The Cute’s Innocent Expression Art Photography PART ONE










The Driwan’s  Cybermuseum


part one


If You want to choose a girlfriend,fiance or Wife,please look rthdeir innocent exprsession like the art photography below.
















the end @ copyright Dr Iwan suwandy 2011


The Sinking of Lampong Poetry about Krakatoa Mount Eruption 1883











The Driwan’s  Cybermuseum

The sinking of Lampong poetry

The eruption of Mount Krakatau


Top of Form

Long before foreign researchers wrote about the eruption of Mount Krakatau (Krakatoa, Carcata) on 26, 27, and August 28, 1883, a native witness has written a very rare and interesting, three months after the eruption of  Krakatoa through Lampung Karang (Lampong sinking) poetry .


“Scientific studies and bibiliografi about Krakatoa almost missed include only indigenous written sources, which record the testimonies of the eruption of Krakatoa in 1883. Two years of research, I found the only native testimony in written form, “he said. Before the eruption on 26, 27, and August 28, 1883, the Krakatoa volcano has coughed since May 20, 1883. Krakatoa eruption caused pyroclastic as high as 70 km and 40-meter high tsunami that killed about 36,000 people.

Before the 1883 eruption, Mount Krakatoa had never exploded around the year 1680 / 1.

The eruption that led to the three islands adjacent to each other; Sertung Island, Little Rakata Island, and the island of Rakata. Suryadi explained, as long as it is to be reading about the eruption of Mount Krakatoa is a complete research report GJ Symons et al, The Eruption of Krakatoa and Subsequent Phenomena: Report of the Krakatoa Committee of the Royal Society (London, 1888).

While the indigenous written sources published in Singapore in printed form stones (litography) in 1883/1884. Kolofonnya recorded in 1301 AH (November 1883-October 1884).


The first edition is titled Poetry Lampung District Water and Rain ridden by Abu (42 pages). “A short time later came the second edition of this poem with the title This is the poem Lampung ridden Sea (42 pages). The second edition was also published in Singapore on 2 Safar 1302 H (21 November 1884), “he explained.
The third edition of the poem titled Lampung and Anyer and the Cape Coral Sea Rise (49 pages), published by Haji Said. This third edition also published in Singapore, bertarikh 27 Rabiulawal 1301 AH (January 3, 1886). In some ads, this third edition of the poem called Anyer Sunset District. “

The fourth edition of this poem, the last edition as far as I know, This is the poem entitled The Karam Lampung (36 pages). This fourth edition also published in Singapore, Safat bertarikh 10 1306 H (October 16, 1888), “said Suryadi, the dozens of research results have been published in various international journals.
According to Suryadi, the fourth edition of the text special poem written in Malay and Arabic wear-Malay (Jawi). From the comparison of the text which he did, there are significant variations between each edition. This indicates that kelisanan influence is still strong in the tradition of literacy that began to grow in the archipelago in the second half of the 19th century.
Suryadi who managed to identify the place where copies of all editions of Lampung Karam poem that still exists in the world until now to mention, Lampung poem written Karam Mohammed Saleh. He admitted writing the poem in Kampung Bangkahulu (then called Bencoolen Street) in Singapore. “Muhammad Saleh claimed was in Cape Coral when the eruption of Krakatoa occurred and witnessed the great natural disaster that with his own eyes. It is likely that the poet was a victim of the eruption of Krakatoa which went fled to Singapore, and brings scary memories of natural disasters mahadahsyat it, “he said.
 Lampung Karam or the sinking of Lampong poetry can be categorized as a poetic journalism, because the more strongly highlight the nuances of journalism. In Lampung Karam Poetry 38 pages in length and 374 verse, Mohammed Saleh dramatically illustrate the great disaster that followed the eruption of Mount Krakatoa in 1883. He told the destruction of villages and mass death caused by the eruption. Areas such as Earth, Kitambang, Gutters, Kupang, Lampasing, Umbulbatu, Benawang, Rhino, Limes, monkey, Mount Bases, Gunung Sari, Minanga, Tanjung, Kampung teba, Middle Village, Kuala, Rajabasa, Cape Coral, Island also Sebesi , Sebuku, and Peacock devastated by the tsunami, mud, and rain of ash and rock.
The author tells how in a heartbreaking situation and turmoil, people are still willing to help each other help each other. However, not a few who take the opportunity to enrich themselves by taking the property and other people’s money is overwritten disaster. Besides tracing the editions published poem Lampung Karam remaining in the world until now, the study also presents transliterations Suryadi (control characters) text of this poem in the Latin alphabet.

another info

The legendary annihilation in 1883 of the volcano-island of Krakatoa — the name has since become a by-word for a cataclysmic disaster — was followed by an immense tsunami that killed nearly 40,000 people. Beyond the purely physical horrors of an event which has only very recently become properly understood, the eruption changed the world in more ways than could possibly be imagined. Dust swirled round the world for years, causing temperatures to plummet and sunsets to turn vivid with lurid and unsettling displays of lght. The effects of the immense waves were felt as far away as France. Barometers in Bogota and Washington went haywire. Bodies were washed up in Zanzibar. The sound of island’s destruction was heard in Australia and India and on islands thousands of miles away.


The 1883 explosion on an uninhabited island in Indonesia was one of the most catastrophic in history. Before the eruption, this island in the Sunda Straits between Java and Sumatra islands was made up of three stratovolcanoes that had grown together.

In the summer of 1883, one of Krakatau’s three cones became active. Sailors reported seeing clouds of ash rising from the island. The eruptions reached a peak in August, culminating in a series of tremendous explosions. The most ear-shattering eruption was heard in Australia, more than 2,000 miles (3,200 kilometers) away.

Ash was sent 50 miles (80 kilometers) into the sky and blanketed an area of 300,000 square miles (800,000 square kilometers), plunging the area into darkness for two and a half days. The ash drifted around the globe, causing spectacular sunsets and halo effects around the moon and sun.

The explosions also sent as much as 5 cubic miles (21 cubic kilometers) of rock fragments into the air. The northern two-thirds of the island collapsed under the sea into the newly vacated magma chamber. Much of the remaining island sank into a caldera about 3.8 miles (6 kilometers) across.

The collapse set off an immense series of tsunamis, or giant sea waves, that traveled as far as Hawaii and South America. The largest wave loomed 120 feet (37 meters) high and destroyed 165 nearby settlements. All vegetation was stripped bare, structures were
demolished, and some 30,000 people were washed out to sea in Java and Sumatra.

Krakatau was quiet until the 1920s, when volcanic activity began again. Since then, eruptions have built a new cone, Anak Krakatau, or “child of Krakatau” in the center of the caldera created in 1883

Krakatoa eruption 1930


Krakatoa mount now


the end @ copyright Dr Iwan Suwandy 2011

The Rare King Farouk , Fuoad and other Egypt Stamps










The Driwan’s  Cybermuseum


Rare Egypt



1.Port Fuoad Overprint Stamps 1926

a. On King Fuoad stamps 

Est. £600-700

On Congres International De Navigations Stamps

Est. £120-150


2.King Fuoad Wedding stamp


Est. £120-150 


Port Fuad



Port Fuad

Port Fuad as seen across the Suez Canal from Port Said.

Port Fuad is located in Egypt

Port Fuad

Location in Egypt

Coordinates: 31°15′N 32°19′E / 31.25°N 32.317°E / 31.25; 32.317
Country  Egypt
Governorate Port Said Governorate
Population (2003)
 – Total 560,000
Time zone EST (UTC+2)
 – Summer (DST) +3 (UTC)

Port Fuad (Arabic: بور فؤاد ‎; Būr Fu’ād) is a city in north-eastern Egypt under the jurisdiction of Port Said Governorate, located across the Suez Canal from Port Said. It forms the northwesternmost part of Sinai Peninsula and has a population of 560,000 (as of 2003). Port Fuad and Port Said together form a metropolitan area.

Port Fuad was established in 1926, principally to relieve overcrowding in Port Said, and was named after King Fuad I (also transliterated as Fuad), the first holder of the title King of Egypt in the modern era (having previously held the title Sultan of Egypt).

The city is located on a triangular island which is bounded by the Mediterranean on the north, the Suez Canal on the west, and the relatively new junction between the Suez Canal and the Mediterranean on the east. The Suez Canal Authority forms the main employment of the city, and its employees comprise most of the population. It has one general hospital.

After the war of 1967 Port Fuad was the only piece of Sinai held by the Egyptians. The Israelis tried to capture Port Fuad countless of times during the War of Attrition, but failed each time. During October War Port Fuad was secured and land was regained around it to ensure it would never be attacked or bombed again by the Israelis. The war ended with a strategic victory for Egypt, and in the Camp David Accord in 1978 Israel agreed to return Sinai to Egypt peacefully, and later the two countries signed a peace treaty. Today Port Fuad is a major Air Defense Position for Egypt.


Local dissatisfaction with Ismail and with European intrusion led to the formation of the first nationalist groupings in 1879, with Ahmad Urabi a prominent figure. In 1882 he became head of a nationalist-dominated ministry committed to democratic reforms including parliamentary control of the budget. Fearing a reduction of their control, the UK and France intervened militarily, bombarding Alexandria and crushing the Egyptian army at the battle of Tel el-Kebir.[31] They reinstalled Ismail’s son Tewfik as figurehead of a de facto British protectorate.[32]

Female nationalists demonstrating in Cairo, 1919

In 1914 the Protectorate was made official, and the title of the head of state, which had changed from pasha to khedive in 1867, was changed to sultan, to repudiate the vestigial suzerainty of the Ottoman sultan, who was backing the Central powers in World War I. Abbas II was deposed as khedive and replaced by his uncle, Hussein Kamel, as sultan.[33]

In 1906, the Dinshaway Incident prompted many neutral Egyptians to join the nationalist movement. After the First World War, Saad Zaghlul and the Wafd Party led the Egyptian nationalist movement to a majority at the local Legislative Assembly.

When the British exiled Zaghlul and his associates to Malta on 8 March 1919, the country arose in its first modern revolution. The revolt led the UK government to issue a unilateral declaration of Egypt’s independence on 22 February 1922.[34]



The new government drafted and implemented a constitution in 1923 based on a parliamentary system.

 Saad Zaghlul was popularly elected as Prime Minister of Egypt in 1924.

 In 1936 the Anglo-Egyptian Treaty was concluded. Continued instability due to remaining British influence and increasing political involvement by the king led to the dissolution of the parliament in a military coup d’état known as the 1952 Revolution. The Free Officers Movement forced King Farouk to abdicate in support of his son Fuad. British military presence in Egypt lasted until 1954.


Farouk of Egypt

King of Egypt and the Sudan
Coat of arms of the Egyptian Kingdom.gifOfficial Seal of the King of Egypt

Photograph of Farouk I by Riad Shehata
Reign 28 April 1936 – 26 July 1952
Coronation 29 July 1937 (aged 17)[1]
Arabic فاروق الأول
Born 11 February 1920(1920-02-11)
Birthplace Abdeen Palace, Cairo, Egypt
Died 18 March 1965(1965-03-18) (aged 45)
Place of death Rome, Italy
Buried Al-Rifa’i Mosque, Cairo, Egypt
Predecessor Fuad I
Successor Fuad II
Consort to Farida (née Safinaz Zulficar)
(m. 1938; div. 1948)
Narriman Sadek
(m. 1951; div. 1954)
Offspring Princess Ferial
Princess Fawzia
Princess Fadia
Fuad II
Dynasty Muhammad Ali Dynasty
Father Fuad I
Mother Nazli Sabri
Religious beliefs Sunni Islam
Signature Farouk I signature.svg

Farouk I of Egypt (Arabic: فاروق الأول Fārūq al-Awwal) (11 February 1920 – 18 March 1965), was the tenth ruler from the Muhammad Ali Dynasty and the penultimate King of Egypt and Sudan, succeeding his father, Fuad I, in 1936.

His full title was “His Majesty Farouk I, by the grace of God, King of Egypt and Sudan, Sovereign of Nubia, of Kordofan, and of Darfur.” He was overthrown in the Egyptian Revolution of 1952, and was forced to abdicate in favor of his infant son Ahmed Fuad, who succeeded him as King Fuad II. He died in exile in Italy.

His sister was Princess Fawzia Fuad, first wife and Queen Consort of the Shah of Iran Mohammad Reza Pahlavi.

Early life


As Crown Prince, Farouk held the rank of First Scout of Egypt.


The great-great-grandson of Khalid Kamel Pasha, Farouk was of Albanian descent as well as native Egyptian and Turkish descent through his mother Queen Nazli Sabri.[2][3] Before his father’s death, he was educated at the Royal Military Academy, Woolwich, England. Upon his coronation, the hugely popular 16-year-old King Farouk made a public radio address to the nation, the first time a sovereign of Egypt had ever spoken directly to his people in such a way:

And if it is God’s will to lay on my shoulders at such an early age the responsibility of kingship, I on my part appreciate the duties that will be mine, and I am prepared for all sacrifices in the cause of my duty… My noble people, I am proud of you and your loyalty and am confident in the future as I am in God. Let us work together. We shall succeed and be happy. Long live the Motherland!

Farouk was enamored of the glamorous royal lifestyle. Although he already had thousands of acres of land, dozens of palaces, and hundreds of cars, the youthful king would often travel to Europe for grand shopping sprees, earning the ire of many of his subjects. It is said that he ate 600 oysters a week.[4]

He was most popular in his early years and the nobility largely celebrated him. For example, during the accession of the young King Farouk, “the Abaza family had solicited palace authorities to permit the royal train to stop briefly in their village so that the king could partake of refreshments offered in a large, magnificently ornamented tent the family had erected in the train station.”[5]

Farouk’s accession initially was encouraging for the populace and nobility, due to his youth and Egyptian roots through his mother Nazli Sabri. However, the situation was not the same with some Egyptian politicians and elected government officials, with whom Farouk quarreled frequently, despite their loyalty in principle to his throne.

During the hardships of World War II, criticism was leveled at Farouk for his lavish lifestyle. His decision to not put out the lights at his palace in Alexandria, during a time when the city was blacked out because of German and Italian bombing, was deemed particularly offensive by Egyptian people. Due to the continuing British occupation of Egypt, many Egyptians, Farouk included, were positively disposed towards Germany and Italy, and despite the presence of British troops, Egypt remained officially neutral until the final year of the war. Consequently, the royal Italian servants of Farouk were not interned, and there is an unconfirmed story that Farouk told British Ambassador Sir Miles Lampson (who had an Italian wife), “I’ll get rid of my Italians when you get rid of yours”.[citation needed] In addition, Farouk was known for harbouring certain Axis sympathies and even sending a note to Hitler saying that an invasion would be welcome.[6] Farouk only declared war on the Axis Powers under heavy British pressure in 1945, long after the fighting in Egypt’s Western Desert had ceased.

Farouk is also reported as having said “The whole world is in revolt. Soon there will be only five Kings left — the King of England, the King of Spades, the King of Clubs, the King of Hearts, and the King of Diamonds.”[7]


Farouk was widely condemned for his corrupt and ineffectual governance, the continued British occupation, and the Egyptian army’s failure to prevent the loss of 78% of Palestine to the newly formed State of Israel in the 1948 Arab-Israeli War. Public discontent against Farouk rose to new levels.[citation needed] In the CIA, the project to overthrow King Farouk, known internally known as “Project FF [Fat Fucker]”,[8] was initiated by CIA operative Kermit Roosevelt, Jr. The CIA was disappointed in King Farouk for not improving the functionality and usefulness of his government,[9] and had actively supported the toppling of King Farouk by the Free Officers.[10] Finally, on 23 July 1952, the Free Officers Movement under Muhammad Naguib and Gamal Abdel Nasser staged a military coup that launched the Egyptian Revolution of 1952. Farouk was forced to abdicate, and went into exile in Monaco and Italy where he lived for the rest of his life.[citation needed] Immediately following his abdication, Farouk’s baby son, Ahmed Fuad was proclaimed King Fuad II, but for all intents and purposes Egypt was now governed by Naguib, Nasser and the Free Officers.[citation needed] On 18 June 1953, the revolutionary government formally abolished the monarchy, ending 150 years of the Muhammad Ali dynasty’s rule, and Egypt was declared a republic.[citation needed]

The revolutionary government quickly moved to auction off the King’s vast collection of trinkets and treasures.[citation needed] Among the more famous of his possessions was one of the rare 1933 Double Eagle coins, though the coin disappeared before it could be returned to the United States.[citation needed] He was also notorious for his collection of pornography.[11]

 Exile and death

Farouk I with his wife Narriman and their son Fuad II in exile in Capri, Italy (1953)

On his exile from Egypt, Farouk settled first in Monaco, and later in Rome, Italy. On 29 April 1958, the United Arab Republic issued rulings revoking the Egyptian citizenship of Farouk.[12] He was granted Monegasque citizenship in 1959 by his close friend Prince Rainier III.[13]

The blue-eyed Farouk was thin early in his reign, but later gained enormous weight. His taste for fine cuisine made him dangerously obese, weighing nearly 300 pounds (136 kg)—an acquaintance described him as “a stomach with a head”. He died in the Ile de France restaurant in Rome, Italy on 18 March 1965. He collapsed and died at his dinner table following a characteristically heavy meal.[14] While some claim he was poisoned by Egyptian Intelligence,[15] no official autopsy was conducted on his body. His will stated that his burial place should be in the Al Rifa’i Mosque in Cairo, but the request was denied by the Egyptian government under Gamal Abdel Nasser, and he was going to be buried in Italy. King Faisal of Saudi Arabia stated he would be willing to have King Farouk buried in Saudi Arabia, upon which President Nasser agreed for the former monarch to be buried in Egypt, not in the Mosque of Al Rifai’ but in the Ibrahim Pasha Burial Site.[citation needed]

A likely apocryphal story about Farouk’s lavish living in exile was that he refused to donate money to relieve poverty on the basis that “If I donate my fortune to buy food, all of Egypt eats today, eats tomorrow, and the day after that they are starving once again”, thus rationalizing his high living.

 Marriages and affairs

Farouk I with his wife Queen Farida and their first-born daughter Ferial (c. 1939)

In addition to an affair with the British writer Barbara Skelton, among numerous others, Farouk was married twice, with a claim of a third marriage (see below). His first wife was Safinaz Zulficar (1921–1988), the daughter of Youssef Zulficar Pasha. Safinaz was renamed Farida upon her marriage. They were married in 1938, and divorced in 1948, producing three daughters.

Farouk’s second wife was a commoner, Narriman Sadek (1934–2005). They were married in 1951, and divorced in 1954, having only one child, the future King Fuad II.

While in exile in Italy, Farouk met Irma Capece Minutolo, an opera singer, who became his companion. In 2005, she claimed that she married the former King in 1957.[16]



The ostentatious king’s name is used to describe imitation Louis XV-style furniture known as “Louis-Farouk”. The imperial French style furniture became fashionable among Egypt’s upper classes during Farouk’s reign so Egyptian artisans began to mass-produce it. The style uses ornate carving, is heavily gilded, and covered in very elaborate cloth.[17] The style, or imitations thereof, remains widespread in Egypt.





Second Arab Scout Jamboree

perforated mini-sheet SG MS513, very fine mint, fresh & very rare

Est 120-150 pounds

THE END @ Copyright Dr Iwan Suwandy 2011


The Rare Asia Vintage Postcard Part Two(A_Z)

Rare Asia Postcard












The Driwan’s  Cybermuseum

The  Rare Asia Vintage Postcard Part Two

Rare Asia Postcard Part One


























a.Lao Bao


b.Quan Yen







Rare Asia Postcard







British camp












France consulate Nagasaki



Japan Occupation




b.Canton China












Kuala lumpur

During the open mining area in the Ampang and Kuala Lumpur, the people who berkelian tin Mandailinglah there, in addition to the furnace, buying tin and business. Bugis kings collect taxes from those who mandailing on the bases of the river.
Even the name “Ampang” itself may be taken in conjunction with the dams built by the mandailing in berkelian tin works. Water used to remove ore from the rock.When Sutan Fasting in Ampang, the son of the king mandailing dealing with Chinese merchants Hiu Siew and his friend Ah Sze Potato from Cobra. Both quarter-Hakka Chinese merchant was then moved to Ampang after being informed by Sutan fast that they can quickly make a profit in Ampang
mile away from the meeting Sungai Gombak and Sungai Klang as a base for their stores. This occurs in approximately 1859. Mouth of both rivers are then called the Kuala Lumpur – perhaps because of sloppy work in the stomach berkelian tin the rivers.





This is Batu Feringhi. Thats Lover’s Isle there in the sea. The beach then was definetly unspoilt and as can be seen, not a hotel in sight.


The famous Mesjid Kapitan Keling. Look at the car, that tells you that this is old.


Chulia Street. Funny, even then it looked old. The car tells you its old.


This is a scene in the ferry. Notice the dressing then. I am told this is taken in 1958.


I think this is somewhere near Padang Kota Lama. I may be wrong.


I am still trying to figure out which place this is. Can anyone help me out here? Hey I am a mainland boy and resides in Penang Island only since 1993 besides the 2 or 3 years in 1984.


The Penang Hill Police Station. The last time I went up that hill was probably 8 years ago and if I am not mistaken, the police station looked the same.


View of Penang Island from the hill. Lots of changes I tell you.


This is Penang Road of old. Notice one thing in particular? What you asked? Look, no jam.


Penang Road again. Trishaws or Lang Chia or some people like to call it lancheows were the king of the road then. Is that a Lambretta?


The Odeon Cinema. Now it plays only Tamil movies. Look at Rajnikant waiting there and again, no jam.


No jam along Penang Road. I think if you know what year the movie Annastasia was shown, it would help in determing the age of this photo.


Hey we had double deckers back then. I don’t know if I had ridden in one or not. If I had, I must have been too young to remember so Kerp, don’t go saying you were in one.


Besides the double decker, this is another of my favourite. Tanjong Tokong and old Malay huts. This is a classic man.


The Botanical Gardens. I remember the excitement of going there and feeding the monkeys. They still do have monkeys now and also two legged ones.













Native tamasek








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 Dr Iwan Suwandy 2011


The rare Asia Vintage Postcard Part One: CHINA

Rare Asia Postcard











The Driwan’s  Cybermuseum

The High Investation Value China  vintage Postcard


1.Ethnic Traditional





Native people


2.City View














e.Tientsin Museum


f.Nanking road




a.Boxer Rebellion

1)foreign pictures



2)China Boxer REVOLT Arsenal Hanyang Hupeh Taken


3).CHINA BOXER REBEL Arsenal after Capture of SHANGHAI OLD


b.Tientsin Massacred




4.Foreign Monument

a.German,America and Japanese Consulate at Shanghai


b.Astor Hotel Shanghai


c.Hotel La Paix Tientsin


d.Russian Cruiser China


5.Old China Monument

a.Beijing monument Tu Lien Pagoda used via foreign Postal


b.Temple Of Heaven



c.Ming Tomb


d.Harbin Church


6.China Old Transportations

a.Tram held by horse


b.Imperial TrainTientsin



c.Sparow Boat


d.Rickshaw at Hongkong





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The end @ copyright

 Dr Iwan Suwandy 2011

The Highest Investation Value Phonecard Collections










The Driwan’s  Cybermuseum




The High Investation Value Of

PHONE CARD Collections







I.Dr Iwan Masterpiece Collections


(not list in any auctions)

Coca Cola Sprint Phone Card/Cells Premier Edition

Limited Hot Cel 1 of 610





(not list in any auctions)

1)McDonald’s In Tokyo Established 1971

Limited Edition

Proof 26 of 28

2)Mc Donald Happy Meal

,Guys French Fries

Diet Cut

Limited editions

113 of 856


3) with this rare card above ,Dr Iwan also found uncommon card

$2.-Card of NBA star profile Charles Barkeley(list in auctions)


II.International Masterpiece Collections

1.Proof Snowflakes Trial :

First Edition Debit Card of Ameritech








2.TAMRA Electric Works Ltd Promotion Test Card


a.NewYork City Skyline,Bridge and twin Tower of WTC

b.Diamond Head & Beach



1).Diamond Head and Waikiki Beach


2)Raibow Valley Issued,eclipse Hawaii

July,11,1991 Overprint



1) 10u Coastal Lights & Hawaii at Bottom-Left (Tel Bold)


2) 3u Hula Girl By Night (Tel)


3) 3u Whales of Hawaii Humpback Whale



1)$49 Jerry Rice 1994

Record breaker 49ers.


2) PhonePak 1996 $100. Jeff Gordon (DuPont, McDonalds) # Printers Proof [210 USD]


1)Smith Coke 1994 Grand Prize Winner Santa & Bear Toasting Coca-Cola


2 1997 Smith:600 m Woman,Co9ke Bottle &Skis GRAND PRIZE WINNER



3.1998 Smith : 600 m Woman (Rede Coat) with Skis GRAND PRIZE WINNER




(1) $3.00 Marlene Dietrich:

a) $3,00,Blue Dress & Large Pendant (by: Watts)


b) $6.00 Marlene Dietrich: In Red Dress & Hat (Artist: Perillo) GOLD


(2)$50. Marilyn Monroe A

 (In White Strapless Dress)










$10. Purple Pope John Paul II Visit To Denver – Rare Prototype


Elvis Presley






RARE Set of 4 Original Coin$aver JUMBOs (Internal) $5,$10,$50,$100. [8995 USD]




7u Telecard Man JUMBO (AmeriVox): 1st Jumbo Card Ever Issued 9/93 [450 USD]



10u Multi-Media Demonstration Center Grand Opening *SAMPLE* [375 USD]



$7.50, $15.,$30.,$60. Back To School (4 Card SAMPLE Set) [1100 USD]













 @copyright Dr Iwan suwandy 2011


The Rare Albania Handstamped Overprint Eagle 1913 stamps











The Driwan’s  Cybermuseum




In 1913 Albania issued a very beautiful and amizing overprint eagle on Turkish Stamps, many Eagle thematic stamps collectors xseeking this stamps. Now the value of the stamps very high espacially postally used on fragment, and until this day I never seen this stamps postally used on Covers,please who have  be kind to show us.

This rare stamps  have three types colours overprint  Black,Violet and Red, I hope the collectors from all over the world will happy to look at this rare stamps and becareful for the fake one.

(Dr Iwan Notes)





The history of Alabnia in 1913

Independence of Albania (1912)

The initial sparks of the first Balkan War in 1912 were ignited by the Albanian uprising between 1908 and 1910[43] which were directed at opposing the Young Turk policies of consolidation of the Ottoman Empire. Following the eventual weakening of the Ottoman Empire in the Balkans, Serbia, Greece and Bulgaria declared war and sought to aggrandize their respective boundaries on the remaining territories of the Empire. Albania was thus invaded by Serbia in the north and Greece in the south, restricting the country to only a patch of land around the southern coastal city of Vlora. In 1912 Albania, still under foreign occupation, declared its independence and, with the aid of Austria-Hungary, the Great Powers drew its present borders. The territorial security of Albania was guaranteed by the Great Powers in the Treaty of London of 1913.

The border between Albania and its neighbors was delineated in 1913 following the dissolution of most of the Ottoman Empire’s territories in the Balkans. The delineation of the new state’s borders left a significant number of Albanian communities outside Albania. This population was largely divided between Montenegro and Serbia (which then included what is now Kosovo and the Republic of Macedonia). A substantial number of Albanians thus found themselves under Serbian rule. At the same time, an uprising in the country’s south by local Greeks, led to the formation of the Autonomous Republic of Northern Epirus in the southern provinces (1914). After a period of political instability brought about by the First World War, the country adopted a republican form of government in 1920.[44] The territorial security of Albania was guaranteed by a League of Nations declaration of November 9, 1921, which entrusted the defense of that state to Italy




the end @ copyright dr Iwan suwandy 2011


Indonesia SEA GAMES 2001 Live Now










The Driwan’s  Cybermuseum

















the end @ copyright dr Iwan suwnady 2001

The Haemophilia Disease Informations










The Driwan’s  Cybermuseum


clotting factor VIII (haemophilia A) and 

factor IX deficiency(haemophilia B)

Classification and external resources

Deficiency in coagulation factor VIII is the most common cause of haemophilia.
ICD10 D66D68
ICD9 286
OMIM 306700 306900 264900
DiseasesDB 5555 5561 29376
MedlinePlus 000537
eMedicine med/3528
MeSH D025861

Haemophilia (English pronunciation: /hiːməˈfɪliə/; also spelled hemophilia in North America, from the Greek haima αἷμα ‘blood’ and philia φιλος ‘love’[1]) is a group of hereditary genetic disorders that impair the body’s ability to control blood clotting or coagulation, which is used to stop bleeding when a blood vessel is broken. Haemophilia A (clotting factor VIII deficiency) is the most common form of the disorder, present in about 1 in 5,000–10,000 male births.[2] Haemophilia B (factor IX deficiency) occurs in around 1 in about 20,000–34,000 male births.

Like most recessive sex-linked, X chromosome disorders, haemophilia is more likely to occur in males than females. This is because females have two X chromosomes while males have only one, so the defective gene is guaranteed to manifest in any male who carries it. Because females have two X chromosomes and haemophilia is rare, the chance of a female having two defective copies of the gene is very low, so females are almost exclusively asymptomatic carriers of the disorder. Female carriers can inherit the defective gene from either their mother or father, or it may be a new mutation. Although it is not impossible for a female to have haemophilia, it is unusual: a female with Haemophilia A or B would have to be the daughter of both a male haemophiliac and a female carrier, while the non-sex-linked Haemophilia C, which can affect either sex, is extremely rare.

Haemophilia lowers blood plasma clotting factor levels of the coagulation factors needed for a normal clotting process. Thus when a blood vessel is injured, a temporary scab does form, but the missing coagulation factors prevent fibrin formation, which is necessary to maintain the blood clot. A haemophiliac does not bleed more intensely than a person without it, but can bleed for a much longer time. In severe haemophiliacs even a minor injury can result in blood loss lasting days or weeks, or even never healing completely. In areas such as the brain or inside joints, this can be fatal or permanently debilitating.


 Signs and symptoms

Characteristic symptoms vary with severity. In general symptoms are internal or external bleeding episodes, which are called “bleeds”.[3][4] Patients with more severe haemophilia suffer more severe and more frequent bleeds, while patients with mild haemophilia typically suffer more minor symptoms except after surgery or serious trauma. Moderate haemophiliacs have variable symptoms which manifest along a spectrum between severe and mild forms.

Prolonged bleeding and re-bleeding are the diagnostic symptoms of haemophilia. Internal bleeding is common in people with severe haemophilia and some individuals with moderate haemophilia. The most characteristic type of internal bleed is a joint bleed where blood enters into the joint spaces.[5] This is most common with severe haemophiliacs and can occur spontaneously (without evident trauma). If not treated promptly, joint bleeds can lead to permanent joint damage and disfigurement.[5] Bleeding into soft tissues such as muscles and subcutaneous tissues is less severe but can lead to damage and requires treatment.

Children with mild to moderate haemophilia may not have any signs or symptoms at birth especially if they do not undergo circumcision. Their first symptoms are often frequent and large bruises and haematomas from frequent bumps and falls as they learn to walk. Swelling and bruising from bleeding in the joints, soft tissue, and muscles may also occur. Children with mild haemophilia may not have noticeable symptoms for many years. Often, the first sign in very mild haemophiliacs is heavy bleeding from a dental procedure, an accident, or surgery. Females who are carriers usually have enough clotting factors from their one normal gene to prevent serious bleeding problems, though some may present as mild haemophiliacs.


Severe complications are much more common in severe and moderate haemophiliacs. Complications may be both directly from the disease or from its treatment:[6]

  • Deep internal bleeding, e.g. deep-muscle bleeding, leading to swelling, numbness or pain of a limb.
  • Joint damage from haemarthrosis, potentially with severe pain, disfigurement, and even destruction of the joint and development of debilitating arthritis.
  • Transfusion transmitted infection from blood transfusions that are given as treatment.
  • Adverse reactions to clotting factor treatment, including the development of an immune inhibitor which renders factor replacement less effective.
  • Intracranial haemorrhage is a serious medical emergency caused by the buildup of pressure inside the skull. It can cause disorientation, nausea, loss of consciousness, brain damage, and death.

 Life expectancy

Like most aspects of the disorder, life expectancy varies with severity and adequate treatment. People with severe haemophilia who don’t receive adequate, modern treatment have greatly shortened lifespans and often do not reach maturity. Prior to the 1960s when effective treatment became available, average life expectancy was only 11 years.[5] By the 1980s the life span of the average haemophiliac receiving appropriate treatment was 50–60 years.[5] Today with appropriate treatment, males with haemophilia typically have a near normal quality of life with an average lifespan approximately 10 years shorter than an unaffected male.[7]

Since the 1980s the primary leading cause of death of people with severe haemophilia has shifted from haemorrhage to HIV/AIDS acquired through treatment with contaminated blood products.[5] The second leading cause of death related to severe haemophilia complications is intracranial haemorrhage which today accounts for one third of all deaths of patients with haemophilia. Two other major causes of death include: hepatitis infections causing cirrhosis and, obstruction of air or blood flow due to soft tissue haemorrhage.[5]


  • Haemophilia A is a recessive X-linked genetic disorder involving a lack of functional clotting Factor VIII and represents 80% of haemophilia cases.
  • Haemophilia B is a recessive X-linked genetic disorder involving a lack of functional clotting Factor IX. It comprises approximately 20% of haemophilia cases.[8]
  • Haemophilia C is an autosomal genetic disorder (i.e. not X-linked) involving a lack of functional clotting Factor XI. Haemophilia C is not completely recessive: heterozygous individuals also show increased bleeding.[9]


X-linked recessive inheritance

Females possess two X-chromosomes, males have one X and one Y-chromosome. Since the mutations causing the disease are X-linked, a woman carrying the defect on one of her X-chromosomes may not be affected by it, as the equivalent allele on her other chromosome should express itself to produce the necessary clotting factors, due to X inactivation. However, the Y-chromosome in men has no gene for factors VIII or IX. If the genes responsible for production of factor VIII or factor IX present on a male’s X-chromosome are deficient there is no equivalent on the Y-chromosome to cancel it out, so the deficient gene is not masked and he will develop the illness.

Since a male receives his single X-chromosome from his mother, the son of a healthy female silently carrying the deficient gene will have a 50% chance of inheriting that gene from her and with it the disease; and if his mother is affected with haemophilia, he will have a 100% chance of being a haemophiliac. In contrast, for a female to inherit the disease, she must receive two deficient X-chromosomes, one from her mother and the other from her father (who must therefore be a haemophiliac himself). Hence haemophilia is far more common among males than females. However, it is possible for female carriers to become mild haemophiliacs due to lyonisation (inactivation) of the X-chromosomes. Haemophiliac daughters are more common than they once were, as improved treatments for the disease have allowed more haemophiliac males to survive to adulthood and become parents. Adult females may experience menorrhagia (heavy periods) due to the bleeding tendency. The pattern of inheritance is criss-cross type. This type of pattern is also seen in colour blindness.

A mother who is a carrier has a 50% chance of passing the faulty X-chromosome to her daughter, while an affected father will always pass on the affected gene to his daughters. A son cannot inherit the defective gene from his father.

Genetic testing and genetic counselling is recommended for families with haemophilia. Prenatal testing, such as amniocentesis, is available to pregnant women who may be carriers of the condition.

As with all genetic disorders, it is of course also possible for a human to acquire it spontaneously through mutation, rather than inheriting it, because of a new mutation in one of their parents’ gametes. Spontaneous mutations account for about 33% of all cases of haemophilia A. About 30% of cases of haemophilia B are the result of a spontaneous gene mutation.

If a female gives birth to a haemophiliac child, either the female is a carrier for the disease or the haemophilia was the result of a spontaneous mutation. Until modern direct DNA testing, however, it was impossible to determine if a female with only healthy children was a carrier or not. Generally, the more healthy sons she bore, the higher the probability that she was not a carrier.

If a male is afflicted with the disease and has children with a female who is not even a carrier, his daughters will be carriers of haemophilia. His sons, however, will not be affected with the disease. The disease is X-linked and the father cannot pass haemophilia through the Y-chromosome. Males with the disorder are then no more likely to pass on the gene to their children than carrier females, though all daughters they sire will be carriers and all sons they father will not have haemophilia (unless the mother is a carrier).


There are numerous different mutations which cause each type of haemophilia. Due to differences in changes to the genes involved, patients with haemophilia often have some level of active clotting factor. Individuals with less than 1% active factor are classified as having severe haemophilia, those with 1-5% active factor have moderate haemophilia, and those with mild haemophilia have between 5-40% of normal levels of active clotting factor.[5]


Haemophilia A can be mimicked by von Willebrand disease.

von Willebrand Disease

  • von Willebrand Disease could significantly affect as many as 1 in 10,000 people.[10]
  • von Willebrand Disease type 2A, where decreased levels of von Willebrand Factor can lead to premature proteolysis of Factor VIII. In contrast to haemophilia, vWD type 2A is inherited in an autosomal dominant fashion.
  • von Willebrand Disease type 2N, where von Willebrand Factor cannot bind Factor VIII, autosomal recessive inheritance. (i.e.; both parents need to give the child a copy of the gene).
  • von Willebrand Disease type 3, where lack of von Willebrand Factor causes premature proteolysis of Factor VIII. In contrast to haemophilia, vWD type 3 is inherited in an autosomal recessive fashion.

Additionally, severe cases of vitamin K deficiency can present similar symptoms to haemophilia. This is because vitamin K is necessary for the human body to produce several protein clotting factors. This vitamin deficiency is rare in adults and older children but is common in newborns. Infants are born with naturally low levels of vitamin K and do not yet have the symbiotic gut flora to properly synthesise their own vitamin K. Bleeding issues due to vitamin K deficiency in infants is known as “haemorrhagic disease of the newborn“, to avoid this complication newborns are routinely injected with vitamin K supplements.

Condition Prothrombin time Partial thromboplastin time Bleeding time Platelet count
Vitamin K deficiency or warfarin prolonged prolonged unaffected unaffected
Disseminated intravascular coagulation prolonged prolonged prolonged decreased
von Willebrand disease unaffected prolonged prolonged unaffected
Haemophilia unaffected prolonged unaffected unaffected
Aspirin unaffected unaffected prolonged unaffected
Thrombocytopenia unaffected unaffected prolonged decreased
Early Liver failure prolonged unaffected unaffected unaffected
End-stage Liver failure prolonged prolonged prolonged decreased
Uremia unaffected unaffected prolonged unaffected
Congenital afibrinogenemia prolonged prolonged prolonged unaffected
Factor V deficiency prolonged prolonged unaffected unaffected
Factor X deficiency as seen in amyloid purpura prolonged prolonged unaffected unaffected
Glanzmann’s thrombasthenia unaffected unaffected prolonged unaffected
Bernard-Soulier syndrome unaffected unaffected prolonged unaffected [11]


Commercially produced factor concentrates such as “Advate”, a recombinant Factor VIII produced by Baxter International, come as a white powder in a vial which must be mixed with sterile water prior to intravenous injection.

Though there is no cure for haemophilia, it can be controlled with regular infusions of the deficient clotting factor, i.e. factor VIII in haemophilia A or factor IX in haemophilia B. Factor replacement can be either isolated from human blood serum, recombinant, or a combination of the two. Some haemophiliacs develop antibodies (inhibitors) against the replacement factors given to them, so the amount of the factor has to be increased or non-human replacement products must be given, such as porcine factor VIII.

If a patient becomes refractory to replacement coagulation factor as a result of circulating inhibitors, this may be partially overcome with recombinant human factor VII (NovoSeven), which is registered for this indication in many countries.

In early 2008, the US Food and Drug Administration (FDA) approved Xyntha (Wyeth) anti-haemophilic factor, genetically engineered from the genes of Chinese hamster ovary cells. Since 1993 (Dr. Mary Nugent) recombinant factor products (which are typically cultured in Chinese hamster ovary (CHO) tissue culture cells and involve little, if any human plasma products) have been available and have been widely used in wealthier western countries. While recombinant clotting factor products offer higher purity and safety, they are, like concentrate, extremely expensive, and not generally available in the developing world. In many cases, factor products of any sort are difficult to obtain in developing countries.

In Western countries, common standards of care fall into one of two categories: prophylaxis or on-demand. Prophylaxis involves the infusion of clotting factor on a regular schedule in order to keep clotting levels sufficiently high to prevent spontaneous bleeding episodes. On-demand treatment involves treating bleeding episodes once they arise. In 2007, a clinical trial was published in the New England Journal of Medicine comparing on-demand treatment of boys (< 30 months) with haemophilia A with prophylactic treatment (infusions of 25 IU/kg body weight of Factor VIII every other day) in respect to its effect on the prevention of joint-diseases. When the boys reached 6 years of age, 93% of those in the prophylaxis group and 55% of those in the episodic-therapy group had a normal index joint-structure on MRI.[12] Prophylactic treatment, however, resulted in average costs of $300,000 per year. The author of an editorial published in the same issue of the NEJM supports the idea that prophylactic treatment not only is more effective than on demand treatment but also suggests that starting after the first serious joint-related haemorrhage may be more cost effective than waiting until the fixed age to begin.[13] This study resulted in the first (October 2008) FDA approval to label any Factor VIII product to be used prophylactically.[14] As a result, the factor product used in the study (Bayer’s Kognate) is now labelled for use to prevent bleeds, making it more likely that insurance carriers in the US will reimburse consumers who are prescribed and use this product prophylactically. Despite Kognate only recently being “approved” for this use in the US, it and other factor products have been well studied and are often prescribed to treat Haemophilia prophylactically to prevent bleeds, especially joint bleeds.[15]

Preventive exercises

It is recommended that people affected with haemophilia do specific exercises to strengthen the joints, particularly the elbows, knees, and ankles.[16] Exercises include elements which increase flexibility, tone, and strength of muscles, increasing their ability to protect joints from damaging bleeds. These exercises are recommended after an internal bleed occurs and on a daily basis to strengthen the muscles and joints to prevent new bleeding problems. Many recommended exercises include standard sports warm-up and training exercises such as stretching of the calves, ankle circles, elbow flexions, and quadriceps sets.

Alternative medicine

While not a replacement for traditional treatments, preliminary scientific studies indicate that hypnosis and self-hypnosis may be effective at reducing bleeds and the severity of bleeds and thus the frequency of factor treatment.[17][18][19][20] Herbs which strengthen blood vessels and act as astringents may benefit patients with haemophilia, however there are no peer reviewed scientific studies to support these claims.[17]


Anticoagulants such as Heparin and Warfarin are contraindicated for people with haemophilia as these can aggravate clotting difficulties. Also contraindicated are those drugs which have “blood thinning” side effects. For instance, medications which contain aspirin, ibuprofen, or naproxen sodium should not be taken because they are well known to have the side effect of prolonged bleeding.[21]

Also contraindicated are activities with a high likelihood of trauma, such as motorcycling and skateboarding. Popular sports with very high rates of physical contact and injuries such as American football, hockey, boxing, wrestling, and rugby should be avoided by people with haemophilia.[21][22] Other active sports like soccer, baseball, and basketball also have a high rate of injuries, but have overall less contact and should be undertaken cautiously and only in consultation with a doctor.[21]


Haemophilia is rare, with only about 1 instance in every 10,000 births (or 1 in 5,000 male births) for haemophilia A and 1 in 50,000 births for haemophilia B.[23] About 18,000 people in the United States have haemophilia. Each year in the US, about 400 babies are born with the disorder. Haemophilia usually occurs in males and less often in females.[24] It is estimated that about 2500 Canadians have haemophilia A, and about 500 Canadians have haemophilia B.[25]


“About seventy or eighty years ago, a woman by name of Smith, settled in the vicinity of Plymouth, New Hampshire, and transmitted the following idiosyncrasy to her descendants. It is one, she observed, to which her family is unfortunately subject, and had been the source not only of great solicitude, but frequently the cause of death. If the least scratch is made on the skin of some of them, as mortal a hemorrhagy will eventually ensue as if the largest wound is inflicted. (…) So assured are the members of this family of the terrible consequences of the least wound, that they will not suffer themselves to be bled on any consideration, having lost a relation by not being able to stop the discharge occasioned by this operation.”

John C. Otto, 1803[26]

 Scientific discovery

The first written account of haemophilia occurred in the 2nd century in the Babylonian Talmud. In it Rabbi Judah haNasi, redactor of the Mishneh, wrote: “If she circumcised her first child and he died, and a second one also died, she must not circumcise her third child.” This passage refers to both the prolonged bleeding caused by circumcision and to the maternal inheritance of the disease.[27] The first medical professional to describe a disease was Albucasis. In the tenth century he described families whose males died of bleeding after only minor traumas.[28][dead link] While many other such descriptive and practical references to the disease appear throughout historical writings, scientific analysis did not begin until the start of the nineteenth century.

In 1803, Dr. John Conrad Otto, a Philadelphian physician, wrote an account about “a hemorrhagic disposition existing in certain families” in which he called the affected males “bleeders.”[29] He recognised that the disorder was hereditary and that it affected mostly males and was passed down by healthy females. His paper was the second paper to describe important characteristics of an X-linked genetic disorder (the first paper being a description of colour blindness by John Dalton who studied his own family). Otto was able to trace the disease back to a woman who settled near Plymouth in 1720. The idea that affected males could pass the trait onto their unaffected daughters was not described until 1813 when John Hay published an account in The New England Journal of Medicine.[30][31]

A Finnish Doctor in 1924 discovered a heredity bleeding disorder similar to Haemophilia localised in a group of islands (called the “Aland Islands”) which are located to the southwest of Finland. This bleeding disorder is called “Von Willebrand Disease”.

The term “haemophilia” is derived from the term “haemorrhaphilia” which was used in a description of the condition written by Friedrich Hopff in 1828, while he was a student at the University of Zurich.[29][32] In 1937, Patek and Taylor, two doctors from Harvard, discovered anti-haemophilic globulin.[27] In 1947, Pavlosky, a doctor from Buenos Aires, found haemophilia A and haemophilia B to be separate diseases by doing a lab test. This test was done by transferring the blood of one haemophiliac to another haemophiliac. The fact that this corrected the clotting problem showed that there was more than one form of haemophilia.

 European royalty

Queen Victoria passed haemophilia on to some of her descendants.

Haemophilia has featured prominently in European royalty and thus is sometimes known as “the royal disease”. Queen Victoria passed the mutation for Haemophilia B[33][34] to her son Leopold and, through some of her daughters, to various royals across the continent, including the royal families of Spain, Germany, and Russia. In Russia, Tsarevich Alexei Nikolaevich, son of Nicholas II, was a descendant of Queen Victoria through his mother Empress Alexandra and suffered from haemophilia.


It was claimed that Rasputin was successful at treating the Tsarevich‘s haemophilia.

Rasputin The Mad Monk
Russia’s greatest love machine!

Rasputin (1869-1916) was a Russian mystic and preacher. Born of illiterate peasant parents, he arrived in Saint Petersburg in the early 20th century, where he had some success in treating Tsarevich Alexei, who suffered from haemophilia. He managed to turn this, and the fascination in upper-class Russian circles with religious mysticism, healing, and sex, into becoming a close associate of the Tsar family and an important figure in pre-revolution Russia. 

Due to his many affairs and drunkenness (his personal faith required sin, in his case alcohol and sex, followed by repentance), he became a target of anti-Romanov and anti-Tsarist groups in Russia. He was murdered in 1916. The accounts from the murderers, primarily Felix Yusupov, were widely published, but also very exaggerated and were changed frequently. According to popular myth, he was first poisoned, then beaten, then shot, and finally drowned before he died. In reality, the poison evaporated while baked, and he died of the gunshot wounds before he was thrown in the river. 


Trope Namer for Rasputinian Death. The frequent myths and interesting history around him has made him a frequent target for a Historical Villain Upgrade or Beethoven Was an Alien Spy, as well as a figure in a Conspiracy Theory


  • Alan Rickman did a sympathetic portrayal of the man in Rasputin. It is notable his portrayal argued Rasputin may actually have been a saint with legitimate supernatural powers derived from God and at the very least didn’t deserve the crap piled on his memory.
  • In the Don Bluth film Anastasia, Rasputin was an undead sorcerer. Nevermind the other historical inaccuracies.
    • The Nostalgia Chick review included a call-in from the historical Rasputin, who argued he was a holy man who didn’t deserve this.
  • A Team Fortress 2 achievement for the Heavy references Rasputin. The Heavy needs to suffer several types of damage in a single life.
  • Showed up as a Big Bad (though not THE Big Bad, since he basically shows up in the middle of the game) in Shadow Hearts 2: Covenant. Turns out, he’s secretly a demon. Fortunately, you’ve got the help of a camera-wielding Princess Anastasia, and her magical, flying Farberge Egg!
  • He shows up as a Camp Gay fighter in the World Heroes series.
  • He gets a mention in Assassin’s Creed 2, as an agent of the Templars who stole the Staff of Eden from Czar Nicholas and thus precipitated the revolution that would follow. The Assassin order were the ones who killed him, though naturally, it took a while.
  • A robot from the future made in the image of Rasputin shows up as an antagonistic Devil Summoner in Raidou Kuzunoha vs. The Soulless Army (set years after his supposed death and in Japan no less).
  • Razputin is the psychic prodigy star of Psychonauts, with no other real connection to his namesake.
  • He is an antagonist (in service of an Eldritch Abomination ) in Hellboy.
  • He is also an ancestor of Colossus in X-Men. An ancestor that is very eager to be reincarnated in one of his blood.
  • Appeared in about a dozen books in the old World of Darkness… and each of them told a different story with him as another type of supernatural. They are all true, Rasputin became a Wraith after death and possessed all the supernaturals he was featured as.
  • The Doctor Who Past Doctor Adventures novel Wages of Sinis set in pre-Revolution Russia and has Rasputin as a character. It’s a historically-straight portrayal mostly, although his famous hard-to-kill-ness does turn out to be due to a time traveller trying to keep him alive.
    • He gets far more hilarious in Faction Paradox. To start with, the Faction recruited him a few days before his death, took him to the Eleven-Day Empire, and replaced him with an exact duplicate. Then the Celestis came along, didn’t realise the Faction had made the switch, and offered him their standard deal that includes resurrection. The duplicate had been briefed not to argue with any War-era powers it met, and so accepted the deal. By the time of the assassination attempt, the Great Houses noticed something was going on, assumed the Faction would try to take him to the Empire at the point of death, and so implanted a device that would replace the Faction duplicate with a Great House duplicate. House constructs are by default immune to poisoning. As such, when the poison failed, he was shot. Then the Celesti protocols resurrected him, producing a creature whose mind was struggling between Great Houses, Celesti, and Faction protocols which had to be shot repeatedly and beaten to death simply to get it to lie down long enough to be thrown ino the river, where it finally froze to death. As a result, none of the three powers involved like to talk about it and everyone in the War agreed to leave celebrities well alone. The real Rasputin, meanwhile, persuaded Anastasia (who was also a Faction recruit) to set up a rival state, then went mad and died under mysterious circumstances. Anastasia’s Thirteen-Day Republic was shortly afterwards annihilated.
  • He was the subject of an episode of the TV version of The Crow.
  • In an Animaniacs short, Rasputin has the ability to hypnotize others instantly into doing his will…until he meets the Warners.
  • Wizardry has Rattkin NPC named Ratsputin. Though he’s a ninja, not monk — name is due to mice- and rat- related puns Theme Naming.
  • Tom Baker played a darkly charismatic Rasputin in the historical biopic Nicholas and Alexandra before taking up the scarf.
  • Alan Rickman played him in the HBO original movie.
  • And Leonard Nimoy played a Rasputin-like character in “The Choice”, an episode of Mission: Impossible, indestructibility and all.
  • One Dilbert comic had the Pointy-Haired Boss hiring Rasputin, saying he had “charisma”. He then proceeded to suffocate Asok with a Death Glare. After that, he tried to do the same to Wally, but his powerful anti-charisma caused him to choke instead.
  • A Cahill from the Tomas branch in The 39 Clues.
  • The band Boney Mhas a song about him. The chorus refers to Rasputin as “Russia’s greatest love machine.”
  • When Karl Kesel homaged elements of Kamandi in Superboy he introduced a Ratsputin as the Evil Chancellor of Great Caesar.
  • Rasputin shows up among the army of wax droids in an episode of Red Dwarf, serving mainly as Caligula’s lackey.
  • Rasputin is the final boss of Lime-iro Senkitan. He’s presented as a monk, at least. He’s also presented as a villain mastermind with his own henchmen and an intent to take over Russia (and then, presumably, the world.)
  • Rasputin (in one of his coolest appearances) is the main villain of the Dungeons and Dragons game the main characters of The Word Weary play.
  • Rasputin was the Big Bad for both the comic series and film, Hell Boy.
  • Makes an appearance as a literal Disc One Final Boss in Shadow Hearts: Covenant. Actually plays pretty close to what history claims about him – with the sorcery and demonic influences taken Up to Eleven.
  • Hammer did a movie about him called Rasputin the Mad Monk, with Christopher Lee in the title role.

 At the time, a common treatment administered by professional doctors was to use aspirin, which worsened rather than lessened the problem. It is believed that, by simply advising against the medical treatment, Rasputin could bring visible and significant improvement to the condition of Alexei.

In Spain, Queen Victoria’s youngest daughter, Princess Beatrice, had a daughter Victoria Eugenie of Battenberg, who later became Queen of Spain. Two of her sons were haemophiliacs and both died from minor car accidents: Her eldest son, Prince Alfonso of Spain, Prince of Asturias, died at the age of 31 from internal bleeding after his car hit a telephone booth. Her youngest son, Infante Gonzalo, died at age 19 from abdominal bleeding following a minor car accident where he and his sister hit a wall while avoiding a cyclist. Neither appeared injured or sought immediate medical care and Gonzalo died two days later from internal bleeding.

Blood contamination issues

Ryan White was an American haemophiliac who became infected with HIV/AIDS through contaminated blood products.

Prior to 1985, there were no laws enacted within the U.S. to screen blood. As a result, many haemophilia patients who received untested and unscreened clotting factor prior to 1992 were at an extreme risk for contracting HIV and hepatitis C via these blood products. It is estimated that more than 50% of the haemophilia population, over 10,000 people, contracted HIV from the tainted blood supply in the United States alone.[35]

As a direct result of the contamination of the blood supply in the late 1970s and early/mid 1980s with viruses such as hepatitis and HIV, new methods were developed in the production of clotting factor products. The initial response was to heat-treat (pasteurise) plasma-derived factor concentrate, followed by the development of monoclonal factor concentrates, which use a combination of heat treatment and affinity chromatography to inactivate any viral agents in the pooled plasma from which the factor concentrate is derived. The Lindsay Tribunal in Ireland investigated, among other things, the slow adoption of the new methods

the end @ copyright Dr Iwan suwandy 2011

The GuillaIn Barre Syndrome Informations



Georges Guillain.
Georges Guillain
Jean-Alexandre Barré.
Jean-Alexandre Barré










The Driwan’s  Cybermuseum

Guillain–Barré syndrom


Andy Griffith

Andy Griffith

Andy Griffith receiving the Presidential Medal of Freedom.
Born Andy Samuel Griffith
June 1, 1926 (1926-06-01) (age 85)
Mount Airy, North Carolina, United States
Nationality American
Education Mount Airy High School
Alma mater University of North Carolina at Chapel Hill
Occupation Actor, comedian, director, producer, singer (country, bluegrass & southern gospel), writer
Years active 1954–present
Notable works The Andy Griffith Show
Political party Democrat
Spouse Barbara Bray Edwards (m. 1949–72) (divorced)
Solica Cassuto (m. 1975–81) (divorced)
Cindi Knight (1983–present)American actor Andy Griffith developed Guillain-Barré syndrome in 1983

Andy Samuel Griffith (born June 1, 1926) is an American actor, director, producer, Grammy Award-winning Southern-gospel singer, and writer.[1] He gained prominence in the starring role in director Elia Kazan‘s epic film A Face in the Crowd (1957) before he became better known for his television roles, playing the lead characters in the 1960–68 situation comedy, The Andy Griffith Show, and in the 1986–95 legal drama, Matlock. Griffith was awarded the Presidential Medal of Freedom by US President George W. Bush on November 9, 2005.

Guillain-Barré syndrome
Classification and external resources
ICD10 G61.0
ICD9 357.0
OMIM 139393
DiseasesDB 5465
MedlinePlus 000684
eMedicine emerg/222 neuro/7 pmr/48 neuro/598
MeSH D020275

Guillain–Barré syndrome (GBS) (French pronunciation: [ɡiˈlɛ̃ baˈʁe], English pronunciation: /ˈɡlænˈbɑr/), sometimes called Landry’s paralysis, is an acute inflammatory demyelinating polyneuropathy (AIDP), a disorder affecting the peripheral nervous system. Ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk, is the most typical symptom. It can cause life-threatening complications, particularly if the breathing muscles are affected or if there is dysfunction of the autonomic nervous system. The disease is usually triggered by an acute infection. Guillain–Barré syndrome is a form of peripheral neuropathy.

The diagnosis is usually made by nerve conduction studies. With prompt treatment by intravenous immunoglobulins or plasmapheresis, together with supportive care, the majority will recover completely. Guillain–Barré syndrome is rare, at 1–2 cases per 100,000 people annually, but is one of the leading causes of acute non-trauma-related paralysis in the world. The syndrome is named after the French physicians Georges Guillain and Jean Alexandre Barré, who described it in 1916.

Guillain Barré Syndrome Support Group Trust

Welcome to the website of the Guillain Barré (pronounced gee-lane bah-ray) Syndrome Support Group New Zealand Trust.

Georges Guillain.
Georges Guillain
Jean-Alexandre Barré.
Jean-Alexandre Barré

Guillain Barré syndrome was discovered by the French physicians Jean-Alexandre Barré, Georges Guillain and Andre Strohl in the early 1900s following tests on soldiers returning from World War 1. Many cases of an identical condition had been described over the preceding 80 years but these neurologists identified one of the characterising features of the disease – the increased concentration of protein in the spinal fluid without evidence of inflammation.

GBS is a polyneuritis (an inflammation of many nerves) that affects the peripheral nerves connecting the skin and muscles to the central nervous system and leads to progressive weakness in the arms and legs. It is caused by the body’s own immune system turning on itself and attacking the nerves by mistake


Guillain-Barré syndrome (GBS) (pengucapan Prancis: [ɡilɛ baʁe], pengucapan bahasa Inggris: / ɡi lænbɑreɪ ː /), kadang-kadang disebut kelumpuhan Landry, adalah suatu polineuropati demielinasi inflamasi akut (AIDP), gangguan yang mempengaruhi sistem saraf perifer. Ascending kelumpuhan, kelemahan awal pada kaki dan tangan dan bermigrasi ke bagasi, adalah gejala paling khas. Hal ini dapat menyebabkan komplikasi yang mengancam jiwa, terutama jika otot-otot pernapasan dipengaruhi atau jika ada disfungsi dari sistem saraf otonom. Penyakit ini biasanya dipicu oleh infeksi akut. Guillain-Barré syndrome adalah bentuk neuropati perifer.

Diagnosis biasanya dibuat dengan studi konduksi saraf. Dengan pengobatan prompt dengan imunoglobulin intravena atau plasmapheresis, bersama-sama dengan perawatan suportif, mayoritas akan sembuh sepenuhnya. Sindrom Guillain-Barré jarang, pada 1-2 kasus per 100.000 orang per tahun, namun merupakan salah satu penyebab utama akut non-trauma yang berhubungan dengan kelumpuhan di dunia.


Georges Guillain.
Georges Guillain
Jean-Alexandre Barré.
Jean-Alexandre Barré

Sindrom ini dinamai setelah Georges Guillain dan Jean dokter Alexandre Barre dari Perancis , yang digambarkan pada tahun 1916

contoh kasus di Indonesia

Askes Tanggung Biaya Pengobatan Penderita GBS


M. Azka Arriziq, (4), penderita penyakit langka Guillain Barre Syndrome (GBS) yang tengah menjalani perawatan di RSUP Cipto Mangungkusumo. (ist/doc)  � PT Askes (Persero) akhirnya menjamin seluruh biaya pengobatan M. Azka Arriziq, (4), penderita penyakit langka Guillain Barre Syndrome (GBS) yang tengah menjalani perawatan di RSUP Cipto Mangungkusumo.

Seperti diketahui, sebelum dirawat di RSCM, Azka yang merupakan anak satu-satunya dari pasangan Anto Ariyanto, (42), dan Rina, (38), sudah dirawat sejak 21 Juli 2011 diruang Perinatal Intensive Care Unit, RS Azra, Bogor. Namun, sejak Selasa (2/8) lalu, Azka dipindahkan perawatannya ke RSCM Jakarta.

Direktur Utama PT Askes (Persero), I Gede Subawa usai mengunjugi Azka di RSUP Cipto Manungunkusumo, kepada waratwan mengatakan  saat ini Askes sudah menjamin seluruh kebutuhan medis Azka, sampai hari ke-6 per 8 Agustus 2011. Gede, juga menekankan bahwa penyakit GBS, termasuk dalam kategori penyakit katastropik.

Gede menambahkan, sejak dirawat di RS Azra Bogor, biaya pengobatan Azka mencapai Rp87.557.000. Meski RS tersebut tidak bekerja sama dengan Askes, namun Gede mengatakan akan memberikan penggantian penuh atas biaya perawatannya.

�Kita sudah bayar biaya sebesar Rp32 juta dari total Rp87.557.000. Sisanya, akan dibayarkan secara bertahap. Dan ked epannya, Azka akan dijamin biaya kesehatannya tanpa ada batasan biaya dan hari rawat sesuai sistem yang dianut oleh PT. Askes sesuai prosedur dan aturan berlaku,� jelasnya.

Di tempat yang sama, Anto Ariyanto mengaku lega karena PT Askes mau menanggung seluruh biaya medis yang dibutuhkan Azka termasuk hutang di RS Azra Bogor. �Kami berterima kasih kepada Askes karena menanggulangi seluruh biaya pengobatan Aska secara utuh. Sebelumnya saya sempat stress karena biaya yang dibutuhkan untuk mengobatan Azka rata-rata Rp10 juta per hari,� ucapnya.

Guillain Barre Syndrome (GBS) merupakan penyakit langka dan menyerang satu dari 100.000 ribu orang per tahun. Hingga kini, belum diketahui penyebab dan bagaimana awal munculnya penyakit GBS ini. Berdasarkan catatan medis, GBS disebabkan oleh auto imun yang menghasilkan antibodi berlebih saat menghadapi virus atau bakteri juga menyerang syaraf tepi.

Sebelumnya, gerakan kepedulian seribu rupiah bagi penderita penyakit langka Guillain-Barre Syndrome (GBS) yang menimpa Muhammad Azka Arriziq dan Shafa dimulai Minggu (7/8) lalu. Aksi sosial tersebut dilakukan setelah kedua bocah malang berusia 4 tahun itu tidak sanggup membayar biaya pengobatan yang mencapai ratusan juta rupiah.

�Gerakan ini untuk menghimpun dana kemanusiaan masyarakat luas untuk meringankan biaya pengobatan dan perawatan Shafa dan Azka,” ungkap Ketua Gerakan Rp1.000, Silvia Wahyuni, di Jakarta belum lama ini



Six different subtypes of Guillain–Barré syndrome exist:[citation needed]

  • Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common form of GBS, and the term is often used synonymously with GBS. It is caused by an auto-immune response directed against Schwann cell membranes.
  • Miller Fisher syndrome (MFS) is a rare variant of GBS and manifests as a descending paralysis, proceeding in the reverse order of the more common form of GBS. It usually affects the eye muscles first and presents with the triad of ophthalmoplegia, ataxia, and areflexia. Anti-GQ1b antibodies are present in 90% of cases.
  • Acute motor axonal neuropathy (AMAN),[1] also known as Chinese paralytic syndrome, attacks motor nodes of Ranvier and is prevalent in China and Mexico. It is probably due to an auto-immune response directed against the axoplasm of peripheral nerves. The disease may be seasonal and recovery can be rapid. Anti-GD1a antibodies[2] are present. Anti-GD3 antibodies are found more frequently in AMAN.
  • Acute motor sensory axonal neuropathy (AMSAN) is similar to AMAN but also affects sensory nerves with severe axonal damage. Like AMAN, it is probably due to an auto-immune response directed against the axoplasm of peripheral nerves. Recovery is slow and often incomplete.[3]
  • Acute panautonomic neuropathy is the most rare variant of GBS, sometimes accompanied by encephalopathy. It is associated with a high mortality rate, owing to cardiovascular involvement, and associated dysrhythmias. Impaired sweating, lack of tear formation, photophobia, dryness of nasal and oral mucosa, itching and peeling of skin, nausea, dysphagia, constipation unrelieved by laxatives or alternating with diarrhea occur frequently in this patient group. Initial nonspecific symptoms of lethargy, fatigue, headache, and decreased initiative are followed by autonomic symptoms including orthostatic lightheadedness, blurring of vision, abdominal pain, diarrhea, dryness of eyes, and disturbed micturition. The most common symptoms at onset are related to orthostatic intolerance, as well as gastrointestinal and sudomotor dysfunction (Suarez et al. 1994). Parasympathetic impairment (abdominal pain, vomiting, constipation, ileus, urinary retention, dilated unreactive pupils, loss of accommodation) may also be observed.
  • Bickerstaff’s brainstem encephalitis (BBE), is a further variant of Guillain–Barré syndrome. It is characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or Babinski’s sign. The course of the disease can be monophasic or remitting-relapsing. Large, irregular hyperintense lesions located mainly in the brainstem, especially in the pons, midbrain and medulla are described in the literature. BBE despite severe initial presentation usually has a good prognosis. Magnetic resonance imaging (MRI) plays a critical role in the diagnosis of BBE. A considerable number of BBE patients have associated axonal Guillain–Barré syndrome, indicative that the two disorders are closely related and form a continuous spectrum.

 Signs and symptoms

The disorder is characterized by symmetrical weakness which usually affects the lower limbs first, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs, manifesting as “rubbery legs” or legs that tend to buckle, with or without dysesthesias (numbness or tingling). As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness, oropharyngeal dysphagia (drooling, or difficulty swallowing and/or maintaining an open airway) and respiratory difficulties. Most patients require hospitalization and about 30% require ventilatory assistance for treatment of Type II respiratory failure.[4] [5] Facial weakness is also commonly a feature, but eye movement abnormalities are not commonly seen in ascending GBS, but are a prominent feature in the Miller-Fisher variant (see below.) Sensory loss, if present, usually takes the form of loss of proprioception (position sense) and areflexia (complete loss of deep tendon reflexes), an important feature of GBS. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising. These pains are self-limited and should be treated with standard analgesics. Bladder dysfunction may occur in severe cases but should be transient. If severe, spinal cord disorder should be suspected.

Fever should not be present, and if it is, another cause should be suspected.

In severe cases of GBS, loss of autonomic function is common, manifesting as wide fluctuations in blood pressure, orthostatic hypotension, and cardiac arrhythmias.

Acute paralysis in Guillain–Barré syndrome may be related to sodium channel blocking factor in the cerebrospinal fluid (CSF). Significant issues involving intravenous salt and water administration may occur unpredictably in this patient group, resulting in SIADH. SIADH is one of the causes of hyponatremia and can be accompanied with various conditions such as malignancies, infections and nervous system diseases. Symptoms of Guillain-Barré syndrome such as general weakness, decreased consciousness, and seizure are similar to those of hyponatremia

The symptoms of Guillain–Barré syndrome are also similar to those for progressive inflammatory neuropathy.[6]

indonesia version

Tanda dan gejala
Kelainan ini ditandai oleh kelemahan simetris yang biasanya mempengaruhi tungkai bawah pertama, dan dengan cepat berkembang dalam mode menaik. Pasien umumnya menyadari kelemahan di kaki mereka, mewujudkan sebagai “kaki karet” atau kaki yang cenderung gesper, dengan atau tanpa dysesthesias (mati rasa atau kesemutan). Sebagai kelemahan berlangsung ke atas, biasanya selama periode jam untuk hari, lengan dan otot-otot wajah juga menjadi terpengaruh. Sering, saraf kranial yang lebih rendah mungkin akan terpengaruh, menyebabkan kelemahan bulbar, disfagia orofaringeal (air liur, atau kesulitan menelan dan / atau mempertahankan jalan napas terbuka) dan kesulitan pernafasan. Kebanyakan pasien memerlukan rawat inap dan sekitar 30% memerlukan bantuan ventilasi untuk pengobatan kegagalan pernafasan Tipe II [4] [5]. Kelemahan wajah juga sering fitur, tapi mata kelainan gerakan yang tidak biasa terlihat dalam ascending GBS, tetapi fitur yang menonjol di varian Miller-Fisher (lihat di bawah.) kehilangan sensorik, jika ada, biasanya mengambil bentuk hilangnya proprioception (rasa posisi) dan areflexia (hilangnya lengkap refleks tendon dalam), sebuah fitur penting dari GBS. Hilangnya sensasi nyeri dan suhu biasanya ringan. Bahkan, nyeri adalah gejala yang umum di GBS, menyajikan sebagai nyeri yang dalam, biasanya pada otot melemah, yang pasien dibandingkan dengan rasa sakit dari overexercising. Rasa sakit adalah diri terbatas dan harus diobati dengan analgesik standar. Disfungsi kandung kemih dapat terjadi pada kasus yang berat tetapi harus sementara. Jika parah, gangguan sumsum tulang belakang harus dicurigai.

Demam tidak harus hadir, dan jika itu, penyebab lain harus dicurigai.

Dalam kasus yang parah GBS, hilangnya fungsi otonom adalah umum, mewujudkan sebagai fluktuasi luas dalam tekanan darah, hipotensi ortostatik, dan aritmia jantung.

Kelumpuhan akut pada sindrom Guillain-Barré mungkin berkaitan dengan saluran natrium memblokir faktor dalam cairan cerebrospinal (CSF). Isu-isu signifikan yang melibatkan garam intravena dan administrasi air dapat terjadi tak terduga pada kelompok pasien ini, sehingga SIADH. SIADH adalah salah satu penyebab hiponatremia dan dapat disertai dengan berbagai kondisi seperti keganasan, infeksi dan penyakit sistem saraf. Gejala sindrom Guillain-Barré seperti kelemahan umum, penurunan kesadaran, dan kejang yang mirip dengan hiponatremia

Gejala-gejala sindrom Guillain-Barré juga mirip dengan yang untuk neuropati inflamasi progresif


Structure of a typical neuron

All forms of Guillain–Barré syndrome are due to an immune response to foreign antigens (such as infectious agents) that is mistargeted at host nerve tissues instead. The targets of such immune attack are thought to be gangliosides, compounds naturally present in large quantities in human nerve tissues. The most common antecedent infection is the bacterium Campylobacter jejuni.[7][8] However, 60% of cases do not have a known cause. One study suggests that a minority of cases may be triggered by the influenza virus, or by an immune reaction to the influenza virus.[9]

The end result of such autoimmune attack on the peripheral nerves is damage to the myelin, the fatty insulating layer of the nerve, and a nerve conduction block, leading to a muscle paralysis that may be accompanied by sensory or autonomic disturbances.

However, in mild cases, nerve axon (the long slender conducting portion of a nerve) function remains intact and recovery can be rapid if remyelination occurs. In severe cases, axonal damage occurs, and recovery depends on the regeneration of this important tissue. Recent studies on the disorder have demonstrated that approximately 80% of the patients have myelin loss, whereas, in the remaining 20%, the pathologic hallmark of the disorder is indeed axon loss.

Guillain-Barré, unlike disorders such as multiple sclerosis (MS) and Lou Gehrig’s disease (ALS), is a peripheral nerve disorder and does not generally cause nerve damage to the brain or spinal cord.


Becoming infected with influenza increases both the risk of developing GBS and the risk of death (up to 1 in 10,000 who get influenza will die from it). While influenza vaccines have sometimes been suspected to raise the incidence of GBS, the evidence is equivocal, as shown below. Moreover, the highest level of suspected risks from the influenza vaccine is less than one-tenth the risk from the influenza disease itself, as discussed in more detail in the next section.[10][11][12]

Influenza vaccine

GBS may be a rare side-effect of influenza vaccines; a study of the Vaccine Adverse Event Reporting System (VAERS) indicates that it is reported as an adverse event potentially associated with the vaccine at a rate of 1 per million vaccines (over the normal risk).[13] There were reports of GBS affecting 10 per million who had received swine flu immunizations in the 1976 U.S. outbreak of swine flu—25 of which resulted in death from severe pulmonary complications, leading the United States Center of Disease Control to end that immunization campaign within the United States. (By comparison, the average flu season kills around 30,000 people in the United States).[14] However, the role of the vaccine even in those 25 cases in 1976 has remained unclear, partly because GBS had an unknown but very low incidence rate in the general population making it difficult to assess whether the vaccine was really increasing the risk for GBS. Later research has pointed to the absence of, or only a very small increase in, the GBS risk due to the 1976 swine flu vaccine.[15] Furthermore, the GBS may not have been directly due to the vaccine but to a bacterial contamination of the 1976 vaccine.[16]

Since 1976, no other influenza vaccines have been linked to GBS, though as a precautionary principle, caution is advised for certain individuals, particularly those with a history of GBS.[17][18]

From October 6 to November 24, 2009, the U.S. CDC, through the VAERS reporting system, received ten reports of Guillain-Barré syndrome cases associated with the H1N1 vaccine and identified two additional probable cases from VAERS reports (46.2 million doses were distributed within the U.S. during this time). Only four cases, however, meet the Brighton Collaboration case criteria for Guillain–Barré syndrome, while four do not meet the criteria and four remain under review.[19] A preliminary report by the CDC‘s Emerging Infections Programs (EIP) calculates the rate of GBS observed in patients who previously received the 2009 H1N1 influenza vaccination is an excess of 0.8 per million cases, which is on par with the rate seen with the seasonal trivalent influenza vaccine.[20]

Although one review gives an incidence of about one case per million vaccinations,[21] a large study in China, reported in the NEJM covering close to 100 million doses of vaccine against the 2009 H1N1 “swine” flu found only eleven cases of Guillain-Barré syndrome (0.1%) total incidence in persons vaccinated, actually lower than the normal rate of the disease in China, and no other notable side effects; “The risk-benefit ratio, which is what vaccines and everything in medicine is about, is overwhelmingly in favor of vaccination.”[22]


The diagnosis of GBS usually depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as nerve conduction studies) are common tests ordered in the diagnosis of GBS.

Typical CSF findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100–1000 mg/dL), without an accompanying increased cell count pleocytosis. A sustained increased white blood cell count may indicate an alternative diagnosis such as infection.
  • Electrodiagnostics
Electromyography (EMG) and nerve conduction study (NCS) may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.

Diagnostic criteria

Required:[citation needed]

  • Progressive, relatively symmetrical weakness of two or more limbs due to neuropathy
  • Areflexia
  • Disorder course < 4 weeks
  • Exclusion of other causes (see below)

Supportive:[citation needed]

  • relatively symmetric weakness accompanied by numbness and/or tingling
  • mild sensory involvement
  • facial nerve or other cranial nerve involvement
  • absence of fever
  • typical CSF findings obtained from lumbar puncture
  • electrophysiologic evidence of demyelination from electromyogram

Differential diagnosis:[citation needed]


Supportive care with monitoring of all vital functions is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm. Early intubation should be considered in any patient with a vital capacity (VC) <20 ml/kg, a negative inspiratory force (NIF) that is less negative (i.e., closer to zero) than -25 cmH2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.

Once the patient is stabilized, treatment of the underlying condition should be initiated as soon as possible. Either high-dose intravenous immunoglobulins (IVIg) at 400 mg/kg for 5 days or plasmapheresis can be administered,[23][24] as they are equally effective and a combination of the two is not significantly better than either alone. Therapy is no longer effective two weeks after the first motor symptoms appear, so treatment should be instituted as soon as possible. IVIg is usually used first because of its ease of administration and safety profile, with a total of five daily infusions for a total dose of 2 g/kg body weight (400 mg/kg each day). The use of intravenous immunoglobulins is not without risk, occasionally causing hepatitis, or in rare cases, renal failure if used for longer than five days. Glucocorticoids have not been found to be effective in GBS. If plasmapheresis is chosen, a dose of 40-50 mL/kg plasma exchange (PE) can be administered four times over a week.

Following the acute phase, the patient may also need rehabilitation to regain lost functions. This treatment will focus on improving ADL (activities of daily living) functions such as brushing teeth, washing, and getting dressed. Depending on the local structuring on health care, a team of different therapists and nurses will be established according to patient needs. An occupational therapist can offer equipment (such as wheelchair and special cutlery) to help the patient achieve ADL independence. A physiotherapist would plan a progressive training program and guide the patient to correct functional movement, avoiding harmful compensations which might have a negative effect in the long run. There is also some evidence supporting physiotherapy in helping patients with Guillain–Barré syndrome regain strength, endurance, and gait quality,[25] as well as helping them prevent contractures, bedsores, and cardiopulmonary difficulties.[26] A speech and language therapist would be essential in the patient regaining speaking and swallowing ability if they were intubated and received a tracheostomy. The speech and language therapist would also offer advice to the medical team regarding the swallowing abilities of the patient and would help the patient regain their communication ability pre-dysarthria. There would also be a doctor, nurse and other team members involved, depending on the needs of the patient. This team contribute their knowledge to guide the patient towards his or her goals, and it is important that all goals set by the separate team members are relevant for the patient’s own priorities. After rehabilitation the patient should be able to function in his or her own home and attend necessary training as needed.


Most of the time recovery starts after the fourth week from the onset of the disorder. Approximately 80% of patients have a complete recovery within a few months to a year, although minor findings may persist, such as areflexia. About 5–10% recover with severe disability, with most of such cases involving severe proximal motor and sensory axonal damage with inability of axonal regeneration. However, this is a grave disorder and despite all improvements in treatment and supportive care, the death rate among patients with this disorder is still about 2–3% even in the best intensive care units. Worldwide, the death rate runs slightly higher (4%), mostly from a lack of availability of life support equipment during the lengthy plateau lasting four to six weeks, and in some cases up to one year, when a ventilator is needed in the worst cases. About 5–10% of patients have one or more late relapses, in which case they are then classified as having chronic inflammatory demyelinating polyneuropathy (CIDP).

Poor prognostic factors include: 1) age, over 40 years, 2) history of preceding diarrheal illness, 3) requiring ventilator support, 4) high anti-GM1 titre and 5) poor upper limb muscle strength.


The incidence of GBS during pregnancy is 1.7 cases per 100,000 of the population.[27] The mother will generally improve with treatment but death of the fetus is a risk. The risk of Guillain–Barré syndrome increases after delivery, particularly during the first two weeks postpartum. There is evidence of Campylobacter jejuni as an antecedent infection in approximately 26% of disease cases, requiring special care in the preparation and handling of food. Congenital and neonatal Guillain–Barré syndrome have also been reported.[28]


The disorder was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and André Strohl diagnosed two soldiers with the illness and discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count.[29]

GBS is also known as acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis, French polio, Landry’s ascending paralysis and Landry Guillain Barré syndrome.

Canadian neurologist C. Miller Fisher described the variant that bears his name in 1956.[30]

Notable cases

American actor Andy Griffith developed Guillain-Barré syndrome in 1983. Griffith is seen here receiving an award at the White House in 2005

Case Report From Indonesia (Lois)

In 1982 my younger sister suddenly paralyzed after a few days before experiencing pain colds / flu-like. The beginning of a limp leg and quickly loose all over his body, but does not affect the face, the power of memory and can speak normally. The doctor said the pain is GBS as contained in this post. Time was already seeing where where in Indonesia and also to China, but my sister still remains paralyzed from the waist down.

While my brother was not able to walk and uses a wheelchair, he can run the business legacy of our parents’ shop. Hopefully those who also suffer from GBS disease now can get the treatment that is more up to date …. until the paralysis is not permanent

Indonesia version

Laporan Kasus Dari indonesia(Lois)

Tahun 1982 adik perempuan saya tiba tiba lumpuh setelah beberapa hari sebelumnya mengalami sakit masuk angin/seperti flu. Permulaan kaki yang lemas dan dengan cepat lemas sekujur badan, tapi tidak mempengaruhi wajah, daya ingatan dan bisa berbicara normal. Kata dokter sakitnya adalah GBS seperti yang termuat dalam posting ini. Waktu itu udah berobat kemana mana di Indonesia dan juga sampai ke China, tapi adik saya sampai sekarang masih tetap lumpuh dari pinggang kebawah.

Walau adik saya itu tidak bisa jalan dan menggunakan kursi roda, dia bisa menjalankan usaha toko peninggalan orang tua kami. Semoga mereka yang juga menderita penyakit GBS sekarang ini bisa mendapatkan pengobatan yang lebih up to date…. hingga kelumpuhan tidak bersifat permanen