


3. In this patient reversible, first wave aggregation is seen with ADP, adrenaline and collagen and only partial agglutination with ristocetin. The picture is clearly different from the two traces above 1) or 2): the results suggest a failure of granule release and and is consistent with either platelet storage pool disorder or a defect in nucleotide release.

  1. 3.    Pada pasien ini reversibel, agregasi gelombang pertama terlihat dengan ADP, adrenalin dan kolagen dan hanya aglutinasi parsial dengan ristocetin. Gambar jelas berbeda dari dua jejak di atas 1) atau 2): hasil menunjukkan kegagalan pelepasan granul dan dan konsisten dengan baik gangguan kolam penyimpanan trombosit atau cacat dalam rilis nukleotida 
  2. 4.    Its useful to summarise the ‘commonly’ described abnormalities seen with light transmission aggregometry although in practice many of these are extremely rare. The table below summarises these:

Tes ini   berguna untuk merangkum kelainan ‘umum’ dijelaskan dilihat dengan aggregometry transmisi cahaya meskipun dalam prakteknya banyak di antaranya sangat langka. Tabel di bawah ini merangkum ini

 

Disorder

Characteristic Findings on LTA

Glanzmann’s Thrombasthenia
OR afibrinogenaemia
Absent or markedly impaired aggregation to all agonists except ristocetin. Ristocetin-induced agglutination shows only primary wave – aggregation cannot occur because fibrinogen cannot bind.
Afibrinogenaemia gives similar results.
Absen atau gangguan nyata agregasi untuk semua agonis kecuali ristocetin. Ristocetin-diinduksi aglutinasi hanya menunjukkan gelombang primer – agregasi tidak bisa terjadi karena fibrinogen tidak dapat mengikat.
Afibrinogenaemia memberikan hasil yang sama
Bernard Soulier Syndrome OR Von Willebrand Disease Absent or markedly reduced platelet agglutination with ristocetin. Absen atau nyata mengurangi trombosit aglutinasi dengan ristocetin
Storage Pool Disorder OR Platelet Release Defect Primary aggregation only with ADP, adrenaline and collagen and only partial agglutination with ristocetin suggesting a failure of granule release or a deficiency of platelet granules. Primer agregasi hanya dengan ADP, adrenalin dan kolagen dan hanya aglutinasi parsial dengan ristocetin menunjukkan kegagalan pelepasan granul atau butiran kekurangan trombosit
Aspirin [or defects in the COX pathway] Absent aggregation to arachadonic acid.
Primary wave aggregation only with ADP.
Decreased or absent aggregation with collagen.
Absen agregasi untuk asam arachadonic.
Gelombang primer agregasi hanya dengan ADP.
Penurunan atau tidak ada agregasi dengan kolagen
Clopidogrel Absent aggregation with ADP
2B VWD/Platelet-type [pseudo]VWD Aggregation with low dose ristocetin e.g. 0.5 mg/mL.

 

What test next?

On the basis of an abnormal platelet aggregation trace, you should establish if this fits in with any recognisable disorder. All abnormal results should be repeated and you may wish to undertake flow cytometry and nucleotide studies. Genetic testing can be of value in some cases.

Don’t forget to establish a family pedigree – some of the rare platelet disorders are commoner in consanguineous relationships.

Apa tes berikutnya?
Atas dasar suatu jejak agregasi platelet normal, Anda harus menentukan apakah ini cocok dengan gangguan dikenali. Semua hasil yang abnormal harus diulang dan Anda mungkin ingin melakukan cytometry aliran dan studi nukleotida. Pengujian genetik dapat menjadi nilai dalam beberapa kasus.
Jangan lupa untuk membuat silsilah keluarga – beberapa gangguan trombosit langka biasa dalam hubungan kerabat

Data Interpretation

Click HERE to go to the Data Interpretation Exercises.

Comments

1. You can also see the principles of Light Transmission Aggregometry on this site [http://www.platelet-research.org/3/aggregometry.htm].

References

1. Remuzzi, G., et al., Platelet hyperaggregability and the nephrotic syndrome. Thromb Res, 1979. 16(3-4): p. 345-54.

2. Lages, B. and H.J. Weiss, Biphasic aggregation responses to ADP and epinephrine in some storage pool deficient platelets: relationship to the role of endogenous ADP in platelet aggregation and secretion. Thromb Haemost, 1980. 43(2): p. 147-53.

3. Guidelines on platelet function testing. The British Society for Haematology BCSH Haemostasis and Thrombosis Task Force.

4. Lages, B. and H.J. Weiss, Heterogeneous defects of platelet secretion and responses to weak agonists in patients with bleeding disorders. Br J Haematol, 1988. 68(1): p. 53-62.

5. Hardisty, R.M., Disorders of platelet secretion. Baillieres Clin Haematol, 1989. 2(3): p. 673-94.

6. Michelson, A.D., Flow cytometry: a clinical test of platelet function. Blood, 1996. 87(12): p. 4925-36.

7. Rao, A.K., Congenital disorders of platelet function: disorders of signal transduction and secretion. Am J Med Sci, 1998. 316(2): p. 69-76.

8. Rodgers, G.M., Overview of platelet physiology and laboratory evaluation of platelet function. Clin Obstet Gynecol, 1999. 42(2): p. 349-59.

9. Shapiro, A.D., Platelet function disorders. Haemophilia, 2000. 6 Suppl 1: p. 120-7.

10. Kottke-Marchant, K. and G. Corcoran, The laboratory diagnosis of platelet disorders. Arch Pathol Lab Med, 2002. 126(2): p. 133-46.

11. Handin, R.I., Inherited platelet disorders. Hematology Am Soc Hematol Educ Program, 2005: p. 396-402.

12. Harrison, P., Platelet function analysis. Blood Rev, 2005. 19(2): p. 111-23.

13. Bolton-Maggs, P.H., et al., A review of inherited platelet disorders with guidelines for their management on behalf of the UKHCDO. Br J Haematol, 2006. 135(5): p. 603-33.

14. Hayward, C.P., Diagnostic approach to platelet function disorders. Transfus Apher Sci, 2008. 38(1): p. 65-76.

15. Harrison, P. and A. Mumford, Screening tests of platelet function: update on their appropriate uses for diagnostic testing. Semin Thromb Hemost, 2009. 35(2): p. 150-7.

16. Mezzano, D., T. Quiroga, and J. Pereira, The level of laboratory testing required for diagnosis or exclusion of a platelet function disorder using platelet aggregation and secretion assays. Semin Thromb Hemost, 2009. 35(2): p. 242-54.

17. Zhou L, Schmaier AH. Platelet aggregation testing in platelet-rich plasma: description of procedures with the aim to develop standards in the field. Am J Clin Pathol. 2005 Feb;123(2):172-83.

18. Simon D, Kunicki T, Nugent D. Platelet function defects. Haemophilia. 2008 Nov;14(6):1240-9.

19. Truss, N.J., Armstrong, P.C., Liverani, E., Vojnovic, I. & Warner, T.D. (2009) Heparin but not citrate anticoagulation of blood preserves platelet function for prolonged periods. J Thromb Haemost, 7, 1897-1905.

20. Quiroga et al BJH 2009

21. Nurden A, Nurden P. Advances in our understanding of the molecular basis of disorders of platelet function. J Thromb Haemost 2011;9 Suppl 1:76-91.

 

Top of Form

Data Interpretasi
Klik DI SINI untuk pergi ke Latihan Interpretasi data.
Komentar
1. Anda juga dapat melihat prinsip-prinsip Aggregometry Transmisi Cahaya di situs ini [http://www.platelet-research.org/3/aggregometry.htm].
Referensi
1. Remuzzi, G., et al., Hyperaggregability trombosit dan sindrom nefrotik. Thromb Res, 1979. 16 (3-4): p. 345-54.

2. Lages, B. dan HJ Weiss, respon agregasi Biphasic ke ADP dan epinefrin dalam beberapa trombosit storage pool kekurangan: hubungan peran ADP endogen dalam agregasi platelet dan sekresi. Thromb Haemost, 1980. 43 (2): p. 147-53.

3. Pedoman pengujian fungsi platelet. Masyarakat Inggris untuk Haemostasis BCSH Hematologi dan Angkatan Trombosis Tugas.

4. Lages, B. dan HJ Weiss, cacat heterogen sekresi platelet dan tanggapan terhadap agonis lemah pada pasien dengan gangguan perdarahan. Br J Haematol, 1988. 68 (1): p. 53-62.

5. Hardisty, R.M., Gangguan sekresi platelet. Baillieres Clin Haematol, 1989. 2 (3): p. 673-94.

6. Michelson, AD, Arus cytometry: tes klinis fungsi platelet. Darah, 1996. 87 (12): p. 4925-36.

7. Rao, AK, gangguan kongenital fungsi trombosit: gangguan transduksi sinyal dan sekresi. Am J Med Sci, 1998. 316 (2): p. 69-76.

8. Rodgers, GM, Ikhtisar fisiologi trombosit dan evaluasi laboratorium fungsi platelet. Clin Obstet Gynecol, 1999. 42 (2): p. 349-59.

9. Shapiro, M, gangguan fungsi trombosit. Hemofilia, 2000. 6 Suppl 1: p. 120-7.

10. Kottke-Marchant, K. dan G. Corcoran, Diagnosis laboratorium kelainan trombosit. Arch Pathol Lab Med, 2002. 126 (2): p. 133-46.

11. Handin, R.I., warisan gangguan trombosit. Hematologi Am Soc Hematol Educ Program, 2005: p. 396-402.

12. Harrison, P., analisis fungsi trombosit. Darah Rev, 2005. 19 (2): p. 111-23.

13. Bolton-Maggs, PH, et al, Sebuah tinjauan gangguan trombosit diwariskan dengan pedoman untuk manajemen mereka atas nama UKHCDO.. Br J Haematol, 2006. 135 (5): p. 603-33.

14. Hayward, CP, pendekatan Diagnostik gangguan fungsi trombosit. Transfus Apher Sci, 2008. 38 (1): p. 65-76.

15. Harrison, P. dan A. Mumford, Screening tes fungsi platelet: update pada penggunaan yang sesuai untuk tes diagnostik. Semin Thromb Hemost, 2009. 35 (2): p. 150-7.

16. Mezzano, D., T. Quiroga, dan J. Pereira, Tingkat pengujian laboratorium diperlukan untuk diagnosis atau pengecualian dari gangguan fungsi trombosit menggunakan agregasi platelet dan tes sekresi. Semin Thromb Hemost, 2009. 35 (2): p. 242-54.

17. Zhou L, Schmaier AH. Agregasi platelet pengujian di platelet-kaya plasma: deskripsi prosedur dengan tujuan untuk mengembangkan standar di lapangan. Am J Clin Pathol. 2005 Feb, 123 (2) :172-83.

18. Simon D, Kunicki T, Nugent D. cacat fungsi trombosit. Hemofilia. 2.008 November, 14 (6) :1240-9.

19. Truss, NJ, Armstrong, PC, Liverani, E., Vojnovic, I. & Warner, TD (2009) Heparin tetapi tidak sitrat antikoagulasi darah mempertahankan fungsi trombosit untuk waktu yang lama. J Thromb Haemost, 7, 1.897-1.905.

20. Quiroga et al BJH 2.009

21. Nurden A, Nurden P. Kemajuan dalam pemahaman kita tentang dasar molekul dari gangguan fungsi trombosit. J Thromb Haemost 2011; 9 Suppl 1:76-91.

 

 

BELAJAR KETERAMPILAN-KETERAMPILAN


Anda harus belajar keterampilan diabetes manajemen dasar. Mereka akan membantu mencegah masalah dan kebutuhan untuk perawatan medis. Keterampilan ini meliputi:
• Bagaimana menguji dan merekam glukosa darah Anda (Lihat: pemantauan glukosa darah)
• Apa yang harus makan dan kapan
• Bagaimana untuk mengambil obat, jika diperlukan
• Bagaimana mengenali dan mengobati gula darah rendah dan tinggi
• Bagaimana menangani hari sakit
• Dimana dapat membeli persediaan diabetes dan bagaimana menyimpannya
Ini mungkin membutuhkan beberapa bulan untuk mempelajari keterampilan dasar. Selalu terus belajar tentang diabetes, komplikasi, dan bagaimana mengontrol dan hidup dengan penyakit. Tetap up-to-date pada penelitian baru dan perawatan.

MENGELOLA GULA DARAH ANDA
Pengujian diri berarti bahwa Anda memeriksa gula darah Anda di rumah sendiri. Memeriksa kadar gula darah Anda di rumah dan menuliskan hasilnya akan memberitahu Anda seberapa baik Anda mengelola diabetes Anda.

Perangkat yang disebut glucometer bisa memberi Anda membaca gula darah yang tepat.

Ada berbagai jenis perangkat. Biasanya, Anda menusuk jari Anda dengan jarum kecil yang disebut lanset. Ini akan memberikan Anda setetes kecil darah. Anda menempatkan darah pada strip tes dan menempatkan strip ke dalam perangkat. Hasil yang diberikan dalam 30 – 45 detik.

Sebuah perawatan kesehatan atau pendidik diabetes akan membantu mengatur jadwal di rumah pengujian untuk Anda. Dokter akan membantu Anda menetapkan tujuan darah gula.
• Kebanyakan orang dengan diabetes tipe 2 hanya perlu memeriksa gula darah mereka sekali atau dua kali sehari.
• Jika kadar gula darah Anda berada di bawah kontrol, Anda mungkin hanya perlu memeriksa mereka beberapa kali seminggu.
• Anda dapat menguji diri sendiri ketika Anda bangun tidur, sebelum makan, dan sebelum tidur.
• Anda mungkin perlu menguji lebih sering ketika Anda sakit atau sedang stres.

Hasil tes dapat digunakan untuk mengubah makanan Anda, aktivitas, atau obat-obatan untuk menjaga kadar gula darah dalam kisaran yang tepat.

 

 Pengujian dapat mengidentifikasi kadar gula darah tinggi dan rendah sebelum Anda memiliki masalah serius.

Mencatat gula darah Anda untuk diri sendiri dan penyedia layanan kesehatan Anda. Ini akan membantu jika Anda mengalami kesulitan mengelola diabetes.

 

 

 

DIET DAN PENGENDALIAN BERAT
Bekerja sama dengan dokter, perawat, dan ahli diet untuk mengetahui berapa banyak lemak, protein, dan karbohidrat yang Anda butuhkan dalam diet Anda. Rencana makan Anda harus sesuai dengan gaya hidup sehari-hari dan kebiasaan, dan harus mencoba untuk memasukkan makanan yang Anda sukai.

Mengelola berat badan dan makan makanan yang seimbang adalah penting.

 

Beberapa orang dengan diabetes tipe 2 dapat berhenti memakai obat setelah kehilangan berat badan (meskipun mereka masih memiliki diabetes).
Lihat juga:
• Diabetes diet
• Ngemil bila Anda memiliki diabetes


Pasien sangat gemuk yang diabetes tidak dikelola dengan baik dengan diet dan obat-obatan dapat mempertimbangkan bariatrik (berat badan) operasi.
Lihat:
• operasi pintas lambung
• Laparoskopi gastric banding

 

 

 

KEGIATAN  FISIK REGULER

Dapat Mencegah 58 % terjadinya Diabetes type 2


Olahraga teratur adalah penting bagi semua orang.

 

 Hal ini bahkan lebih penting Anda memiliki diabetes.

 

Latihan di mana jantung Anda berdetak lebih cepat dan Anda bernapas lebih cepat membantu menurunkan tingkat gula darah Anda tanpa pengobatan.

 

 Hal ini juga membakar kalori ekstra dan lemak sehingga Anda dapat mengelola berat badan Anda.

Olahraga dapat membantu kesehatan Anda dengan meningkatkan aliran darah dan tekanan darah.

 

Olahraga juga meningkatkan tingkat energi tubuh, menurunkan ketegangan, dan meningkatkan kemampuan Anda untuk menangani stres.

Tanyakan pada dokter Anda sebelum memulai program latihan. Orang dengan diabetes tipe 2 harus mengambil langkah khusus sebelum, selama, dan setelah aktivitas fisik yang intensif atau berolahraga. Lihat juga: Diabetes dan olahraga

 

 

 

PENGOBATAN UNTUK MENGOBATI DIABETES

OBAT  METFORMIN HANYA 28 % MENCEGAH TIMBULNYA DIABETES TYPE 2

 

Jika diet dan olahraga tidak membantu menjaga gula darah pada tingkat normal atau mendekati normal, dokter mungkin meresepkan obat.

 

Karena obat ini membantu menurunkan kadar gula darah dengan cara yang berbeda, dokter Anda mungkin telah mengambil lebih dari satu obat.


Beberapa jenis yang paling umum dari obat tercantum di bawah ini. Mereka diminum atau injeksi.
• Alpha-glukosidase inhibitor (seperti acarbose)
Biguanides (Metformin)
• injeksi obat-obatan (termasuk exenatide, mitiglinide, pramlintide, sitagliptin saxagliptin, dan)
• meglitinides (termasuk repaglinide dan Nateglinide)
• Sulfonylureas (seperti glimepiride, glyburide, dan tolazamide)
• thiazolidinediones (seperti rosiglitazone dan pioglitazone). (Rosiglitazone dapat meningkatkan risiko gangguan jantung Bicarakan dengan dokter Anda..)

Obat ini dapat diberikan dengan insulin, atau insulin dapat digunakan sendiri.

 

 Anda mungkin perlu insulin jika Anda terus memiliki kontrol glukosa darah yang buruk. Ini harus disuntikkan di bawah kulit menggunakan jarum suntik insulin atau perangkat pena. Hal ini tidak dapat diambil melalui mulut. Lihat juga: Diabetes tipe 1

Tidak diketahui apakah obat hiperglikemia diminum aman untuk digunakan dalam kehamilan. Wanita yang memiliki diabetes tipe 2 dan hamil dapat beralih ke insulin selama kehamilan dan saat menyusui.

 

MENCEGAH KOMPLIKASI
Dokter mungkin meresepkan obat atau perawatan lain untuk mengurangi peluang Anda untuk mengembangkan penyakit mata, penyakit ginjal, dan kondisi lain yang lebih sering terjadi pada penderita diabetes.

 

Lihat juga:
• Diabetes – mencegah serangan jantung dan stroke

Konsultasi dengan dokter ahli Jantung


• Komplikasi jangka panjang diabetes

 

PERAWATAN KAKI
Orang dengan diabetes lebih mungkin untuk memiliki masalah kaki. Diabetes dapat merusak saraf, yang berarti Anda mungkin tidak merasa cedera pada kaki sampai Anda mendapatkan sakit besar atau infeksi.

 

Diabetes juga dapat merusak pembuluh darah.
Diabetes juga menurunkan kemampuan tubuh untuk melawan infeksi.

Infeksi kecil dapat dengan cepat memburuk dan menyebabkan kematian kulit dan jaringan lain.

Untuk mencegah cedera pada kaki Anda, memeriksa dan merawat kaki Anda setiap hari.

 

 Lihat juga: Diabetes kaki
Dukungan Grup
Untuk informasi lebih lanjut, lihat sumber diabetes.


Harapan (prognosis)

Setelah bertahun-tahun, diabetes dapat menyebabkan masalah serius dengan mata, ginjal, saraf, jantung, pembuluh darah, atau daerah lain dalam tubuh Anda.

Jika Anda memiliki diabetes, risiko serangan jantung adalah sama dengan seseorang yang sudah mengalami serangan jantung.

 

Baik wanita maupun pria dengan diabetes memiliki risiko. Anda mungkin tidak memiliki tanda-tanda normal dari serangan jantung.

Jika Anda mengontrol gula darah dan tekanan darah, Anda dapat mengurangi risiko kematian, stroke, gagal jantung, dan masalah diabetes lainnya.

Beberapa orang dengan diabetes tipe 2 tidak lagi membutuhkan obat jika mereka menurunkan berat badan dan menjadi lebih aktif.
 
Ketika mereka mencapai berat badan ideal mereka, insulin tubuh mereka dan diet yang sehat dapat mengendalikan kadar gula darah mereka.


Komplikasi
Setelah bertahun-tahun, diabetes dapat menyebabkan masalah serius:
• Anda bisa memiliki masalah mata, termasuk kesulitan untuk melihat (terutama pada malam hari), dan sensitivitas cahaya. Anda bisa menjadi buta.
• Kaki dan kulit dapat mengembangkan luka dan infeksi.

Setelah lama, kaki atau kaki mungkin perlu dihapus. Infeksi juga dapat menyebabkan nyeri dan gatal-gatal di bagian lain dari tubuh.
• Diabetes dapat membuat lebih sulit untuk mengontrol tekanan darah dan kolesterol. Hal ini dapat menyebabkan serangan jantung, storke, dan masalah lainnya.

 

 Hal ini dapat menjadi lebih sulit untuk darah mengalir ke kaki dan kaki.

 


• Saraf dalam tubuh Anda dapat rusak, menyebabkan nyeri, kesemutan, dan hilangnya perasaan.


• Karena kerusakan saraf, Anda bisa memiliki masalah mencerna makanan yang Anda makan. Anda bisa merasakan kelemahan atau kesulitan pergi ke kamar mandi. Kerusakan saraf dapat membuat lebih sulit bagi pria untuk memiliki ereksi.


• gula darah tinggi dan masalah lainnya dapat menyebabkan kerusakan ginjal. Ginjal tidak dapat bekerja dengan baik, dan mereka bahkan dapat berfungsi lagi.
Infeksi pada kulit, saluran kelamin wanita, dan saluran kemih juga lebih umum.

Untuk mencegah masalah dari diabetes, kunjungi dokter anda atau pendidik diabetes setidaknya empat kali setahun. Bicara tentang masalah yang Anda mengalami.

 

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Apa Hubungan antara Trigliserida dan Diabetes?

Trigliserida ini telah disebut sebagai “lemak jelek” tapi itu lebih merupakan respons emosional dari satu yang kukuh berakar pada fakta ilmiah.Namun hubungannya dengan diabetes tidak bisa diabaikan.

Kolesterol telah diidentifikasi sebagai faktor risiko penyakit jantung. Ada iklan yang tak terhitung jumlahnya dan outlet informasi yang mengkonfirmasi masalah yang berhubungan dengan diet yang tidak terkontrol.

Demikian juga ada pil dan pilihan makanan yang dipromosikan sebagai bagian dari solusi.

Konsumen mendapatkan hasil yang bervariasi tergantung pada genetik dan tahap di mana kondisi ini ditangkap.

Program latihan juga direkomendasikan sebagai bagian dari proses hidup sehat.


Pertanyaannya tetap, apakah semua intervensi ini telah efektif atau apakah mereka hanya cara bagi instansi periklanan untuk membuat lebih banyak uang.


• Kumpulan lemak yang dapat menyebabkan kerusakan: Dengan konsensus, trigliserida adalah bundel kecil lemak yang ditemukan dalam aliran darah. Mereka meningkat jumlahnya setelah kita mengkonsumsi makanan.

 

Tubuh akan memproduksi lemak-lemak dari makanan yang kita makan terutama jika mereka lemak di alam.

 

Diperkirakan bahwa 90% dari seluruh kandungan lemak non-daging tanpa lemak terdiri dari trigliserida.

 

Oleh karena itu kebiasaan belanja dari kelompok risiko harus mencerminkan bahaya.
• Trigliserida tidak universal buruk:

Diet yang seimbang harus mengandung semua elemen yang relevan. Telah diperkirakan bahwa trigliserida memiliki proporsi 99% dari semua lemak yang tersimpan dalam tubuh manusia.

 

Anda mendapatkan sumber energi jangka panjang dari deposito ini lemak. Mereka benar-benar disimpan dalam lebih padat daripada protein dari otot atau bahkan pati.

 

 Insulin diperlukan untuk membentuk lemak. Antara makan dan semalam, trigliserida diubah menjadi energi.

 

Kadar insulin puasa dan rendah akan memicu reaksi ini. Sel-sel lemak memiliki kapasitas penyimpanan yang sangat tinggi dan ini dapat menyebabkan obesitas pada situasi tertentu.

 

 Jika Anda sedang menjalani puasa luas atau sama sekali tidak ada insulin dalam tubuh maka hati akan mengkonversi produk pemecahan lemak menjadi keton.


• komplikasi kesehatan dan manifestasi mereka:

 

 Hal ini sering terjadi rendahnya tingkat HDL atau kolesterol baik dikaitkan dengan tingkat tinggi trigliserida.

 

Ini kemudian didiagnosis sebagai dislipidemia diabetik. Ini adalah kombinasi dari faktor-faktor yang dapat menempatkan hidup pasien dalam bahaya.

 

Pasien dalam situasi ini akan memiliki kelompok kecil, padat dan akhirnya berbahaya dari LDL atau kolesterol berbahaya.

 

Format yang terakhir ini tidak diinginkan berdasarkan sifat aterogenik nya. Akhirnya orang tersebut akan mengembangkan

obesitas sentral.

Ini adalah salah satu fitur mendefinisikan sindrom metabolik.


• Sekitar 80% dari semua penderita diabetes tipe 2 akan memiliki kondisi ini. Akhirnya orang tersebut meninggal lebih cepat akibat penyakit jantung.
• Menetapkan tolok ukur untuk orang yang sehat: Sangat penting bahwa Anda memiliki beberapa tujuan pada seberapa banyak trigliserida yang Anda akan merekam pada skala standar. Ini merupakan indikator yang mendasari kondisi sehat. Oleh karena itu

 

Anda akan berada dalam posisi untuk menerapkan strategi pencegahan bila diperlukan untuk melakukannya.

 

 Tingkat normal trigliserida adalah 150 mg / dl. Angka batas adalah antara 150 dan 199.

 

 Tingginya adalah antara 200 dan 499 sedangkan apa pun lebih dari 500 adalah hal yang mendesak.

 

Keadaan puasa normal akan memiliki tingkat membaca antara 100 dan 150 mg / dl.

 

Setelah makan yang normal angkanya akan meningkat menjadi 300.

 

Pasien dengan diabetes tipe 2 akan mengalami peningkatan kadar di kedua saat baik  puasa dan maupun sesudah makan.

 

Sebelum tes lipid panel, Anda harus memiliki beberapa puasa semalam setidaknya selama 12 jam.

 

 Demikian juga tidak dianjurkan untuk mengambil alkohol minimal 24 jam sebelum tes.
• Mengelola tingkat trigliserida dalam tubuh Anda:

 

 Hal ini untuk keuntungan Anda bahwa Anda menjaga kadar zat ini relatif rendah.

 

 

 

 Pasien dengan diabetes tipe 2 memiliki faktor risiko tinggi dan perlu bekerja sedikit yang ekstra untuk memastikan bahwa tingkat mereka 150 mg / dl atau bahkan lebih rendah. Ini akan membantu mereka mengurangi kemungkinan terkena penyakit kardiovaskular.

 

Beberapa orang dalam kategori ini telah melakukan tingkat yang lebih dari 400. Setelah Anda mulai memukul tanda 1000 maka Anda akan menderita lesi kulit atau xanthomas, kehilangan memori, pankreas dan sakit perut. Intervensi diperlukan pada tahap ini untuk menyelamatkan hidup Anda.

 

Tips diet diabetic type 2

 

Tips for Eating Well

with Diabetes

 

Knowing what to eat with type 2 diabetes is the best way to feel in control and feel better.

This first lesson in your quick-start guide gives an overview of the five simple key things to know:

 

 

1. Eating the Right Balanced Mix of Foods

 

2. Portions: How to Fill Your Plate

 

3. Calories Needed to Lose Weight

 

4. How Food Choices Can Lower Blood Sugar

 

5. Easy Ways to Count Carbs

 

Posted on December 18th, 2007 by DietMan

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Diet diabetes tipe 2:

Dengan lebih dari 14,6 juta orang Amerika menderita diabetes, telah menjadi masalah kesehatan utama di Amerika Serikat saat ini.

Diet Diabetes Tipe 2  perlu dibarengi dengan gaya hidup sehat dalam rangka untuk menempatkan cek pada diabetes tipe 2.

Diet diabetes Tipe 2  bersama dengan olahraga teratur, dapat membantu signifikan dalam mengendalikan gula darah Anda dan mengelola diabetes Anda.
Dengan mengurangi asupan kalori dan termasuk latihan rutin Anda, Anda dapat membuat tubuh Anda lebih sensitif terhadap insulin nya.

  Idealnya, Anda harus mengikuti rencana diet yang mengurangi asupan gula sederhana dan karbohidrat olahan.


  Diet kaya karbohidrat serat dan kompleks direkomendasikan untuk pasien diabetes tipe 2.
Karbohidrat kompleks yang ditemukan dalam buah-buahan, biji-bijian, dan sayuran dipecah sangat lambat akibat yang pelepasan glukosa dalam aliran darah diperlambat.

  Sebaliknya, karbohidrat sederhana dipecah dalam tidak ada waktu yang mengarah ke peningkatan pesat dalam tingkat gula darah.

Pasien diabetes tipe 2 dapat mencakup lebih sedikit lemak jenuh dalam makanan mereka.

Diabetes rencana diet: Sebuah rencana diet diabetes harus diikuti hanya setelah berkonsultasi seorang dokter ahli. Dokter Anda juga akan mempertimbangkan masalah kesehatan lainnya, jika ada, sebelum resep Anda rencana diet diabetes.

 

Original info

Type 2 diabetes diet: With more than 14.6 million Americans suffering from diabetes, it has become a major health concern in the United States today.

 

Type 2 diabetes diet needs to be coupled with a healthy lifestyle in order to put a check on type 2 diabetes.

 

Type 2 diabetes diet along with regular exercise, can be of significant help in controlling your blood sugar and managing your diabetes.

By reducing your calorie intake and including exercise in your routine, you can make your body more sensitive to its insulin.

 

 Ideally, you need to follow a diet plan that reduces your intake of simple sugars and refined carbohydrates.

 A diet rich in fiber and complex carbohydrates is recommended for type 2 diabetes patients.

Complex carbohydrates found in fruits, whole grains, and vegetables are broken down very slowly as a result of which the release of glucose in the bloodstream is slowed down.

 

 On the contrary, simple carbohydrates are broken down within no time leading to a rapid rise in the blood sugar levels.

 

Type 2 diabetic patients can include less saturated fat in their diet.

 

Diabetes diet plan: A diabetes diet plan should be followed only after consulting an expert physician. Your doctor will also take into account any other health problems, if any, before prescribing you a diabetes diet plan.

 

Diet yang direkomendasikan oleh American Diabetes Association: Diet yang direkomendasikan oleh American Diabetes Association adalah semua tentang membuat pilihan makanan sehat.

 

Diet meletakkan lebih menekankan pada buah-buahan, non – sayuran bertepung

(wortel, bayam, kacang hijau, brokoli),

 kacang kering, dan lentil.

Anda dapat memilih untuk makan makanan gandum bukan produk gandum olahan dan juga termasuk beras merah dalam diet Anda.

 

 

 


Diet yang disarankan oleh American Diabetes Association dapat membantu Anda mengelola diabetes Anda secara efektif asalkan Anda menonton ukuran porsi saat makan.

Bahkan makanan sehat, jika dimakan dalam jumlah besar, dapat meningkatkan berat badan Anda membuat manajemen diabetes lebih sulit.

 

Original info

Diet recommended by American Diabetes Association: The diet recommended by American Diabetes Association is all about making healthy food choices.

 

The diet lays more emphasis on fruits, non – starchy vegetables (carrots, spinach, green beans, broccoli), dried beans, and lentils.

 

You may choose to eat whole grain foods instead of processed grain products and also include brown rice in your diet.

 

The diet recommended by American Diabetes Association can help you manage your diabetes effectively provided that you watch the portion sizes while eating.

 

Even healthy foods, if eaten in large quantities, can increase your weight making diabetes management more difficult.

 

 

 

An Excellent Type 2 Diabetes Diet program

 

 

 

Rencana makan sehat Diabetes Tipe 2 adalah hanya untuk mereka yang memiliki tipe yang paling khas dari diabetes, tipe 2.

 

Hal ini terjadi ketika tubuh Anda tidak dapat mengembangkan insulin yang cukup, yang penting untuk membantu Anda menyerap glukosa dalam sel sampai kembali atau keperluan energi.

Apa yang menghentikan insulin dari fungsi ini seringkali dibangun lemak, itu sebabnya rencana diet mutlak diperlukan untuk membantu Anda mengendalikan penyakit dan kemudian menghentikannya dari semakin buruk.

Maka persis bagaimana seharusnya setiap orang memulai / nya nya 2 rencana diabetes makan agar benar-benar akan menghasilkan efek?

1. Mencatat segala macam hal yang terutama mengkonsumsi dan minum.

Tanpa diragukan lagi, kebenaran menyakitkan, tetapi banyak kali orang harus telah mengungkap semua dari mereka dan menghadapi mereka sehingga kami dapat melampaui semua masalah ini.

 

 Membuat daftar hanya apa yang Anda sering makan pasti akan membuat Anda menemukan bahwa kita satu-satunya yang dapat tetap mengontrol kesehatan kita sendiri dan kesehatan dan kita dapat melestarikan atau merusaknya. (Menyembuhkan diabetes tipe 2)

2. Temukan produk yang lebih sehat.
Sekarang ada tentu akan menjadi pengganti bahkan jika pada awalnya, mereka mungkin tampak tidak mudah untuk menemukan. Misalnya, sangat sangat mudah untuk hanya memindahkan dari roti normal untuk

roti gandum!

 

Apa yang perlu Anda lakukan adalah memiliki sedikit kesabaran pada eksplorasi tentang alternatif signifikan lebih sehat yang akan memberikan kesehatan yang lebih baik dalam jangka panjang.

3. Hilangkan Praktik Negatif resep diet diabetes
Gula pemanis soda bersama-sama dengan minuman dapat dengan mudah menyebabkan kondisi lebih buruk, jadi tinggal dengan

 

 

air dan teh sehat.

Ketika Anda minum soda terlalu banyak, hal ini dapat meningkatkan gula darah, yang tidak akan menstabilkan perkembangan insulin darah.

Demikian juga, daripada makan junk food serta makanan cepat saji, kenapa tidak mencoba

buah dan sayuran sebagai camilan?

 

 Anda juga bisa mencoba popcorn bebas lemak. Berkaitan dengan saus, Anda juga dapat mencoba mustard bukan mayones terlalu banyak.

Mencoba mengatakan pelayaran bon untuk produk makanan goreng hanya karena benar-benar diisi dengan lemak dan kalori.

Anda mungkin dapat mencoba

 memanggang, mengukus, panas sekali, atau panfrying menggunakan sedikit minyak zaitun sebagai pengganti.

 

Tak bisakah kau melihat bahwa ada begitu banyak pilihan?

Perlu diingat bahwa tidak ada diet mudah. Jika ingin melihat hasil yang baik, maka Anda benar-benar perlu melalui diet diabetes tipe 2 yang sulit.

 

Original info

Type 2 Diabetes Healthy eating plan is just for those who have the most typical type of diabetes, Type 2. This happens when your body cannot develop enough insulin, that is important to help you absorb glucose in the cells for back up or energy purposes. What stops insulin from functioning is oftentimes built up fat, that is why a diet plan is definitely needed to help you control the illness and then stop it from getting worse.

And so exactly how should everyone start up her / his 2 diabetes meal plan in order that it’ll really yield effects?

1. Take note of all kinds of things you mainly consume and drink.
Without a doubt, the truth hurts, but many times people have to have uncover all of them and face them so that we’re able to go beyond all these issues. Creating listing just what you frequently eat will definitely make you discover that we’re the only ones who can keep control of our own health and wellness and we can conserve it or wreck it. (cure for type 2 diabetes)

2. Discover more healthy products.
Now there will certainly be substitutes even if in the beginning, they might seem not easy to discover. For instance, it is very very easy to just move from normal bread to whole wheat bread! What you need to do is to have a little patience on exploring regarding significantly more healthy alternatives which will give you a better health in the long run.

3. Eliminate Negative Practices for the diabetes diet recipes
Sugar sweetened sodas together with drinks can easily cause the condition even worse, so stay with waters and healthful teas. When you drink too much soda, this could increase the blood sugar, which will not stabilize the blood insulin development.

Likewise, rather than of eating junk food as well as fast food, why not try fruits and vegetables as snacks? You could likewise try fat free popcorn. Relating to sauces, you can also try mustard instead of too much mayo.

Attempt saying bon voyage to fried food products simply because these are really stuffed with fats and calories. You possibly can try grilling, steaming, broiling, or panfrying using a bit of olive oil as a substitute. Cannot you see that there are so many choices?

Keep in mind that there is no effortless diet. If you’d like see the good results, then you really need to go through a difficult type 2 diabetes diet.

Resource: EzineArticles.Com

 

 

 

 

Respon klinis:

 

Kombinasi obat dan manajemen diet dapat memiliki hasil positif. Pertama-tama Anda harus bertujuan untuk pengendalian glukosa. Sebuah resep khas akan mencakup Statin seperti Zocor, Lipitor, Pravachol, Zetia, Crestor dan Vytorin.

 

 Obat-obat ini dimaksudkan untuk menurunkan kadar kolesterol Anda secara umum. Pasien diabetes tipe 2 mungkin memerlukan terapi kombinasi untuk mencapai tingkat yang aman dari trigliserida.

 

Anda juga harus memikirkan cara-cara menurunkan kadar LDL Anda.

Kadang-kadang dokter akan merekomendasikan serangkaian fibrate seperti gemfibrozil Lopid, Trico fenofibrate dan asam nikotinat atau niasin. Hal ini juga dianjurkan untuk memasukkan minyak ikan dalam diet Anda.


Setelah menyadari bahaya yang dapat timbul dari trigliserida dalam kaitannya dengan diabetes, Anda harus datang dengan perubahan gaya hidup praktis yang akan membantu Anda menghindari fase berbahaya.

Dalam beberapa kasus Anda mungkin harus membatasi asupan lemak Anda sepenuhnya. Masalahnya adalah bahwa langkah ini dapat menyebabkan Anda mengambil karbohidrat bahkan lebih dan karena itu meningkatkan tingkat trigliserida dalam aliran darah Anda.

 Beberapa buku merekomendasikan lemak substitusi sehat seperti minyak zaitun dan lemak tak jenuh tunggal lainnya.
 

Tidak meningkatkan asupan produk tepung gula atau putih. Asupan Alkohol harus disimpan ke minimum.

Ambil minyak ikan seperti tuna, sarden, salmon, makarel dan ikan.

Mereka mengandung asam lemak omega-3 yang dikenal untuk mengurangi trigliserida.

 

Kelainan genetik seperti hipotiroidisme dapat menggabungkan dengan penyakit untuk memperburuk situasi.


Mengambil obat-obatan seperti steroid, pil KB dan Tamoxifen juga bisa menimbulkan masalah. Anda beresiko jika Anda menderita penyakit ginjal, gagal hati dan tekanan darah tinggi

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Drag with shift key to reorder.

 

Original Info

Type 2 diabetes

Definition

Type 2 diabetes is a lifelong (chronic) disease in which there are high levels of sugar (glucose) in the blood. Type 2 diabetes is the most common form of diabetes.

Alternative Names

Noninsulin-dependent diabetes; Diabetes – type 2;

 

 Adult-onset diabetes

 

 

Causes, incidence, and risk factors

Diabetes is caused by a problem in the way your body makes or uses insulin. Insulin is needed to move blood sugar (glucose) into cells, where it is stored and later used for energy.

 

When you have type 2 diabetes, your fat, liver, and muscle cells do not respond correctly to insulin.

 

This is called insulin resistance.

 

 As a result, blood sugar does not get into these cells to be stored for energy.

 

When sugar cannot enter cells, high levels of sugar build up in the blood. This is called hyperglycemia.

 

Type 2 diabetes usually occurs slowly over time. Most people with the disease are overweight when they are diagnosed. Increased fat makes it harder for your body to use insulin the correct way.

 

Type 2 diabetes can also develop in people who are thin. This is more common in the elderly.

 

Family history and genes play a large role in type 2 diabetes.

Low activity level, poor diet, and excess body weight around the waist increase your risk.

 

See also: Type 2 diabetes for a list of risk factors.

Symptoms

Often, people with type 2 diabetes have no symptoms at first. They may not have symptoms for many years.

The early symptoms of diabetes may include:

  • Bladder, kidney, skin, or other infections that are more frequent or heal slowly
  • Fatigue
  • Hunger
  • Increased thirst
  • Increased urination

The first symptom may also be:

Signs and tests

Your health care provider may suspect that you have diabetes if your blood sugar level is higher than 200 mg/dL. To confirm the diagnosis, one or more of the following tests must be done.

Diabetes blood tests:

Read more

Hemoglobin A1c Test – facts

The AccuBase A1c Test Kit is a highly accurate test (CV’s less than 1.0%) capable of detecting abnormal and/or silent hemoglobin variants such as hemoglobin S, and C and F and over 850 others. Each sample is first screened for presence of abnormal hemoglobins and/or disturbed erythrocyte kinetics (abnormal age or volume of red blood cells) Example; anemia (which can falsely lower the A1c value).


Individuals with long-standing diabetes may present with a condition called erythropoietin (EPO) deficiency. EPO deficiency and/or anemia are considered serious conditions requiring appropriate medical intervention. DEK can adversely affect the A1c answer and each sample should be screened for the presence of DEK.

Estimates report that over 650,000 Black Americans with diabetes are know to have the Sickle Cell Trait (Hb “S, C or F”) “Don’t be fooled by claims of accuracy when an A1c method and/or disposable monitoring device has CV’s (coefficient of variation) greater than 2.0% or can not detect an abnormal hemoglobin”.

“An A1c method and/or monitoring device with a CV of 7.0 % could mean that if your actual A1c level was 6.5% it could be reported anywhere from 5.0% to 8.0% providing false and/or misleading therapeutic information,” not to mention the impact of an abnormal hemoglobin on the A1c value that the particular method or device is incapable of detecting.

Each AccuBase A1c sample is analyzed by an HPLC-IE procedure with resulting printed Chromatogram as shown below. The laboratory staff is available to discuss individual chromatograms with your physician and/or medical personnel.

The AccuBase A1c Test Kit is a non-fasting, finger stick, mail-in test, considered the most accurate and precise A1c test available. The test is considered sensitive and specific enough to detect diabetes (less than 2.0% CV’s). CV’s are under 1.0%. CV’s indicate the level of repeated accuracy compared to a known laboratory A1c value. The lower the CV’s the more accurate the A1c test.

The AccuBase A1c Test Kit method is NGSP certified (values referenced to the DCCT). The AccuBase A1c Test Kit does not require any drying time, samples can be collected and mailed within minutes. The kit comes complete with patient positive ID vials and plastic capillary tubes/device.

The analytical method is interference free. Samples are stable for 30 day un-refrigerated. Each test result comes with a Mean Blood Glucose calculation based on the DCCT MBG Equation: % A1c X 31.7 – 66.1 = MBG in mg/dl. Test results are typically available within 5 to 7 days form mailing. Special handling can be arranged to provide, next-day, two-day or three day results. Ideal for confidential diabetes (mean blood glucose) screening, outreach programs and clinical trails.

The first graph demonstrates a normal chromatogram with no hemoglobin variants present and a normal A1c level.

The Chromatogram on the second graph demonstrates an highly elevated level of hemoglobin F (25.6%). This elevated level of Hb F resulted in a sub-normal A1c value of 3.2%. Normal range of A1c assay (4.2% – 6.0%).

Unless you have been screened for hemoglobin variants you would not know you carry the hereditary persistent variant, or be aware of its associated impact on your A1c level.

Increased levels of Hemoglobin F may represent an increased risk for SIDS in infants, and may represent as association in various types of leukemia and/or solid tumors. Mothers that smoke or have been exposed to environmental pollution during pregnancy may have a much higher level of Hb F in the baby which may increase the risk of SIDS in the newborn.

AccuBase A1c Test Kit Cleared for OTC use by the FDA (no prescription needed in most states). Patients can receive a copy of the test results. Electronic reporting to managed care health organizations/providers is available.

The AccuBase A1cTest Kit uses the “gold standard” HPLC-IE or BA methodology to collect and analyze A1c samples in alternate site locations such as the home, physicians office and/or clinic

 

Diabetes screening is recommended for:

  • Overweight children who have other risk factors for diabetes, starting at age 10 and repeated every 2 years
  • Overweight adults (BMI greater than 25) who have other risk factors
  • Adults over age 45 every 3 years

You should see your health care provider every 3 months. At these visits, you can expect your health care provider to:

  • Check your blood pressure
  • Check the skin and bones on your feet and legs
  • Check to see if your feet are becoming numb
  • Examine the back part of the eye with a special lighted instrument called an ophthalmoscope

The following tests will help you and your doctor monitor your diabetes and prevent problems:

  • Have your blood pressure checked at least every year (blood pressure goals should be 130/80 mm/Hg or lower).
  • Have your hemoglobin A1c test (HbA1c) every 6 months if your diabetes is well controlled; otherwise every 3 months.
  • Have your cholesterol and triglyceride levels checked yearly (aim for LDL levels below 70-100 mg/dL).
  • Get yearly tests to make sure your kidneys are working well (microalbuminuria and serum creatinine).
  • Visit your eye doctor at least once a year, or more often if you have signs of diabetic eye disease.
  • See the dentist every 6 months for a thorough dental cleaning and exam. Make sure your dentist and hygienist know that you have diabetes.

Treatment

The goal of treatment at first is to lower high blood glucose levels. The long-term goals of treatment are to prevent problems from diabetes.

 

The main treatment for type 2 diabetes is exercise and diet.

 

 

LEARN THESE SKILLS

You should learn basic diabetes management skills. They will help prevent problems and the need for medical care. These skills include:

  • How to test and record your blood glucose (See: Blood glucose monitoring)
  • What to eat and when
  • How to take medications, if needed
  • How to recognize and treat low and high blood sugar
  • How to handle sick days
  • Where to buy diabetes supplies and how to store them

It may take several months to learn the basic skills. Always keep learning about diabetes, its complications, and how to control and live with the disease. Stay up-to-date on new research and treatments.

 

 

MANAGING YOUR BLOOD SUGAR

Self testing means that you check your blood sugar at home yourself. Checking your blood sugar levels at home and writing down the results will tell you how well you are managing your diabetes.

 

A device called a glucometer can give you an exact blood sugar reading.

 

There are different types of devices. Usually, you prick your finger with a small needle called a lancet. This gives you a tiny drop of blood. You place the blood on a test strip and put the strip into the device. Results are given in 30 – 45 seconds.

A health care provider or diabetes educator will help set up an at-home testing schedule for you. Your doctor will help you set your blood sugar goals.

  • Most people with type 2 diabetes only need to check their blood sugar once or twice a day.
  • If your blood sugar levels are under control, you may only need to check them a few times a week.
  • You may test yourself when you wake up, before meals, and at bedtime.
  • You may need to test more often when you are sick or under stress.

The results of the test can be used to change your meals, activity, or medications to keep your blood sugar levels in the right range. Testing can identify high and low blood sugar levels before you have serious problems.

 

Keep a record of your blood sugar for yourself and your health care provider. This will help if you are having trouble managing your diabetes.

 

DIET AND WEIGHT CONTROL

Work closely with your doctor, nurse, and dietitian to learn how much fat, protein, and carbohydrates you need in your diet. Your meal plans should fit your daily lifestyle and habits, and should try to include foods that you like.

Managing your weight and eating a well-balanced diet are important. Some people with type 2 diabetes can stop taking medications after losing weight (although they still have diabetes).

See also:

Very overweight patients whose diabetes is not well managed with diet and medicine may consider bariatric (weight loss) surgery.

See:

REGULAR PHYSICAL ACTIVITY

Regular exercise is important for everyone. It is even more important you have diabetes. Exercise in which your heart beats faster and you breathe faster helps lower your blood sugar level without medication. It also burns extra calories and fat so you can manage your weight.

 

Exercise can help your health by improving blood flow and blood pressure. Exercise also increases the body’s energy level, lowers tension, and improves your ability to handle stress.

 

Ask your health care provider before starting any exercise program. People with type 2 diabetes must take special steps before, during, and after intense physical activity or exercise. See also: Diabetes and exercise

 

MEDICATIONS TO TREAT DIABETES

If diet and exercise do not help keep your blood sugar at normal or near-normal levels, your doctor may prescribe medication. Since these drugs help lower your blood sugar levels in different ways, your doctor may have you take more than one drug.

Some of the most common types of medication are listed below. They are taken by mouth or injection.

  • Alpha-glucosidase inhibitors (such as acarbose)
  • Biguanides (Metformin)
  • Injectable medicines (including exenatide, mitiglinide, pramlintide, sitagliptin, and saxagliptin)
  • Meglitinides (including repaglinide and nateglinide)
  • Sulfonylureas (like glimepiride, glyburide, and tolazamide)
  • Thiazolidinediones (such as rosiglitazone and pioglitazone). (Rosiglitazone may increase the risk of heart problems. Talk to your doctor.)

These drugs may be given with insulin, or insulin may be used alone. You may need insulin if you continue to have poor blood glucose control. It must be injected under the skin using a syringe or insulin pen device. It cannot be taken by mouth. See also: Type 1 diabetes

 

It is not known whether hyperglycemia medications taken by mouth are safe for use in pregnancy. Women who have type 2 diabetes and become pregnant may be switched to insulin during their pregnancy and while breast-feeding.

 

 

PREVENTING COMPLICATIONS

Your doctor may prescribe medications or other treatments to reduce your chances of developing eye disease, kidney disease, and other conditions that are more common in people with diabetes.

See also:

FOOT CARE

People with diabetes are more likely to have foot problems. Diabetes can damage nerves, which means you may not feel an injury to the foot until you get a large sore or infection. Diabetes can also damage blood vessels.

Diabetes also decreases the body’s ability to fight infection.

 

Small infections can quickly get worse and cause the death of skin and other tissues.

 

To prevent injury to your feet, check and care for your feet every day. See also: Diabetes foot care

Support Groups

For more information, see diabetes resources.

 

 

 

 

Expectations (prognosis)

After many years, diabetes can lead to serious problems with your eyes, kidneys, nerves, heart, blood vessels, or other areas in your body.

 

If you have diabetes, your risk of a heart attack is the same as that of someone who has already had a heart attack. Both women and men with diabetes are at risk. You may not even have the normal signs of a heart attack.

 

If you control your blood sugar and blood pressure, you can reduce your risk of death, stroke, heart failure, and other diabetes problems.

 

Some people with type 2 diabetes no longer need medicine if they lose weight and become more active.

 

When they reach their ideal weight, their body’s own insulin and a healthy diet can control their blood sugar levels.

 

 

 

 

 

 

Complications

After many years, diabetes can lead to serious problems:

  • You could have eye problems, including trouble seeing (especially at night), and light sensitivity. You could become blind.
  • Your feet and skin can develop sores and infections. After a long time, your foot or leg may need to be removed. Infection can also cause pain and itching in other parts of the body.
  • Diabetes may make it harder to control your blood pressure and cholesterol. This can lead to a heart attack, storke, and other problems. It can become harder for blood to flow to your legs and feet.
  • Nerves in your body can get damaged, causing pain, tingling, and a loss of feeling.
  • Because of nerve damage, you could have problems digesting the food you eat. You could feel weakness or have trouble going to the bathroom. Nerve damage can make it harder for men to have an erection.
  • High blood sugar and other problems can lead to kidney damage. Your kidneys may not work as well, and they may even stop working.

Infections of the skin, female genital tract, and urinary tract are also more common.

 

To prevent problems from diabetes, visit your health care provider or diabetes educator at least four times a year. Talk about any problems you are having.

 

Calling your health care provider

Call 911 right away if you have:

  • Chest pain or pressure
  • Fainting or unconsciousness
  • Seizure
  • Shortness of breath

These symptoms can quickly get worse and become emergency conditions (such as convulsions or hypoglycemic coma).

Call your doctor if you have:

  • Numbness, tingling, or pain in your feet or legs
  • Problems with your eyesight
  • Sores or infections on your feet
  • Symptoms of high blood sugar (being very thirsty, having blurry vision, having dry skin, feeling weak or tired, needing to urinate a lot)
  • Symptoms of low blood sugar (feeling weak or tired, trembling, sweating, feeling irritable, having trouble thinking clearly, fast heartbeat, double or blurry vision, feeling uneasy)

Prevention

You can help prevent type 2 diabetes by keeping a healthy body weight and an active lifestyle.

 

Stay up-to-date with all your vaccinations and get a flu shot every year.

 

References

American Diabetes Association. Standards of medical care in diabetes–2011. Diabetes Care. 2011;34 Suppl 1:S11-S61.

Eisenbarth GS, Polonsky KS, Buse JB. Type 1 Diabetes Mellitus. In: Kronenberg HM, Melmed S, Polonsky KS, Larsen PR. Kronenberg: Williams Textbook of Endocrinology. 11th ed. Philadelphia, Pa: Saunders Elsevier; 2008:chap 31.

Pignone M, Alberts MJ, colwell JA, Cushman M, Inzucchi SE, Mukherjee D, et al. Aspirin for primary prevention of cardiovascular events in people with diabetes: a position statement of the American Diabetes Association, a scientific statement of the American Heart Association, and an expert consensus document of the American College of Cardiology Foundation. Circulation. 2010;121:2694-2701.

Buchwald H, Estok R, Fahrbach K, Banel D, Jensen MD, Pories WJ, Bantle JP, Sledge I. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med. 2009 Mar;122(3):248-256.e5. Review. PubMed PMID: 19272486.

ACCORD Study Group, Gerstein HC, Miller ME, Genuth S, Ismail-Beigi F, Buse JB, et al. Long-term effects of intensive glucose lowering on cardiovascular outcomes. N Engl J Med. 2011;364:818-828.

Alemzadeh R, Ali O. Diabetes Mellitus. In: Kliegman R, ed. 19th ed. Nelson Textbook of Pediatrics. Philadelphia, Pa: Saunders Elsevier; 2011: chap 583.

Review Date:

6/28/2011

 

Diabetic Diva ~

The triglyceride has been referred to as the “ugly fat” but that is more of an emotional response than one that is firmly anchored in scientific fact.

 

Nonetheless its association with diabetes cannot be ignored.

 

Cholesterol has already been identified as a risk factor for heart disease. There are countless adverts and information outlets which confirm the problems that are associated with an uncontrolled diet.

 

Likewise there are pills and food choices which are promoted as part of the solution.

 

Consumers get variable results depending on their genetic makeup and the stage at which the condition is arrested.

 

Exercise programs are also recommended as part of a healthy living process.

The question remains as to whether all these interventions have been effective or whether they are simply a way for the advertizing agencies to make even more money.

  • Bundles of fat that can cause havoc: By consensus, triglycerides are small bundles of fat which are found in the blood stream. They increase in number after we consume food. The body will manufacture these fats from the foods which we eat especially if they are fatty in nature. It has been estimated that 90% of all the fat content in non-lean meat consists of triglyceride.  Therefore the shopping habits of the risk groups have to reflect this imminent danger.
  • Triglycerides are not universally bad: A balanced diet should contain all the relevant elements. It has been estimated that triglyceride have a proportion of 99% of all the fat stored within the human body. You get long term energy sources from these fatty deposits. They are actually stored in a denser from than muscle protein or even starch.  Insulin is required in order to form fat. Between meals and overnight, the triglycerides are converted into energy. Fasting and low insulin levels will trigger this reaction. The fat cells have a very high storage capacity and this can lead to obesity in certain situations. If you are undergoing extensive fasting or there is absolutely no insulin in the body then the liver will convert the fat breakdown products into ketones.
  • The health complications and their manifestations: It is often the case the low levels of HDL or good cholesterol is associated with high levels of triglyceride. This is then diagnosed as diabetic dyslipidemia.  This is a combination of factors that can place the life of the patient in danger. Patients in this situation will have small, dense and ultimately harmful clusters of LDL or harmful cholesterol. The latter format is undesirable by virtue of its atherogenic properties. Eventually the person will develop central obesity. This is one of the defining features of the metabolic syndrome.
  • Around 80% of all the people with type 2 diabetes will have this condition. Eventually the person will die prematurely from heart disease.
  • Setting the benchmarks for a healthy person: It is imperative that you have some goals on how much triglyceride which you are going to record on the standard scale. This is an indicator of underlying healthy conditions. Therefore you will be in a position to implement a preventative strategy when required to do so. The normal levels of triglycerides are 150 mg/dl. The borderline figure is between 150 and 199. The high level is between 200 and 499 while anything over 500 is a matter of urgency. The normal fasting state will have levels reading between 100 and 150 mg/dl. After a normal meal the figure will rise to 300. Patients with type 2 diabetes will have elevated levels in both the fasting and even state.  Prior to the lipid panel test, you should have some overnight fasting for at least 12 hours. Likewise it is not advisable to take alcohol at least 24 hours prior to the test.
  • Managing the level of triglyceride in your body: It is to your advantage that you keep the levels of this substance relatively low. Patients with type 2 diabetes have high risk factors and need to work that bit extra to ensure that their levels are 150 mg/dl or even lower. This will help them reduce the possibility of developing cardiovascular diseases. Some people in this category have carried levels that are well over 400. Once you start hitting the 1000 mark then you will suffer skin lesions or xanthomas, memory loss, pancreatic and abdominal pain. Intervention is required at this stage in order to save your life.
  • The clinical response: A combination of medication and diet management can have positive results. First of all you have to aim for glucose control. A typical prescription will include Statins such as Zocor, Lipitor, Pravachol, Zetia, Crestor and Vytorin. These medications are meant to lower your cholesterol levels in general. Type 2 diabetes patients may require combination therapy in order to reach the safe levels of triglycerides. You also have to think of ways of lowering your LDL levels. Sometimes the clinician will recommend a series of Fibrates such as Lopid gemfibrozil, Trico fenofibrate and Nicotinic acid or niacin. It is also advisable to include fish oil in your diet.

Having recognized the dangers that can arise from triglycerides in relation to diabetes, you should come up with practical lifestyle changes that will help you avoid the dangerous phases.

 

In some instances you may have to restrict your fat intake completely. The problem is that this step can cause you to take even more carbohydrates and therefore increase the level of triglyceride in your bloodstream.

 

 Some books recommend substitution healthy fats such as olive oil and other monounsaturated fats.

 Do not increase your intake of sugar or white flour products.  Alcohol intake should be kept to a minimum.

 

Take oily fish such as tuna, sardines, salmon, mackerel and anchovies.

 

They contain omega-3 fatty acids which are known to reduce triglycerides.

 

Genetic disorders such as hypothyroidism can combine with diseases in order to exacerbate the situation.

 

 

Taking drugs such as steroids, birth control pills and Tamoxifen can also be problematic. You are at risk if you suffer from kidney disease, liver failure and high blood pressure.

The writer of this article is a blogger of ayurvedic health care tips.

 

BEWARE ALWAYS  NO STARCHY FOOD

 

All food that you eat turns to sugar in your body.

 Carbohydrate-containing foods alter your sugar levels more than any other type of food.

Carbohydrates are found in starchy or sugary foods, such as

bread, rice, pasta, cereal, potatoes, peas, corn, fruit, fruit juice, milk, yogurt, cookies, candy, soda, and other sweets.

Simple carbohydrates are broken down quickly by the body to be used as energy. Simple carbohydrates are found naturally in foods such as fruits, milk, and milk products.

 They are also found in processed and refined sugars such as candy, table sugar, syrups, and soft drinks.

The majority of carbohydrate intake should come from complex carbohydrates (starches) and naturally occurring sugars rather than processed or refined sugars.

All food that you eat turns to sugar in your body. Carbohydrate-containing foods alter your sugar levels more than any other type of food.

Carbohydrates are found in starchy or sugary foods, such as bread, rice, pasta, cereal, potatoes, peas, corn, fruit, fruit juice, milk, yogurt, cookies, candy, soda, and other sweets.

Exercises

 

 

 

Food and insulin release

 

 

Insulin is a hormone secreted by the pancreas in response to increased glucose levels in the blood.

 

Glucose test

 

.

 

 

 

 

 

 

 

Monitor blood glucose – series

Part one

 

Set up the meter according to the specific directions that come with your meter. Get the supplies ready, including a new test strip and disposable lancet. Place the lancet into the lancing device.

 

 

Rabu, 02 Mei 2012

PELATIHAN NASIONAL EDUKATOR DIABETES INDONESIA

Jakarta, 21 April 2012

 

 

Menteri Kesehatan, diwakili oleh Direktur Jenderal Pengendalian Penyakit dan Penyehatan Lingkungan (PP dan PL), Prof. dr. Tjandra Yoga Aditama, Sp.P(K), MARS, DTM&H, DTCE

 membuka secara resmi Pelatihan Nasional Edukator Diabetes Indonesia yang ke 10 yang diselenggarakan oleh Perhimpunan Edukator Diabetes Indonesia (PEDI) di Jakarta (20/4/12).

Kementerian Kesehatan  menyambut baik pelatihan ini, karena 4 hal, yang pertama Diabetes Mellitus (DM) merupakan masalah kesehatan penting di Indonesia, sebab DM merupakan penyebab kematian ke 6, prevalensi DM perkotaan 5,7%, dan prevalensi Toleransi Glukosa Terganggu 10,2%.


Alasan kedua karena pengendalian DM haruslah merupakan continum care, dimana edukasi merupakan salah satu faktor amat penting.

 

 Kemudian para mereka yang sudah dilatih akan langsung dapat menangani pasien DM dan keluarganya sehingga mereka dapat tetap sehat, bugar dan mandiri.

 

 Sedangkan yang terakhir adalah pelatihan ini merupakan bentuk nyata partisipasi aktif masyarakat kesehatan untuk bersama pemerintah menanggulangi masalah kesehatan di Indonesia, dalam hal ini Diabetes Mellitus.

Pelatihan berlangsung selama 3 hari dan diikuti lebih dari 200 peserta, terdiri dari dokter, perawat, diietesien, dan petugas lain. Pelatihan sudah berjalan 10 tahun dan mempunyai 3 tingkatan yaitu dasar, lanjut dan berkelanjutan.

 

Metode pelatihan dalam bentuk : teori, loka karya, serta simulasi.

Berita ini disiarkan oleh Pusat Komunikasi Publik, Sekretariat Jenderal Kementerian Kesehatan RI.

 

 

welcome

 

Dear iwansuwandy,

 

Welcome to Diabetic Living Online! Congratulations on taking control now — we’re glad you’re here! We have the information to help you make the best choices for your health. You can live well with diabetes. Get immediate access and must-have information:

 

More than 1,000 delicious recipes guaranteed by the Better Homes and Gardens® Test Kitchen.

 

Practical and clear answers to your questions about carb counting, weight loss, diabetes meal plans, medications, and much more!

 

FREE recipes and tips delivered to your in-box each week.

 

FREE quick-start diabetes education course on What to Eat with Diabetes.

 

Great deals on Diabetic Living Magazine subscriptions.

 

Be sure to find our page on Facebook and join our community of people with diabetes for support, information, and day-to-day tips on living well with diabetes.

 

Here’s to our good health,

Martha Miller Johnson

Editor of Diabetic Living®, wife, mother, friend, PWD type 1

 

PATHOGENESIS OF DIABETIC  NEUUOROPATHY

 

Nerve Complications

 

Elevated blood sugars can damage the peripheral nerves.

 

 

Symptoms of neuropathy include:

  • pain, numbness, and tingling of hands and feet
  • muscle weakness such as trouble climbing stairs
  • nausea and vomiting
  • dizziness and lightheadedness

 

Elevated levels of blood sugar can injure the blood vessels supplying the peripheral nerves, irritating and damaging them in the process.

Such accumulated nerve damage is called diabetic neuropathy.

Better blood glucose control can help restore healthy nerve function.

Nerve Disease

The nervous system includes our brain (central nervous system) and all of the nerves going from the brain to the rest of the body (peripheral nervous system).

The nervous system is always at work.

Sometimes – when we move or feel something – we are aware of it.

 But much happens automatically, including the control of our heart rate, the movement of food through the stomach and intestines and regulation of our blood pressure.

Your health care provider can determine that your symptoms are related to diabetes and not to some other condition.

The best way to improve all forms of diabetic neuropathy is to

 control your blood sugar levels.

There are two categories of diabetic neuropathy:

  • Sensory and motor neuropathy
  • Autonomic neuropathy

Symptoms of neuropathy include:

  • Pain, numbness, and tingling of hands and feet
  • Muscle weakness such as foot drop, double vision, trouble climbing stairs and getting out of a chair
  • Stomach symptoms including bloating, nausea, vomiting of undigested food many hours after a meal, feeling full without eating much food. This is also referred to as gastroparesis.
  • Bowel trouble such as episodes of diarrhea especially at night
  • Difficulty with bladder emptying
  • Sexual dysfunction
  • Dizziness and lightheadedness from a very fast heart rate and trouble keeping the blood pressure high enough when sitting or standing up.

What is the treatment?

Before any treatment can be decided upon, you need to report any of these symptoms to your health provider.

Your provider needs to make sure that the symptoms are due to diabetic neuropathy and not something else.

Near normal blood sugar control will usually improve all forms of diabetic neuropathy.

Pain medications should be used as needed. Your provider may refer you to an doctor for specialized treatment and evaluation.

Foot Complications

Diabetic blood circulation in foot

 

 

People with diabetes are at risk for blood vessel injury, which may be severe enough to cause tissue damage in the legs and feet.

 

 

Taking good care of your feet prevents serious complications.

  • Get regular foot exams that test for any nerve damage
  • Wash, dry and inspect your feet each day
  • Wear shoes and socks that fit
  • Control your blood glucose

 

Foot problems are caused by neuropathy, poor circulation or a combination of both.

 The loss of feeling that comes with neuropathy is especially dangerous, as you may not be aware of cuts, blisters and bruises.

The loss of sensation can change the way you walk or can damage bones and joints.

Delays in treatment can lead to serious problems. Poor blood circulation means that less oxygen and fewer white blood cells that fight infection can get to a wound.

It also means that antibiotic treatments that travel through the bloodstream are not as effective because they cannot get to the tissue in proper concentrations.

Foot problems

Foot problems include:

  • Changes in sensation from severe pain to numbness
  • Increased likelihood of infection (bacterial and fungal)
  • Slow wound healing
  • Deformation of the joints (Charcot joints, hammertoes, bunions, fallen arches)

Recommendations:

  • If you have foot problems, consult a doctor right away. Early diagnosis can make a dramatic difference. Treatment for infection includes antibiotics and regular wound dressing.

 

  • Impaired circulation sometimes can be helped by blood vessel bypass. This procedure also may help heal wounds and ulcers in combination with skin or tissue growth factors.
  • Unfortunately, in advanced cases of poor circulation and uncontrolled infection, amputation may be necessary, usually just a toe or part of a bone is removed. In the most severe cases, it may necessary to remove part of the foot or leg.

It is important to:

  • Get regular foot exams that test for any nerve damage
  • Not go barefoot
  • Not use sharp objects or over-the-counter chemical treatments such as corn/wart removers
  • Not use excessively hot water, electric blankets or heating pads, hot water bottles
  • Not smoke
  • Wash, dry and inspect your feet each day
  • Check between your toes
  • Wear shoes and socks that fit
  • Make sure there is nothing sharp or irritating in your shoes
  • Report corns and calluses and injuries that don’t heal to your medical provider
  • Cut toenails straight across and not too close to the quick; this will help prevent ingrown nails and associated infections
  • Control your blood glucose

Eye Complications

 

Eye problems range from minor changes to significant visual loss.

Complications include:

  • Retinopathy
  • Cataracts
  • Macular edema
  • Glaucoma

 

People with diabetes are at risk of eye problems, ranging from minor changes with no effect on vision to significant visual loss.

With regular screening and eye exams by an eye doctor (ophthalmologist), and with stable and near normal blood glucose control, most of the serious complications can be avoided or successfully treated.

Vision complications

Putting off an eye exam is very risky. Usually there are few or no symptoms at the time the damage is occurring.

Exams will reveal the problem and allow your eye doctor to treat it. Treatment can slow down the progression and maintain vision even in those who have developed significant eye complications.

 

Eye complications include:

Healthy eyes require that you:

  • Control your blood sugar
  • Control your blood pressure
  • Control your cholesterol
  • Don’t smoke and avoid second hand smoke
  • Use Ultra-violet protected eye glasses
  • See your ophthalmologist regularly and get retinal exams and eye pressure checked

 

Symptoms of eye emergencies:

  • Loss of vision,
  • Holes in vision,
  • Showers of sparking white lights,
  • Black curtains over vision,
  • Spots of fuzzy print, hazy vision,

If you have symptoms of any of the eye emergencies, seek medical care or contact your eye doctor immediately

PENGALAMAN PENDERITA DIABETIC TYPE 2

Gejala awal dari mata berupa sulit melihat waktu gelap(seperti rabun senja), kemudian diikuti dengan sulit melihat huruf kecil seperti presbiopia dan tidak dapat dikoreksi sampai plus 3.

YANG BERLANGSUNG HAMPIR SELAMA SEPULUH TAHUN SECARA PERLAHAN DAN MULAI PENGLIHATAN KABUR KARENA KATARAK DAN RETINAPATI

Pada pemeriksaan retina kelihatan pembuluh darah yang melebar akibat tersumbat dan retina yang mengalami kerusakan bewarna putih

 SERTA ADANYA KATARAK PADA KEDUA MATA, KELAINAN PADA MATA  KANAN LEBIH LUAS DARI KIRI.

Tindakan pertama tiga kali diinjeksi dengan anti perdarahan dosis rendah dalam kurun waktu jaraknya satu bulan, kemudian satu bulan lagi dilakukan penyinaran dengan laser untuk membersihkan kerusakan retina bervariasi 700 sampai seribu tembakan.

 

Hasil pengobatan ini cukup memuaskan tetapi tidak dapat disembuhkan 100 persen ,masih ada tersisa sedikit kabur melihat jauh yang perlu dikoreksi dengan kacamata minus cylendris 0,50 sampai 0,75 umumnya mata kiri dan kanan tidak sama yukurannya sehingga penglihatan jadi doubpe , khususnya bila katarak sudah dioperasi dengan tehnik yang sangat maju dengan memberikan tekanan negating lensa dapat dihancurkan dan disedot keluar,lalu dipasang soft lens , tidak terasa rasa sakit karena cukup dianestesi local dibawah kelopak mata, pasien dilakukan tindakan dikamar operasi secara steril dan setelah itu diberikan antibiotika oral, dan tetes mata selama satu bulan.

Operasi katarak dimulai pada satu mata sekaligus dilakukan penyuntikan antiperdarahan pada kedua mata , dan sebulan kemudian pada mata yang satu lagi.

Tembakan laser begitu juga satu bulan sesudah operasi katarak, pada mata secara berganti , setelah ditembak laser  penglihatan agak kabur selama beberapa jam setelah itu akan kelihatan lebih jelas dan huruf kecil dapat dilihat tanpa kacamata.dengan kacamata cylendris kiri  minus 0,50 dan kanan minus 0,76 ditambah added buat baca plus 3.00 untuk umur 69 tahun penglihatan jadi jelas lagi .

Inilah pengalaman yang dialami sendiri oleh Dr Iwan suwandy,MHA

Pada general check up ditemui kadar gula yang hanya sekita 130 mg puasa, dan postpandial 2 jam tetap tidak melebih batas normal pada umur  tua 67 tahun.

 

Ada faktor turunan, kakek dan ayah juga mengalami dibetes tetapi situasi mereka lebih berat kadar Gula darah pusa sampai 400mg sehingga terpaksa makan obat,diet dan timbulnya ulcus  dan abses pada kaki, tetapi anehnya tidka timbul katarak dan gangguan penglihatn sampaiakhir hidupnya yang terjadi gangguan ginjal dan serangan jantung pada usia diatas 70 tahun.

Setelah dicheck secara menyeluruh tidak ditemukan kelainan lain baik pada Thrombosit, Hb Ac,tensi,jantung,ginjal,scanning seluruh alat,test fungsi ginjal menunjukan normat. Berat badan sudah diatur sesuai ukuran tetapi kelihatan cendrung kelihatan  agak krus, sehingga menjadi permasalah dalam mengatur makan sesuai ataurannya,tetapi latihan olah raga lari pagi dan sore serta senam pada kaki dan perawatan kaki dan gigi yang teratur segala maslah dapat diatasi,

Permaslahan yang masih timbul anatara lain

1.Kaki tidak dapat digantung terlalu lama akan timbul kesemutan dan oedem, dan bila dingin pakai selimut dapat mengatasi perasaan tidka enak pada kaki tersebut.

2.Apakah perlu minum obat atau tidak, prinsipnya bila berat badan normal dan latihan olah raga teratur serta perawatan kaki dan gigi serta diet yang terkontrol tetap tidak dilakukan sambil melihat perkembangan lebih lanjut.

September 2013,umur 68 tahun 7 bulan

Ikutilah followup yang akan ditulis terus menerus ampai akhir hayat.

 

 

 

 

 

 

 

 

 

 

 

.

Prinsip pengobatan diabetes dengan metode stem cell

Stem cell adalah sel induk yang berada dalam tubuh kita sendiri yang memiliki kemampuan memperbaharui dan memulihkan. Dalam kondisi seperti ini, ia dapat dikelompokkan sebagai sel multifungsi, dengan efek memulihkan, melengkapi atau menghapus sel-sel yang rusak, bahkan memmperbaharui organ. Metode stem cell terhadap penyakit diabetes menggunakan kemampuan stem cell yang dapat memulihkan dan memperbaharui sel pancreas yang rusak., sehingga dapat mengurangi penderitaan pasien terhadap insulin dalam jangka waktu yang lama.

Metode stem cell dapat mengobati jenis diabetes di bawah ini

Efek dari terapi stem cell terhadap penyakit diabetes sangat nyata, baik terhadap diabetes I, diabetes II, maupun Gestational diabetes hasilnya sangat efektif.

Kelebihan metode pengobatan Stem cell

Dalam hasil suatu penelitian yang diterbitkan < Journal of American Medical Association> dilaporkan, para dokter ahli melakukan terapi stem cell terhadap 15 orang penderita Diabetes I di Brazil, hasilnya terdapat 13 orang yang berhasil mengatasi ketergantungannya terhadap insulin, juga tidak lagi tergantung pada obat-obatan. Pasien pertama yang menjalani terapi ini sudah berhenti dari insulin selama 3 tahun hingga saat ini.

Efek sampingnya kecil

Terapi Stem cell sangat aman, efek sampingnya pun kecil. Sebelum melakukan terapi stem cell, umumnya mereka menjalani pengobatan untuk anti-body, pengobatan induksi bertarget, serta pengobatan untuk menjaga kestabilan dan serangkaian pemeriksaan demi keamanan lainnya, termasuk uji toksisitas, uji genetik, uji immunotoxicity, dll. Hasilnya membuktikan, metode stem cell tidak memiliki efek samping, aman dan tidak beracun.

Pengobatan dengan menggunakan obat-obatan adalah salah satu cara pengobatan diabetes, menggunakan obat-obatan dalam jangka waktu tertentu dapat mengontrol penyakit diabetes untuk sementara. Selain itu, penggunaan obat-obatan dalam jangka waktu yang lama mempunyai efek samping yang sangat besar, banyak orang yang dikarenakan hal itu terkena dampak, seperti gagal ginjal, rusaknya fungsi hati, dll.

Proses pengobatan yang singkat, hanya 3 minggu

Proses terapi stem cell dangat singkat, hanya membutuhkan waktu 3 minggu. Terapi stem cell terhadap diabetes, pasien hanya diharuskan ada di rumah sakit sekitar 3 minggu, satu proses metodenya membutuhkan waktu sekitar 1 bulan, dalam waktu yang singkat, gangguan yang dialami oleh penderita diabetes akan segera teratasi.

Pada pengobatan tradisional, beberapa pasien terpaksa hidup melalui suntikan insulin, bahkan sampai akhirnya hidupnya pun tidak bisa melepaskan ketergantungannya terhadap insulin.

Proses terapi stem cell

Pemeriksaan sebelum dilakukan tindakan→dipastikan apakah cocok untuk menjalani terapi stem cell→memastikan persiapan sebelum tindakan→Menentukan jenis sel y ang akan digunakan, memberitahu pihak lab mengenai pemisahan, penetralan, dan prosedur ketat lainnya sebelum dilakukan tindakan→Masuk ke ruang bedah→Hari selanjutnya, pasien sudah dapat beraktivitas dengan normal→Hari ke 5 dilakukan pemeriksaan untuk pengecekan respon tubuh terhadap stem cell, sekitar hari ke 7 pasien diperbolehkan pulang

 

OBAT DIABETES TYPE 2

Metformin (a biguanide)

Alpha-glucosidase inhibitors

 

 

TYPE 2 DIABETES MEDICINES

A number of oral medicines (pills) are available to treat type 2 diabetes.

Metformin 

— Most people who are newly diagnosed with type 2 diabetes will immediately begin a medicine called

metformin

(Glucophage®, Gumetza®, Riomet®, Fortamet®).

Metformin improves how your body responds to insulin to reduce high blood sugar levels.

Metformin is a pill that is usually started with the evening meal; a second dose may be added one to two weeks later (with breakfast). The dose may be increased every one to two weeks thereafter.

Side effects — Common side effects of metformin include nausea, diarrhea, and gas. These are usually not severe, especially if you take metformin along with food.

Patients with certain types of kidney, liver, and heart disease, and those who drink alcohol excessively should not take metformin.

You should stop taking metformin 48 hours before any test that uses iodine-based contrast dye (like a CT scan with contrast), and you should stop it before any type of surgery.

When to add a second medicine — Your doctor or nurse might recommend a second medicine within the first two to three months if your blood sugar levels are still higher than your goal. Insulin shots might be recommended if your A1C is higher than 8.5 percent.

(See “Patient information: Diabetes mellitus type 2: Insulin treatment (Beyond the Basics)”.)

Which second medicine is best? 

— If your blood sugar levels are still high after two to three months, but your A1C is close to the goal (between 7 and 8.5 percent), a second medicine might be added.

 The “best” second medicine depends upon individual factors, including the person’s weight, other medical problems, and preferences regarding use of injections. The following are general recommendations:

  • The most commonly recommended second medicine is a short acting sulfonylurea, such as glipizide (see ‘Sulfonylureas’ below).
  • A thiazolidinedione, such as pioglitazone, is an alternative to sulfonylureas, but only for people who are not at increased risk of heart failure or bone fracture (see ‘Thiazolidinediones’ below).
  • A GLP-agonist, such as exenatide, is an option for patients who are overweight and who want to avoid developing low blood sugar. (See ‘GLP-agonists’ below.)
  • A meglitinide, such as repaglinide, is an option for people who cannot take a sulfonylurea or prefer to avoid injections. (See ‘Meglitinides’ below.)

Sulfonylureas

 — Sulfonylureas have been used to treat type 2 diabetes for many years. They work by increasing the amount of insulin your body makes, and can lower blood sugar levels by approximately 20 percent. However, they stop working over time.

Sulfonylureas are generally used if metformin does not adequately control blood sugar levels when taken alone. You should not take a sulfonylurea if you are allergic to sulfa drugs.

A number of sulfonylureas are available (Diabinese®, Orinase®, Glucotrol®, Diabeta®, Micronase®, Glynase®, Amaryl®), and the choice between them depends mainly upon cost and availability; they work similarly.

If you take a sulfonylurea, you can develop low blood sugar, known as hypoglycemia. Low blood sugar symptoms can include:

  • Sweating
  • Shaking
  • Feeling hungry
  • Feeling anxious

Low blood sugar must be treated quickly by eating 10 to 15 grams of fast-acting carbohydrate (eg, fruit juice, hard candy, glucose tablets). It is possible to pass out if you do not treat low blood sugar fast enough. A full discussion of low blood sugar is available separately. (See “Patient information: Hypoglycemia (low blood sugar) in diabetes mellitus (Beyond the Basics)”.)

Insulin — In the past, insulin treatment was reserved for patients with type 2 diabetes whose blood sugars were not controlled with oral medicines and lifestyle changes. However, there is increasing evidence that using insulin at earlier stages may improve overall diabetes control and help to preserve the pancreas’s ability to make insulin.

Insulin injections may be used as a first-line treatment in some people with type 2 diabetes, or it can be added to or substituted for oral medicines. Insulin must be injected by the patient or a family member/friend. (See “Patient information: Diabetes mellitus type 2: Insulin treatment (Beyond the Basics)”.)

Thiazolidinediones — This class of medicines includes pioglitazone (Actos®), which work to lower blood sugar levels by increasing the body’s sensitivity to insulin. They are taken in pill form and usually in combination with other medicines such as metformin, a sulfonylurea, or insulin.

Common side effects of thiazolidinediones include:

  • Weight gain and swelling of the feet and ankles.
  • A small but serious increased risk of developing or worsening heart failure. An early sign of heart failure is swelling of the feet and ankles. People who take thiazolidinediones should monitor for swelling.
  • A small but serious increased risk of developing fluid retention at the back of the eyes (macular edema).
  • A small but serious increased risk of developing certain types of cancer (like bladder cancer).
  • A small increased risk of bone fractures.

GLP-agonists — The GLP-agonists, Exenatide (Byetta®) and liraglutide (Victoza), are injectable medicines. They are not a first-line treatment, but might be considered for people whose blood sugar is not controlled on the highest dose of one or two oral medicines. They may be especially helpful for overweight patients who are gaining weight on oral medicine.

GLP-agonists do not usually cause low blood sugar. They promote weight loss, but can also cause bothersome side-effects, including nausea, vomiting, and diarrhea. Pancreatitis has been reported rarely in patients taking GLP-agonists, but it is not known if the drugs caused the pancreatitis. You should stop taking exenatide or liraglutide if you develop severe abdominal pain. Exenatide should not be used in patients with abnormal kidney function. These drugs are more expensive than insulin. Because they are relatively new drugs, long-term risks and benefits are not known.

 

DPP-IV Inhibitors — This class of medicines includes sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), and vildagliptin (Galvus). Vildagliptin is available in Europe but not in the United States. They lower blood sugar levels by increasing insulin release from the pancreas in response to a meal. They are not a first-line treatment, but they can be given alone in patients who can’t tolerate the first-line medicines (metformin, sulfonylureas), or they can be given with other oral medicines if blood sugars are still higher than goal. These medicines do not cause hypoglycemia or changes in body weight. However, they may cause some nausea and diarrhea. There have been rare reports of pancreatitis and skin reactions. DPP-IV inhibitors are expensive, and the long-term risks and benefits are unknown.

Meglitinides — Meglitinides include repaglinide (Prandin®) and nateglinide (Starlix®). They work to lower blood sugar levels, similar to the sulfonylureas, and might be recommended in people who are allergic to sulfa-based drugs. They are taken in pill form. Meglitinides are not generally used as a first-line treatment because they are more expensive than sulfonylureas and are short-acting, so they must be taken with each meal.

Alpha-glucosidase inhibitors — These medicines, which include acarbose (Precose®) and miglitol (Glyset®), work by interfering with the absorption of carbohydrates in the intestines. This helps to lower blood sugar levels, but not as well as metformin or the sulfonylureas. They can be combined with other medicines if the first medicine does not lower blood sugar levels enough.

The main side effects of alpha-glucosidase inhibitors are gas (flatulence), diarrhea, and abdominal pain; starting with a low dose may minimize these side effects. The medicine is usually taken three times per day with the first bite of each meal.

 

 

Living With Diabetic Type 2

People with type 2 diabetes often feel stress related to their disease and the increased responsibilities that come with diabetes, including blood sugar testing, watching the diet, exercise, doctor visits, the need for medicines, and the potential risks of complications.

 

 It is not uncommon to become depressed as a result of this stress, and this can make taking care of yourself more difficult.

Committing to new treatments and lifestyle changes can be difficult, and it is not uncommon to feel that the benefits of treatment are not worth the effort. Having an open and honest discussion with a doctor or nurse can help you to understand your diagnosis and the need for treatment.

Involving family and friends can help you to manage your disease by offering reminders to take medicine, test blood sugar levels, and providing a ride to appointments. Family and friends can also give encouragement and support to eat a healthy diet and stick with an exercise plan.

Working with a psychotherapist or social worker can help you cope with new responsibilities and worries.

 

 A number of studies have shown that people who have psychotherapy in addition to traditional medical care have reduced stress and improved blood sugar control compared with people who received only traditional care [1].

 Related Articles

Managing Diabetes Through Behavior Modification

// Managing diabetes requires lifestyle changes. You need to pay close attention to your diet and your physical activity. You should probably monitor your calories in (diet) and your calories burned (exercise). Modifying your behavior might prove challenging, but it is the only sure way to achieve control. A large part of this process involves addressing the beliefs that keep you from living a healthier lifestyle and replacing problem behaviors with healthy behaviors. Setting goals, keeping records, and evaluating your progress also play an important role.

To jumpstart the behavior modification process, follow these tips:

Develop a Positive Attitude

While assessing your habits and learning to control them might seem difficult at first, the rewards of accepting personal responsibility are worth the effort. Concentrate on developing a positive attitude.

Have You Ever Said…

  • “I have to entertain in my job” or “I am big-boned” or “I do not have time to exercise.” Blaming outside forces only delays your resolve.
  • “I do not have any willpower.” If you do not have control, who does? Willpower is not an inborn trait. You need to develop and practice this skill to get better at it. You can control your responses to foods; you have just convinced yourself you cannot.
  • “I simply cannot lose weight.” Translation: You think you are unworthy of trying again. Banish negative thoughts.
  •  

These rationalizations conveniently remove the responsibility from the individual. Accepting personal responsibility means recognizing that these statements impede success. Apply positive solutions to your problems and focus on what you can do to control your behavior.

Develop a Sense of Personal Responsibility

To take charge of your eating, follow these steps:

  1. 1.   STOP. As soon as you feel the urge to eat something decadent, count to 20. This momentary pause allows you time to exercise your willpower.
  2. 2.   THINK. Give your defenses a chance to kick-in.
  3. 3.   LISTEN. To yourself, not the food. Talk yourself out of a temptation and the urge will pass. Determine whether the treat you crave is worth the consequences.
  4. 4.   ESTABLISH SITUATIONAL CONTROLS. Remove the temptation before it grows too strong to resist. The best situational control? Do not keep your “weakness” in the house, be it ice cream, cookies or potato chips. Be good to yourself.

Assert Your Right to a Healthy Weight

When you watch what you eat to help manage your diabetes, you can help manage your weight as well. Identify “diet” saboteurs:

“Have some more lasagna…,” “Split a piece of pie with me….”

Sometimes the people around you seem like enemies when you try to change your eating habits. They might wonder if the new you will resemble the old friend. Do not be afraid to assert your right to make healthy food choices.

 

 

 

 

 

 

Ask for Help

Help those around you understand how their actions influence you, and give them suggestions for showing more support.

  1. 1.   State the problem areas and situations in which you need help or support.
  2. 2.   Explain how you feel about the problem and why you need help with its resolution.
  3. 3.   Detail the action you wish your supporters to take.
  4. 4.   Describe to them the results that you expect.

Work Toward a Healthy Lifestyle

  • Fill your evenings with people and activities. Do you eat out of boredom? Find something productive to do. Volunteer. Ride an exercise bike while watching your favorite sitcom. Visit a friend. Take a night class.
  • Read food labels and become more aware of the calories in the choices you make. You can make a difference in controlling your blood sugar by keeping alert. When eating out, speak up. Ask for dressings on the side. Request small portions of lean meats. Ask for a doggie bag. If you can’t resist the rolls and butter, send them back to the kitchen.
  • Get out of the house and away from the fridge! Plan evening walks, bicycle rides, and other physical activities. Changing the focal point of your family time from eating to activity will help everyone rethink their habits and provide you with company as well.
  • Act positively. Moaning and groaning about saying no to chocolate cake will not elicit sympathy from your family. Let your family see a happier, healthier you and they’ll be more likely to support you and your new lifestyle.
  • Listen to your body. Spread your meals out throughout the day for better blood sugar control. Create a balanced meal plan with a dietitian that provides the calories you need based on your sex, age, weight, physical activity level, and lifestyle, and stick to it. When someone offers you food, do not feel pressured to eat.

Don’t Forget Exercise

You cannot achieve long-term weight loss by diet alone. To maintain a healthy diet, you should watch your calorie intake and increase activity.

 

Remind yourself about the benefits of exercise. Regular exercise reduces your risk of heart disease, lowers your cholesterol and blood pressure, and raises your metabolism.

Not only do you burn calories during a workout, but you also use more calories all day long. Why? Because exercise builds muscle, and muscle uses more calories than fat.

Take a look at these exercise facts and fallacies.

  • No pain, no gain.
    False. Exercising to the point of discomfort can signal bone, joint and muscle injury.
  • You can “sweat” the weight off.
    False. Perspiration loss during exercise can account for some temporary weight loss. But, you will “regain” it with the first glass of water you drink!
  • Exercise makes you hungry.
    False. Moderate activity will not increase your appetite. Exercising fuels feelings of control and accomplishment.
  • Spot reducing eliminates fat deposits in problem areas.
    False. Spot reducing can tone and firm an area to make it look thinner, but if excess fat exists in the area, it will never look as firm as you want with spot exercises alone!
  • Cellulite is not the same as other fat.
    False. Fat by any other name still equals fat! While some areas of the body resist fat loss more than others, no amount of creams or massages will reduce or eliminate the dimpled, fatty deposits known as cellulite. To shed these fat cells, you will need to use the same program of diet and exercise you’re using for generalized weight reduction.
  • Your scale is the best measure of your exercise program.
    False. When you exercise, heavier, lean muscle tissue increases while lighter fat decreases. In fact, you might even gain a pound or two when you start to exercise. Instead of just checking the pounds, measure your success by evaluating the decrease in your body fat
  • ·

 

Whole fruit can reduced risk of Diabetc type 2

Researchers found that consuming whole fruit than juice can  preventing risk of diabetic type 2 in 7 %

Diabetes mellitus type 2 (formerly noninsulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes) is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency.[2]

 

This is in contrast to diabetes mellitus type 1, in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas.[3]

 

The classic symptoms are excess thirst, frequent urination, and constant hunger.

 

Type 2 diabetes makes up about 90% of cases of diabetes with the other 10% due primarily to diabetes mellitus type 1 and gestational diabetes.

 

Obesity is thought to be the primary cause of type 2 diabetes in people who are genetically predisposed to the disease.

 

Type 2 diabetes is initially managed by increasing exercise and dietary modification.

 

If blood glucose levels are not adequately lowered by these measures, medications such as metformin or insulin may be needed. In those on insulin, there is typically the requirement to routinely check blood sugar levels.

Rates of type 2 diabetes have increased markedly over the last 50 years in parallel with obesity: As of 2010 there are approximately 285 million people with the disease compared to around 30 million in 1985.[4][5]

 

Long-term complications from high blood sugar can include heart disease, strokes, diabetic retinopathy where eyesight is affected, kidney failure which may require dialysis, and poor circulation in the limbs leading to amputations.

The acute complication of ketoacidosis, a feature of type 1 diabetes, is uncommon.[6]

However, nonketotic hyperosmolar coma may occur

Signs and symptoms

 

 

Overview of the most significant symptoms of diabetes.

The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.[7]

Other symptoms that are commonly present at diagnosis include: a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue.

Many people, however, have no symptoms during the first few years and are diagnosed on routine testing.

 

People with type 2 diabetes mellitus may rarely present with nonketotic hyperosmolar coma (a condition of very high blood sugar associated with a decreased level of consciousness and low blood pressure).[3]

Complications

Main article: Complications of diabetes mellitus

Type 2 diabetes is typically a chronic disease associated with a ten-year-shorter life expectancy.[4]

This is partly due to a number of complications with which it is associated, including: two to four times the risk of cardiovascular disease, including ischemic heart disease and stroke; a 20-fold increase in lower limb amputations, and increased rates of hospitalizations.[4]

In the developed world, and increasingly elsewhere, type 2 diabetes is the largest cause of nontraumatic blindness and kidney failure.[8]

It has also been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer’s disease and vascular dementia.[9] Other complications include: acanthosis nigricans, sexual dysfunction, and frequent infections.[7]

Cause

The development of type 2 diabetes is caused by a combination of lifestyle and genetic factors.[8][10]

While some are under personal control, such as diet and obesity, others, such as increasing age, female gender, and genetics, are not.[4]

A lack of sleep has been linked to type 2 diabetes.[11] This is believed to act through its effect on metabolism.[11]

The nutritional status of a mother during fetal development may also play a role, with one proposed mechanism being that of altered DNA methylation.[12]

 

 

 

Lifestyle

Main article: Lifestyle causes of diabetes mellitus type 2

A number of lifestyle factors are known to be important to the development of type 2 diabetes, including: obesity (defined by a body mass index of greater than thirty), lack of physical activity, poor diet, stress, and urbanization.[4] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[3] Those who are not obese often have a high waist–hip ratio.[3]

Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[13][14]

The type of fats in the diet are also important, with saturated fats and trans fatty acids increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.[10]

 

Eating lots of white rice appears to also play a role in increasing risk.[15]

A lack of exercise is believed to cause 7% of cases.[16]

Genetics

Main article: Genetic causes of diabetes mellitus type 2

Most cases of diabetes involve many genes, with each being a small contributor to an increased probability of becoming a type 2 diabetic.[4]

If one identical twin has diabetes, the chance of the other developing diabetes within his lifetime is greater than 90% while the rate for nonidentical siblings is 25-50%.[3]

As of 2011, more than 36 genes have been found that contribute to the risk of type 2 diabetes.[17]

All of these genes together still only account for 10% of the total heritable component of the disease. The TCF7L2allele, for example, increases the risk of developing diabetes by 1.5 times and is the greatest risk of the common genetic variants. Most of the genes linked to diabetes are involved in beta cell functions.[3]

There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes or “other specific types of diabetes”).[3][4] These include maturity onset diabetes of the young (MODY), Donohue syndrome, and Rabson-Mendenhall syndrome, among others.[4] Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people.[18]

Medical conditions

There are a number of medications and other health problems that can predispose to diabetes.[19] Some of the medications include: glucocorticoids, thiazides, beta blockers, atypical antipsychotics,[20] and statins.[21]

Those who have previously had gestational diabetes are at a higher risk of developing type 2 diabetes.[7]

Other health problems that are associated include: acromegaly, Cushing’s syndrome, hyperthyroidism, pheochromocytoma, and certain cancers such as glucagonomas.[19]

 

Testosterone deficiency is also associated with type 2 diabetes.[22][23]

Pathophysiology

Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[3]

Insulin resistance, which is the inability of cells to respond adequately to normal levels of insulin, occurs primarily within the muscles, liver, and fat tissue.[24]

In the liver, insulin normally suppresses glucose release. However, in the setting of insulin resistance, the liver inappropriately releases glucose into the blood.[4]

The proportion of insulin resistance versus beta cell dysfunction differs among individuals, with some having primarily insulin resistance and only a minor defect in insulin secretion and others with slight insulin resistance and primarily a lack of insulin secretion.[3]

Other potentially important mechanisms associated with type 2 diabetes and insulin resistance include: increased breakdown of lipids within fat cells, resistance to and lack of incretin, high glucagon levels in the blood, increased retention of salt and water by the kidneys, and inappropriate regulation of metabolism by the central nervous system.[4] However, not all people with insulin resistance develop diabetes, since an impairment of insulin secretion by pancreatic beta cells is also required.[3]

Diagnosis

Diabetes diagnostic criteria[25][26]  edit

Condition

2 hour glucose

Fasting glucose

HbA1c

 

mmol/l(mg/dl)

mmol/l(mg/dl)

%

Normal

<7.8 (<140)

<6.1 (<110)

<6.0

Impaired fasting glycaemia

<7.8 (<140)

≥ 6.1(≥110) & <7.0(<126)

6.0–6.4

Impaired glucose tolerance

≥7.8 (≥140)

<7.0 (<126)

6.0–6.4

Diabetes mellitus

≥11.1 (≥200)

≥7.0 (≥126)

≥6.5

The World Health Organization definition of diabetes (both type 1 and type 2) is for a single raised glucose reading with symptoms, otherwise raised values on two occasions, of either:[27]

  • fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl)

or

A random blood sugar of greater than 11.1 mmol/l (200 mg/dL) in association with typical symptoms[7] or a glycated hemoglobin (HbA1c) of greater than 6.5% is another method of diagnosing diabetes.[4]

 

In 2009 an International Expert Committee that included representatives of the American Diabetes Association (ADA), the International Diabetes Federation (IDF), and the European Association for the Study of Diabetes (EASD) recommended that a threshold of ≥6.5% HbA1c should be used to diagnose diabetes.

 

 

This recommendation was adopted by the American Diabetes Association in 2010.[28]

Positive tests should be repeated unless the person presents with typical symptoms and blood sugars >11.1 mmol/l (>200 mg/dl).[29]

Threshold for diagnosis of diabetes is based on the relationship between results of glucose tolerance tests, fasting glucose or HbA1c and complications such as retinal problems.[4]

A fasting or random blood sugar is preferred over the glucose tolerance test, as they are more convenient for people.[4]

HbA1c has the advantages that fasting is not required and results are more stable but has the disadvantage that the test is more costly than measurement of blood glucose.[30]

It is estimated that 20% of people with diabetes in the United States do not realize that they have the disease.[4]

Diabetes mellitus type 2 is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency.[2]

 This is in contrast to diabetes mellitus type 1 in which there is an absolute insulin deficiency due to destruction of islet cells in the pancreas and gestational diabetes mellitus that is a new onset of high blood sugars in associated with pregnancy.[3]

Type 1 and type 2 diabetes can typically be distinguished based on the presenting circumstances.[29] If the diagnosis is in doubt antibody testing may be useful to confirm type 1 diabetes and C-peptide levels may be useful to confirm type 2 diabetes,[31] with C-peptide levels normal or high in type 2 diabetes, but low in type 1 diabetes.

Screening

No major organization recommends universal screening for diabetes as there is no evidence that such a program would improve outcomes.[32]

Screening is recommended by the United States Preventive Services Task Force in adults without symptoms whose blood pressure is greater than 135/80 mmHg.[33]

For those whose blood pressure is less, the evidence is insufficient to recommend for or against screening.[33]

The World Health Organization recommends only testing those groups at high risk.[32]

High-risk groups in the United States include: those over 45 years old; those with a first degree relative with diabetes; some ethnic groups, including Hispanics, African-Americans, and Native-Americans; a history of gestational diabetes; polycystic ovary syndrome; excess weight; and conditions associated with metabolic syndrome.[7]

Prevention

Main article: Prevention of diabetes mellitus type 2

Onset of type 2 diabetes can be delayed or prevented through proper nutrition and regular exercise.[34][35]

 

Intensive lifestyle measures may reduce the risk by over half.[8]

The benefit of exercise occurs regardless of the person’s initial weight or subsequent weight loss.[36]

 Evidence for the benefit of dietary changes alone, however, is limited,[37]

with some evidence for a diet high in green leafy vegetables[38]

and some for limiting the intake of sugary drinks.[13]

 

In those with impaired glucose tolerance, diet and exercise either alone or in combination with metformin or acarbose may decrease the risk of developing diabetes.[8][39]

 

Lifestyle interventions are more effective than metformin.[8]

 

Management

Further information: Diabetes management

Management of type 2 diabetes focuses on lifestyle interventions, lowering other cardiovascular risk factors, and maintaining blood glucose levels in the normal range.[8] Self-monitoring of blood glucose for people with newly diagnosed type 2 diabetes was recommended by the British National Health Service in 2008,[40] however the benefit of self monitoring in those not using multi-dose insulin is questionable.[8][41]

 Managing other cardiovascular risk factors, such as hypertension, high cholesterol, and microalbuminuria, improves a person’s life expectancy.[8]

 

Intensive blood pressure management (less than 130/80 mmHg) as opposed to standard blood pressure management (less than 140–160/85–100 mmHg) results in a slight decrease in stroke risk but no effect on overall risk of death.[42]

 

Intensive blood sugar lowering (HbA1c<6%) as opposed to standard blood sugar lowering (HbA1c of 7–7.9%) does not appear to change mortality.[43][44]

 

The goal of treatment is typically an HbA1c of less than 7% or

 

a fasting glucose of less than 6.7 mmol/L (120 mg/dL) however these goals may be changed after professional clinical consultation, taking into account particular risks of hypoglycemia and life expectancy.[7]

It is recommended that all people with type 2 diabetes get regular ophthalmology examination.[3]

Lifestyle

A proper diet and exercise are the foundations of diabetic care,[7] with a greater amount of exercise yielding better results.[45]

 

Aerobic exercise leads to a decrease in HbA1c and improved insulin sensitivity.[45]

 Resistance training is also useful and the combination of both types of exercise may be most effective.[45]

 

A diabetic diet that promotes weight loss is important.[46] While the best diet type to achieve this is controversial[46] a low glycemic index diet has been found to improve blood sugar control.[47]

Culturally appropriate education may help people with type 2 diabetes control their blood sugar levels, for up to six months at least.[48]

 

 If changes in lifestyle in those with mild diabetes has not resulted in improved blood sugars within six weeks, medications should then be considered.[7]

Medications

 

 

Metformin 500mg tablets

There are several classes of anti-diabetic medications available. Metformin is generally recommended as a first line treatment as there is some evidence that it decreases mortality.[8]

A second oral agent of another class may be used if metformin is not sufficient.[49]

Other classes of medications include: sulfonylureas, nonsulfonylurea secretagogues, alpha glucosidase inhibitors, thiazolidinediones, glucagon-like peptide-1 analog, and dipeptidyl peptidase-4 inhibitors.[8][50] Metformin should not be used in those with severe kidney or liver problems.[7] Injections of insulin may either be added to oral medication or used alone.[8]

Most people do not initially need insulin.[3] When it is used, a long-acting formulation is typically added at night, with oral medications being continued.[7][8]

Doses are then increased to effect (blood sugar levels being well controlled).[8] When nightly insulin is insufficient twice daily insulin may achieve better control.[7]

The long acting insulins glargine and detemir are equally safe and effective,[51] and do not appear much better than neutral protamine Hagedorn (NPH) insulin, but as they are significantly more expensive, they are not cost effective.[52][note 1]

In those who are pregnant insulin is generally the treatment of choice.[7]

Surgery

Weight loss surgery in those who are obese is an effective measure to treat diabetes.[53] Many are able to maintain normal blood sugar levels with little or no medications following surgery[54] and long-term mortality is decreased.[55] There however is some short-term mortality risk of less than 1% from the surgery.[56] The body mass index cutoffs for when surgery is appropriate are not yet clear.[55] It is recommended that this option be considered in those who are unable to get both their weight and blood sugar under control.[57]

 

 

 

 

 

Epidemiology

 

 

Prevalence of diabetes worldwide in 2000 (per 1000 inhabitants). World average was 2.8%.

no data

≤ 7.5

7.5–15

15–22.5

22.5–30

30–37.5

37.5–45

45–52.5

52.5–60

60–67.5

67.5–75

75–82.5

≥ 82.5

Globally as of 2010 it was estimated that there were 285 million people with type 2 diabetes making up about 90% of diabetes cases.[4] This is equivalent to about 6% of the world’s adult population.[58] Diabetes is common both in the developed and the developing world.[4] It remains uncommon, however, in the underdeveloped world.[3]

Women seem to be at a greater risk as do certain ethnic groups,[4][59] such as South Asians, Pacific Islanders, Latinos, and Native Americans.[7] This may be due to enhanced sensitivity to a Western lifestyle in certain ethnic groups.[60] Traditionally considered a disease of adults, type 2 diabetes is increasingly diagnosed in children in parallel with rising obesity rates.[4] Type 2 diabetes is now diagnosed as frequently as type 1 diabetes in teenagers in the United States.[3]

Rates of diabetes in 1985 were estimated at 30 million, increasing to 135 million in 1995 and 217 million in 2005.[5] This increase is believed to be primarily due to the global population aging, a decrease in exercise, and increasing rates of obesity.[5] The five countries with the greatest number of people with diabetes as of 2000 are India having 31.7 million, China 20.8 million, the United States 17.7 million, Indonesia 8.4 million, and Japan 6.8 million.[61] It is recognized as a global epidemic by the World Health Organization.[62]

History

Main article: History of diabetes

Diabetes is one of the first diseases described[63] with an Egyptian manuscript from c. 1500 BCE mentioning “too great emptying of the urine.”[64] The first described cases are believed to be of type 1 diabetes.[64] Indian physicians around the same time identified the disease and classified it as madhumeha or honey urine noting that the urine would attract ants.[64] The term “diabetes” or “to pass through” was first used in 230 BCE by the Greek Appollonius Of Memphis.[64] The disease was rare during the time of the Roman empire with Galen commenting that he had only seen two cases during his career.[64]

Type 1 and type 2 diabetes were identified as separate conditions for the first time by the Indian physicians Sushruta and Charaka in 400-500 AD with type 1 associated with youth and type 2 with being overweight.[64] The term “mellitus” or “from honey” was added by the Briton John Rolle in the late 1700s to separate the condition from diabetes insipidus which is also associated with frequent urination.[64] Effective treatment was not developed until the early part of the 20th century when the Canadians Frederick Banting and Charles Best discovered insulin in 1921 and 1922.[64] This was followed by the development of the long acting NPH insulin in the 1940s.[64]

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Recognition of Any Warning Symptoms for Diabetic Neuropathy

By Hendra Excel

 

Recognition of any warning symptoms for DIABETIC NEUROPATHY happen to be for serious great importance given that that will lose him or her can get daily life switching or violent strikes.

Diabetic neuropathy is certainly because of any the wall surfaces within the problematic veins who supply any phobia being more powerful.

 

The decreases the option within the phobia that will run impulses back in the brain.

 

 Sorbitol at the same time methods together with gathers during the Schwann debris inducing deeper sensors conduction disadvantages.

 

One can find several different types of neuropathies which can mode utilizing diabetes; polynueropathies together with mononeuropathies.

 

When the warning symptoms seem to be would depend what precisely phobia components happen to be infected.

 

Any warning symptoms may vary among the consumers as well as being impacted by the sum of hurt finished into the phobia.

 

Many other warning symptoms consist of some sort of soreness problems, a good eliminating or simply blasting impression, or simply becoming like your story own frigid your feet.

 

When the neuropathy progresses any warning symptoms consist of drunken sensations for problems, impression, environment, vibration, together with two-point discrimination.

 

 In order to remedy polyneuropathy is certainly thru direction within the diabetes again.

Mononeuropathies happen to be remoted gatherings the fact that change simple phobia.

 

Any warning symptoms for this style of neuropathy happen to be wholly impacted by which unfortunately a sensor is certainly infected.

 

They’ll change any coulometer sensors which unfortunately lead to annoyance, total eye problems together with some sort of failing to safely move a person’s eye in any focus.

 

Most of the victims of diabetes, irrespective of whether model 1 or simply model a pair of, have to pay attention to any warning symptoms for diabetic neuropathy.

 

The sooner it is actually sent to the interest within the victims of diabetes health-related service providers the sooner it really is monitored thru adequate standard of living opportunities that will be devoted to eating routine, activity, together with adequate health related direction.

 

Diabetic Neuropathy Remedy?

 

The actual DIABETIC NEUROPATHY is actually neural harm to entire body extremities, your toes as well as fingers for instance, in addition neural harm to internal organs, digestive system and also the center for instance

.

Here Are the Actual Diabetic Neuropathy Treatments

*The remedy with regard to diabetic neuropathy very first choice would be to manage the actual blood sugar amounts therefore you will find not really inconsistent levels as well as levels.

 

 Administration consists of diet plan as well as physical exercise, in addition medicine in the event that recommended.

 

* In order to avoid heartburn, physicians claim that diabetes sufferers ought to consume lower foods as well as restrict body fat as well as meals full of dietary fiber.

 

Additionally bloodstream stress medicines probably will advantage the actual diabetic as well.

 

An average lotion is actually capsaicin lotion.

 

The Actual Diabetic Neuropathy Details

1 most unfortunate problems associated with diabetes may be the neural harm already been brought on by diabetes.

 

The actual diabetes neuropathy may cause moderate uneasiness for many people, while with regard to other people this particular condition is actually disabling as well as sometimes crucial.

 

Here Are the Actual Diabetic Neuropathy Signs and Symptoms

The actual DIABETIC NEUROPATHY signs and symptoms tend to be based on the kind as well as which anxiety which obtained impacted.

 

The actual signs and symptoms consist of muscle mass coordination difficulties, heartburn, weak point, numbness, discomfort or even tingling (usually within the ft or even fingers), nausea or vomiting as well as bladder difficulties.

 

It might curiosity you to definitely realize that extended blood sugar levels extreme conditions blood sugar levels that is possibly excessive or even as well reduced with regard to too much time could cause numerous problems, which can result in the diabetic coma.

 

REFRENCESBottom of Form

Bottom of Form

 

 Core Papers 


Label: Dworkin-2003
Title: Advances in neuropathic pain – Diagnosis, mechanisms, and treatment recommendations
Journal: ARCH NEUROL, 60 (11): 1524-1534 NOV 2003
Citations: 274
Authors: Dworkin, RH;Backonja, M;Rowbotham, MC;Allen, RR;Argoff, CR;Bennett, GJ;Bushnell, MC;Farrar, JT;Galer, BS;Haythornthwaite, JA;Hewitt, DJ;Loeser, JD;Max, MB;Saltarelli, M;Schmader, KE;Stein, C;Thompson, D;Turk, DC;Wallace, MS;Watkins, LR;Weinstein, SM
Addresses:
Univ Rochester, Sch Med & Dent, Dept Anesthesiol, 601 Elmwood Ave,Box 604, Rochester, NY 14642 USA
Univ Rochester, Sch Med & Dent, Dept Anesthesiol, Rochester, NY 14642 USA[Back to Map]     Label: Dworkin-2003
Title: Pregabalin for the treatment of postherpetic neuralgia – A randomized, placebo-controlled trial
Journal: NEUROLOGY, 60 (8): 1274-1283 APR 22 2003
Citations: 171
Authors: Dworkin, RH;Corbin, AE;Young, JP;Sharma, U;LaMoreaux, L;Bockbrader, H;Garofalo, EA;Poole, RM
Addresses:
Univ Rochester, Sch Med & Dent, 601 Elmwood Ave,Box 604, Rochester, NY 14642 USA
Univ Rochester, Sch Med & Dent, Rochester, NY 14642 USA
Pfizer Global Res & Dev, Ann Arbor, MI USA

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Label: Ballantyne-2003
Title: Opioid therapy for chronic pain
Journal: N ENGL J MED, 349 (20): 1943-1953 NOV 13 2003
Citations: 162
Authors: Ballantyne, JC;Mao, JR
Addresses:
Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Pain Ctr, 15 Parkman St,WACC 333, Boston, MA 02114 USA
Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Pain Ctr, Boston, MA 02114 USA
Harvard Univ, Sch Med, Boston, MA USA

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Label: Goldstein-2005
Title: Duloxetine vs. placebo in patients with painful diabetic neuropathy
Journal: PAIN, 116 (1-2): 109-118 JUL 2005
Citations: 144
Authors: Goldstein, DJ;Lu, YL;Detke, MJ;Lee, TC;Iyengar, S
Addresses:
Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA
Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA
PRN Consulting, Indianapolis, IN USA
Indiana Univ, Sch Med, Dept Pharmacol & Toxicol, Indianapolis, IN 46202 USA
Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA
McLean Hosp, Dept Psychiat, Belmont, MA 02178 USA
Harvard Univ, Sch Med, Boston, MA USA

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Label: Finnerup-2005
Title: Algorithm for neuropathic pain treatment: An evidence based proposal
Journal: PAIN, 118 (3): 289-305 DEC 5 2005
Citations: 143
Authors: Finnerup, NB;Otto, M;McQuay, HJ;Jensen, TS;Sindrup, SH
Addresses:
Aarhus Univ Hosp, Danish Pain Res Ctr, Dept Neurol, Aarhus Sygehus, Norrebrogade 44, Aarhus 8000, Denmark
Aarhus Univ Hosp, Danish Pain Res Ctr, Dept Neurol, Aarhus Sygehus, Aarhus 8000, Denmark
Odense Univ Hosp, Dept Neurol, Odense 5000, Denmark
Churchill Hosp, Pain Relief Unit, Oxford OX3 7LJ, England

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Label: Gilron-2005
Title: Morphine, gabapentin, or their combination for neuropathic pain
Journal: N ENGL J MED, 352 (13): 1324-1334 MAR 31 2005
Citations: 142
Authors: Gilron, I;Bailey, JM;Tu, DS;Holden, RR;Weaver, DF;Houlden, RL
Addresses:
Queens Univ, Dept Anesthesiol, 76 Stuart St, Kingston, ON K7L 2V7, Canada
Queens Univ, Dept Anesthesiol, Kingston, ON K7L 2V7, Canada
Queens Univ, Dept Pharmacol & Toxicol, Kingston, ON K7L 2V7, Canada
Queens Univ, Dept Math & Stat, Kingston, ON K7L 2V7, Canada
Queens Univ, Dept Epidemiol & Community Hlth, Kingston, ON K7L 2V7, Canada
Queens Univ, Dept Psychol, Kingston, ON K7L 2V7, Canada
Queens Univ, Dept Med, Div Endocrinol, Kingston, ON K7L 2V7, Canada
Dalhousie Univ, Dept Med, Div Neurol, Halifax, NS, Canada
Dalhousie Univ, Dept Chem, Halifax, NS, Canada

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Label: Rosenstock-2004
Title: Pregabalin for the treatment of painful diabetic peripheral neuropathy: a double-blind, placebo-controlled trial
Journal: PAIN, 110 (3): 628-638 AUG 2004
Citations: 141
Authors: Rosenstock, J;Michael, TB;LaMoreaux, L;Sharma, U
Addresses:
Dallas Diabet & Endo Res Ctr, 7777 Forest Lane,C618, Dallas, TX 75230 USA
Dallas Diabet & Endo Res Ctr, Dallas, TX 75230 USA
Palm Beach Neurol Ctr, Palm Beach Gardens, FL USA
Pfizer Global Res & Dev, Ann Arbor, MI USA

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Label: Rowbotham-2003
Title: Oral opioid therapy for chronic peripheral and central neuropathic pain
Journal: N ENGL J MED, 348 (13): 1223-1232 MAR 27 2003
Citations: 127
Authors: Rowbotham, MC;Twilling, L;Davies, PS;Reisner, L;Taylor, K;Mohr, D
Addresses:
Univ Calif San Francisco, Sch Med, Pain Clin, Res Ctr,Dept Neurol, 1701 Divisadero St,Ste 480, San Francisco, CA 94115 USA
Univ Calif San Francisco, Sch Med, Pain Clin, Res Ctr,Dept Neurol, San Francisco, CA 94115 USA
Univ Calif San Francisco, Sch Med, Dept Anesthesia, San Francisco, CA 94115 USA
Univ Calif San Francisco, Sch Pharm, San Francisco, CA 94115 USA

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Label: Arnold-2004
Title: A double-blind, multicenter trial comparing duloxetine with placebo in the treatment of fibromyalgia patients with or without major depressive disorder
Journal: ARTHRITIS RHEUM, 50 (9): 2974-2984 SEP 2004
Citations: 122
Authors: Arnold, LM;Lu, YL;Crofford, LJ;Wohlreich, M;Detke, MJ;Iyengar, S;Goldstein, DJ;Duloxetine Fibromyalgia Trial Grp
Addresses:
Univ Cincinnati, Coll Med, Med Arts Bldg,Suite 8200,222 Piedmont Ave, Cincinnati, OH 45219 USA
Univ Cincinnati, Coll Med, Cincinnati, OH 45219 USA
Eli Lilly & Co, Indianapolis, IN 46285 USA
Univ Michigan, Ann Arbor, MI 48109 USA
Indiana Univ, Sch Med, Indianapolis, IN USA
Harvard Univ, Sch Med, Boston, MA 02115 USA
McLean Hosp, Belmont, MA 02178 USA
PRN Consulting, Indianapolis, IN USA

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Label: Kalso-2004
Title: Opioids in chronic non-cancer pain: systematic review of efficacy and safety
Journal: PAIN, 112 (3): 372-380 DEC 2004
Citations: 122
Authors: Kalso, E;Edwards, JE;Moore, RA;McQuay, HJ
Addresses:
Univ Helsinki, Pain Clin, Dept Anaesthesia & Intens Care Med, Cent Hosp, POB 340, FIN-00029 HUS, Finland
Univ Helsinki, Pain Clin, Dept Anaesthesia & Intens Care Med, Cent Hosp, FIN-00029 HUS, Finland
Univ Oxford, Oxford Radcliffe Hosp, Pain Res & Nuffield Dept Anaesthet, Oxford OX3 7LJ, England

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Label: Goldenberg-2004
Title: Management of fibromyalgia syndrome
Journal: JAMA-J AM MED ASSN, 292 (19): 2388-2395 NOV 17 2004
Citations: 119
Authors: Goldenberg, DL;Burckhardt, C;Crofford, L
Addresses:
Newton Wellesley Hosp, Dept Rheumatol, 2000 Washington St, Newton, MA 02462 USA
Newton Wellesley Hosp, Dept Rheumatol, Newton, MA 02462 USA
Tufts Univ, Sch Med, Dept Med, Boston, MA 02111 USA
Oregon Hlth & Sci Univ, Sch Nursing, Portland, OR USA
Univ Michigan, Sch Med, Dept Internal Med, Div Rheumatol, Ann Arbor, MI USA

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Label: Lesser-2004
Title: Pregabalin relieves symptoms of painful diabetic neuropathy – A randomized controlled trial
Journal: NEUROLOGY, 63 (11): 2104-2110 DEC 14 2004
Citations: 117
Authors: Lesser, H;Sharma, U;LaMoreaux, L;Poole, RM
Addresses:
1415 Portland Ave,Suite 480, Rochester, NY 14621 USA
Univ Rochester, Sch Med & Dent, Rochester, NY USA
Pfizer Global Res & Dev, Ann Arbor, MI USA
Pfizer Global Res & Dev, New London, CT USA

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Label: Crofford-2005
Title: Pregabalin for the treatment of fibromyalgia syndrome – Results of a randomized, double-blind, placebo-controlled trial
Journal: ARTHRITIS RHEUM, 52 (4): 1264-1273 APR 2005
Citations: 110
Authors: Crofford, LJ;Rowbotham, MC;Mease, PJ;Russell, IJ;Dworkin, RH;Corbin, AE;Young, JP;LaMoreaux, LK;Martin, SA;Sharma, U;Pregabalin 1008-15 Study Grp
Addresses:
Kentucky Clin, Room J-503,740 S Limestone St, Lexington, KY 40539 USA
Kentucky Clin, Lexington, KY 40539 USA
Univ Michigan, Ann Arbor, MI 48109 USA
Univ Calif San Francisco, San Francisco, CA 94143 USA
Rheumatol Associates, Seattle, WA USA
Swedish Med Ctr, Seattle, WA USA
Univ Texas, Ctr Hlth Sci, San Antonio, TX USA
Univ Rochester, Sch Med & Dent, Rochester, NY USA
Pfizer Global Res & Dev, Ann Arbor, MI USA

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Label: Sabatowski-2004
Title: Pregabalin reduces pain and improves sleep and mood disturbances in patients with post-herpetic neuralgia: results of a randomised, placebo-controlled clinical trial
Journal: PAIN, 109 (1-2): 26-35 MAY 2004
Citations: 108
Authors: Sabatowski, R;Galvez, R;Cherry, DA;Jacquot, F;Vincent, E;Maisonobe, P;Versavel, M;1008-045 Study Grp
Addresses:
Univ Cologne, Anasthesiol Klin, Dept Anaesthesiol, D-50924 Cologne, Germany
Univ Cologne, Anasthesiol Klin, Dept Anaesthesiol, D-50924 Cologne, Germany
Univ Hosp Virgen Nieves, Pain Clin, Granada, Spain
Flinders Med Ctr, Bedford Pk, SA, Australia
Pfizer Global Res & Dev, Fresnes, France

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Label: Goldstein-2004
Title: Duloxetine in the treatment of depression – A double-blind-placebo-controlled comparison with paroxetine
Journal: J CLIN PSYCHOPHARMACOL, 24 (4): 389-399 AUG 2004
Citations: 107
Authors: Goldstein, DJ;Lu, YL;Detke, MJ;Wiltse, C;Mallinckrodt, C;Demitrack, MA
Addresses:
Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA
Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA
PRN Consulting, Indianapolis, IN USA
Indiana Univ, Sch Med, Dept Pharmacol & Toxicol, Indianapolis, IN 46204 USA
Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46204 USA
McLean Hosp, Dept Psychiat, Belmont, MA 02178 USA
Harvard Univ, Sch Med, Boston, MA 02115 USA
Neuronet Inc, Malvern, PA USA

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Label: Freynhagen-2005
Title: Efficacy of pregabalin in neuropathic pain evaluated in a 12-week, randomised, double-blind, multicentre, placebo-controlled trial of flexible- and fixed-dose regimens
Journal: PAIN, 115 (3): 254-263 JUN 2005
Citations: 97
Authors: Freynhagen, R;Strojek, K;Griesing, T;Whalen, E;Balkenohl, M
Addresses:
Univ Klinikum Dusseldorf, Anasthesiol Klin, Moorenstr 5, D-40225 Dusseldorf, Germany
Univ Klinikum Dusseldorf, Anasthesiol Klin, D-40225 Dusseldorf, Germany
Dept Internal Dis Diabetol & Nephrol, Zabrze, Poland
Pfizer Inc, New York, NY USA
Pfizer Global Pharamceut, Freiburg, Germany

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Label: Detke-2004
Title: Duloxetine in the acute and long-term treatment of major depressive disorder: a placebo- and paroxetine-controlled trial
Journal: EUR NEUROPSYCHOPHARMACOL, 14 (6): 457-470 DEC 2004
Citations: 89
Authors: Detke, MJ;Wiltse, CG;Mallinckrodt, CH;McNamara, RK;Demitrack, MA;Bitter, I
Addresses:
Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA
Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA
Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA
McLean Hosp, Dept Psychiat, Belmont, MA 02178 USA
Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA
Neuronet Inc, Malvern, PA USA
Semmelweis Univ Med, Dept Psychiat & Psychotherapy, H-1085 Budapest, Hungary

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Label: Richter-2005
Title: Relief of painful diabetic peripheral neuropathy with pregabalin: A randomized, placebo-controlled trial
Journal: J PAIN, 6 (4): 253-260 APR 2005
Citations: 83
Authors: Richter, RW;Portenoy, R;Sharma, U;Lamoreaux, L;Bockbrader, H;Knapp, LE
Addresses:
Beth Israel Med Ctr, Dept Pain Med & Palliat Care, 1st Ave 16th St, New York, NY 10003 USA
Beth Israel Med Ctr, Dept Pain Med & Palliat Care, New York, NY 10003 USA
St Johns Hosp, Dept Neurol, Tulsa, OK USA
Pfizer Global Res & Dev, Ann Arbor, MI USA

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Label: Raskin-2005
Title: A double-blind, randomized multicenter trial comparing duloxetine with placebo in the management of diabetic peripheral neuropathic pain
Journal: PAIN MED, 6 (5): 346-356 SEP-OCT 2005
Citations: 78
Authors: Raskin, J;Pritchett, YL;Wang, FJ;D’Souza, DN;Waninger, AL;Iyengar, S;Wernicke, JF
Addresses:
Eli Lilly Canada, Lilly Res Labs, 3650 Danforth Ave, Toronto, ON MIN 2E8, Canada
Eli Lilly Canada, Lilly Res Labs, Toronto, ON MIN 2E8, Canada
Eli Lilly & Co, Lilly Corp Ctr, Lilly Res Labs, Indianapolis, IN 46285 USA

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Label: Eisenberg-2005
Title: Efficacy and safety of opioid agonists in the treatment of neuropathic pain of nonmalignant origin – Systematic review and meta-analysis of randomized controlled trials
Journal: JAMA-J AM MED ASSN, 293 (24): 3043-3052 JUN 22 2005
Citations: 75
Authors: Eisenberg, E;McNicol, ED;Carr, DB
Addresses:
Rambam Med Ctr, Pain Relief Unit, POB 9602, IL-31096 Haifa, Israel
Rambam Med Ctr, Pain Relief Unit, IL-31096 Haifa, Israel
Technion Israel Inst Technol, Haifa Pain Res Grp, Haifa, Israel
Tufts New England Med Ctr, Dept Anesthesia, Boston, MA USA
Tufts New England Med Ctr, Dept Pharm, Boston, MA USA
Tufts New England Med Ctr, Div Clin Care Res, Boston, MA USA
Tufts Univ, Sch Med, Boston, MA 02111 USA

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Label: Arnold-2005
Title: A randomized, double-blind, placebo-controlled trial of duloxetine in the treatment of women with fibromyalgia with or without major depressive disorder
Journal: PAIN, 119 (1-3): 5-15 DEC 15 2005
Citations: 68
Authors: Arnold, LM;Rosen, A;Pritchett, YL;D’Souza, DN;Goldstein, DJ;Iyengar, S;Wernicke, JF
Addresses:
Univ Cincinnati, Coll Med, Womens Hlth Res Program, Dept Psychiat, 222 Piedmont Ave,Suite 8200, Cincinnati, OH 45219 USA
Univ Cincinnati, Coll Med, Womens Hlth Res Program, Dept Psychiat, Cincinnati, OH 45219 USA
Lilly Res Labs, Indianapolis, IN USA
Indiana Univ, Sch Med, Indianapolis, IN 46204 USA
PRN Consulting, Indianapolis, IN 46204 USA

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Label: Furlan-2006
Title: Opioids for chronic noncancer pain: a meta-analysis of effectiveness and side effects
Journal: CAN MED ASSN J, 174 (11): 1589-1594 MAY 23 2006
Citations: 63
Authors: Furlan, AD;Sandoval, JA;Mailis-Gagnon, A;Tunks, E
Addresses:
Toronto Western Hosp, Comprehens Pain Program, 399 Bathurst St,Rm 4F811, Toronto, ON M5T 2S8, Canada
Toronto Western Hosp, Comprehens Pain Program, Toronto, ON M5T 2S8, Canada
Univ Toronto, Ctr Study Pain, Toronto, ON, Canada
Univ Toronto, Inst Work & Hlth, Toronto, ON, Canada
Toronto Western Hosp, Krembil Neurosci Ctr, Toronto, ON M5T 2S8, Canada
McMaster Univ, Chedoke Rehabil Ctr, Hamilton Hlth Sci Hosp, Hamilton, ON, Canada

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Label: Attal-2006
Title: EFNS guidelines on pharmacological treatment of neuropathic pain
Journal: EUR J NEUROLOGY, 13 (11): 1153-1169 NOV 2006
Citations: 50
Authors: Attal, N;Cruccu, G;Haanpaa, M;Hansson, P;Jensen, TS;Nurmikko, T;Sampaio, C;Sindrup, S;Wiffen, P
Addresses:
Hop Ambroise Pare, Ctr Evaluat & Traitement Douleur, EFNS Panel Neuropath Pain, Boulogne, France
Hop Ambroise Pare, Ctr Evaluat & Traitement Douleur, EFNS Panel Neuropath Pain, Boulogne, France
Hop Ambroise Pare, Ctr Evaluat & Traitement Douleur, INSERM, U792, Boulogne, France
Univ Versailles St Quentin, Boulogne, France
Univ Versailles St Quentin, Boulogne, France
Univ Roma La Sapienza, Dept Neurol Sci, Rome, Italy
Helsinki Univ Hosp, Dept Anaesthesiol, Pain Clin, Helsinki, Finland
Helsinki Univ Hosp, Dept Neurosurg, Pain Clin, Helsinki, Finland
Univ Hosp, Karolinska Inst, Dept Mol Med, Stockholm, Sweden
Univ Hosp, Karolinska Inst, Surg Sect Clin Pain Res, Stockholm, Sweden
Univ Hosp, Karolinska Inst, Pain Ctr, Dept Neurosurg, Stockholm, Sweden
Aarhus Univ Hosp, Dept Neurol, DK-8000 Aarhus, Denmark
Aarhus Univ Hosp, Danish Pain Res Ctr, DK-8000 Aarhus, Denmark
Univ Liverpool, Pain Res Inst, Div Neurol Sci, Sch Clin Sci, Liverpool L69 3BX, Merseyside, England
Univ Lisbon, Inst Farmacol & Terapeut Geral, Lisbon Sch Med, P-1699 Lisbon, Portugal
Odense Univ Hosp, Dept Neurol, DK-5000 Odense, Denmark
Cochrane Pain & Palliat Care Review Grp, Oxford, England

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Label: Brannan-2005
Title: Duloxetine 60 mg once-daily in the treatment of painful physical symptoms in patients with major depressive disorder
Journal: J PSYCHIAT RES, 39 (1): 43-53 JAN 2005
Citations: 50
Authors: Brannan, SK;Mallinckrodt, CH;Brown, EB;Wohlreich, MM;Watkin, JG;Schatzberg, AF
Addresses:
Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA
Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA
Cyberon, Houston, TX 77058 USA
Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA

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Label: Martell-2007
Title: Systematic review: Opioid treatment for chronic back pain: Prevalence, efficacy, and association with addiction
Journal: ANN INTERN MED, 146 (2): 116-127 JAN 16 2007
Citations: 46
Authors: Martell, BA;O’Connor, PG;Kerns, RD;Becker, WC;Morales, KH;Kosten, TR;Fiellin, DA
Addresses:
Yale Univ, Sch Med, 333 Cedar St,POB 208025, New Haven, CT 06520 USA
Yale Univ, Sch Med, New Haven, CT 06520 USA
VA Connecticut Hlth Care Syst, West Haven, CT USA
Univ Penn, Sch Med, Philadelphia, PA 19104 USA

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Label: Ballantyne-2007
Title: Opioid dependence and addiction during opioid treatment of chronic pain
Journal: PAIN, 129 (3): 235-255 JUN 2007
Citations: 32
Authors: Ballantyne, JC;LaForge, KS
Addresses:
Massachusetts Gen Hosp, Div Pain Med, Pain Ctr, 15 Parkman St,WACC 333, Boston, MA 02114 USA
Massachusetts Gen Hosp, Div Pain Med, Pain Ctr, Boston, MA 02114 USA
Harvard Univ, Sch Med, Boston, MA 02115 USA
Univ Helsinki, Finnish Genome Ctr, FIN-00014 Helsinki, Finland

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Label: Ives-2006
Title: Predictors of opioid misuse in patients with chronic pain: a prospective cohort study
Journal: BMC HEALTH SERV RES, 6: art. no.-46 APR 4 2006
Citations: 29
Authors: Ives, TJ;Chelminski, PR;Hammett-Stabler, CA;Malone, RM;Perhac, JS;Potisek, NM;Shilliday, BB;DeWalt, DA;Pignone, MP
Addresses:
Univ N Carolina, Sch Med, Dept Med, Div Gen Internal Med, Chapel Hill, NC 27599 USA
Univ N Carolina, Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC USA
Univ N Carolina, Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC USA
Univ N Carolina Hlth Syst, Ctr Excellence Chron Illness Care, Chapel Hill, NC USA

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Label: Arnold-2007
Title: Gabapentin in the treatment of fibromyalgia – A randomized, double-blind, placebo-controlled, multicenter trial
Journal: ARTHRITIS RHEUM, 56 (4): 1336-1344 APR 2007
Citations: 28
Authors: Arnold, LM;Goldenberg, DL;Stanford, SB;Lalonde, JK;Sandhu, HS;Keck, PE;Welge, JA;Bishop, F;Stanford, KE;Hess, EV;Hudson, JI
Addresses:
Univ Cincinnati, Coll Med, Med Arts Bldg,222 Piedmont Ave,Suite 8200, Cincinnati, OH 45219 USA
Univ Cincinnati, Coll Med, Cincinnati, OH 45219 USA
Newton Wellesley Hosp, Newton, MA USA
Tufts Univ, Sch Med, Boston, MA 02111 USA
McLean Hosp, Belmont, MA 02178 USA
Harvard Univ, Sch Med, Boston, MA 02115 USA

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Label: Vinik-2007
Title: Lamotrigine for treatment of pain associated with diabetic neuropathy: Results of two randomized, double-blind, placebo-controlled studies
Journal: PAIN, 128 (1-2): 169-179 MAR 2007
Citations: 28
Authors: Vinik, AI;Tuchman, M;Safirstein, B;Corder, C;Kirby, L;Wilks, K;Quessy, S;Blum, D;Grainger, J;White, J;Silver, M
Addresses:
Eastern Virginia Med Sch, Inst Diabet, 855 W Brandleton, Norfolk, VA 23510 USA
Eastern Virginia Med Sch, Inst Diabet, Norfolk, VA 23510 USA
Palm Beach Neurol Ctr, Palm Beach Gardens, FL USA
Baumel Eisner Neuromed Inst, Bay Harbor, FL USA
COR Clin Res, Oklahoma City, OK USA
Pivotal Res Ctr, Peoria, AZ USA
IMR, Towson, MD USA
GlaxoSmithKline Inc, Res Triangle Pk, NC USA

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Label: Raskin-2007
Title: Efficacy of duloxetine on cognition, depression, and pain in elderly patients with major depressive disorder: An 8-week, double-blind, placebo-controlled trial
Journal: AMER J PSYCHIAT, 164 (6): 900-909 JUN 2007
Citations: 17
Authors: Raskin, J;Wiltse, CG;Siegal, A;Sheikh, J;Xu, J;Dinkel, JJ;Rotz, BT;Mohs, RC
Addresses:
Eli Lilly Canada, Lilly Res Labs, 3650 Danforth Ave, Toronto, ON M1N 2E8, Canada
Eli Lilly Canada, Lilly Res Labs, Toronto, ON M1N 2E8, Canada
Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA
Geriatr & Adult Psychiat LLC, Hamden, CT USA
Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA

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KEYWORDS: NEUROPATHIC PAIN TREATMENT; RANDOMIZED MULTICENTER TRIAL COMPARING DULOXETINE; DIABETIC PERIPHERAL NEUROPATHIC PAIN; CENTRAL NEUROPATHIC PAIN; NEUROPATHIC PAIN EVALUATED.
[5770: (2002-2008_6) (CLI-NEU: ST Diabetes)]

 

 Selesai

The end

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