beriberi

from Wikipedia, the free encyclopedia
Classification according to ICD-10
E51.1 beriberi
ICD-10 online (WHO version 2019)

Beriberi or Beri-Beri , German also sheep walk , as a Japanese loan word Kakke , is the name for various clinical pictures (in particular nerve inflammation, edema and heart dilation) that are attributed to a lack of thiamine (vitamin B 1 ).

Thiamine is a vitamin that is necessary in the body, among other things, for the conversion of carbohydrates into energy. A thiamine deficiency or vitamin B1 avitaminosis mainly affects cells and organs with a high glucose metabolism , for example muscle cells (including heart muscle cells ) and nerve cells . A deficiency can lead to life-threatening conditions. However, with timely treatment (supply of thiamine), these usually subside quickly.

Beriberi occurs more frequently in regions with inadequate nutritional conditions. In Asia in particular, the disease was associated with malnutrition restricted to husked rice and soy products. After 1870, with the increasing availability of husked rice, it occurred en masse and became an important political and humanitarian problem across borders. Different patterns of interpretation as deficiency symptoms or food poisoning have long been controversial. From 1908 to its dissolution in 1938, the Far Eastern Association of Tropical Medicine (FEATM) tried to look at the problem across borders.

The Dutch doctor Christiaan Eijkman discovered thiamine and associated it with beriberi, which won him the Nobel Prize in 1929 .

In richer regions, alcoholism is the greatest risk factor for thiamine deficiency. There are also other disease-promoting factors. It is not clear whether mold toxins are also the cause of certain forms of beriberi. They may hinder the absorption of thiamine from food.

Causes and Development of the Disease

Possible causes are prolonged malnutrition , insufficient intake of the vitamin from food or an increased body requirement.

Course forms and symptoms

Beriberi appears in different, partly overlapping forms with different symptoms:

  • In so-called dry beriberi , the nervous system is particularly affected. Symptoms can be: pain, abnormal sensations in the hands and feet, muscle weakness through to muscle breakdown, walking disorders, speech disorders, fatigue, poor concentration, poor performance, headache, vomiting, apathy and impaired consciousness.
  • The moist beriberi or “wet” form primarily affects the heart and circulation. The heart failure ( cardiac insufficiency ) leads to an accelerated pulse, edema (water retention in the tissue) and breathing difficulties.
  • A severe form of wet beriber is the shoshin beriberi , also called acute pernicious beriberi or fulminant cardiac beriberi or acute beriberi for short, which, if left untreated, leads to acute heart failure (due to right heart failure) and thus death in a short time.
  • Infantile beriberi, or infant beriberi , occurs in children whose nursing mothers are thiamine deficient. Symptoms are poor drinking, vomiting, apathy or restlessness, can be dramatic in acute cases with life-threatening heart failure and, if left untreated, can lead to death within a few hours. In addition to the shape affecting the heart, an aphonic shape has been described, as well as a shape that shows symptoms similar to meningitis .

Prevention and treatment

A varied diet with thiamine-containing foods such as yeast, grain germs, eggs and liver is recommended as a preventive measure. Potatoes and legumes are good vegetable sources of vitamin B 1 .

For treatment, thiamine hydrochloride is given in the form of tablets or as an injection. However, benfotiamine , a lipid-soluble form of thiamine, is increasingly used. Due to its solubility in fat, it is easily permeable to tissue and has a bioavailability that is 5 to 10 times higher .

history

Up until the 19th and early 20th centuries, beriberi was nothing more than an expression for a whole range of symptoms and not an individually distinguishable disease. From the perspective of medical history, Beriberi's epistemic uncertainty, which is clear, is also in productive contradiction to perspectives that, in retrospect, claim to be able to reliably interpret and differentiate historical clinical pictures. The causes of beriberi and other diseases (e.g. infections or fungal and mold infestations, cf. Antoniusfeuer ) have historically not been recognized. The symptoms referred to as beriberi are not always (solely) attributable to a vitamin deficiency. The interpretation as thiamine malnutrition was an important step towards the discovery of vitamins , but it was only slowly gaining acceptance. Additional factors such as deficiency symptoms and stress factors as well as “yellow rice” mycotoxins (citrinine, citreoviridine and others) named after the color of moldy rice can aggravate an existing beriberi . In the case of wet beriberi ( Shoshin-kakke or yellow rice disease in Japan), isolated outbreaks of beriberi through moldy rice and the resulting citreoviridin were explained even after 1905. With the exclusion of moldy rice from the food market, this has not been seen for decades. Even in the wet form, symptoms should be eliminated after administration of thiamine.

A Dutch doctor, Jacob de Bondt , observed and subsequently described a disease called beriberi in Java in 1630 , which is said to have been named after the local word for sheep because of the unsteady gait of the sick. Also Nicolaes Tulp described this disease in the 17th century. The Sinhala word for “I can't, I can't”, which can be traced back to the patient's inability to move in the late phase, is also the origin of the word . A doctor involved in the occupation of Ceylon , Thomas Christie, described the disease and suspected a lack of nutrition as the cause and drew some parallels to scurvy . In the 1830s the disease was described in Madras, the southern area of ​​India, although worm infections in Assam were also mentioned under beriberi in the 1870s. The mix-up was not cleared up until the end of the 19th century. It was not until the end of the 19th century that the disease was described as a mass phenomenon in the sense of a dropsy epidemic in Asia and interpreted as a contagious fever by the British doctor Norman Chevers. Among other things, food poisoning from contaminated cooking oil was interpreted as beriberi. At the beginning of the 20th century there was international talk of a beriberi problem and a large number of deaths and illnesses were reported in Japan, Indonesia, the Malacca Peninsula and Brazil, among others. In 1913, millions of cases were assumed for China based on projections from Hong Kong.

The clinical picture could not be properly separated from food poisoning. It was not until the 19th century that the spread of beriberi became a comparatively large and transnational problem. It was only in the 1870s that mechanical rice mills made the coveted white, peeled rice available in large quantities. Peeled rice did not spoil as quickly and was easier to transport. As the consumption of husked rice spread, beriberi spread and became a mass phenomenon. However, it was much less widespread than in Japan or China , for example, in the area of ​​British India, where rice enhanced by the parboiling process was more popular. In Meiji-era Japan, beriberi became a disease affecting all classes. Beriberi spread further with the travel export from Burma, Thailand and Vietnam to the Philippines, Indonesia and from the 1920s to India.

Role of the FEATM

From 1908 to its dissolution in 1938, the Far Eastern Association of Tropical Medicine (FEATM) tried to look at the problem across borders. The FEATM had just been founded with the appearance of the deficiency thesis. The occurrence, which was limited to Asia and there again differentiated according to nationality, was of worldwide interest. There were also racist views. Among other things, a connection between rice nutrition and a lack of fighting spirit was propagated, for example by the Northern Irish nutrition pioneer Robert McCarrison.

The link between white rice and beriberi put the governments in India and the monsoon belt in a bind. They rejected the radical demands of the FEATM experts, especially Victor Heiser. From 1910 onwards, Heiser called for white rice to be taxed so heavily that only the rich could have afforded it. He and other FEATM experts advocated significant changes in eating habits for health reasons, but politicians feared regional resistance to culturally and religiously based eating habits and outside interference. But the medical establishment also stuck to the pre-1905 prevailing theses of food poisoning as the cause. Important representatives like JWD Megaw of the Indian Medical Service and Chief Surgeon in Madras and Punjab considered the rice mills to be an advance and saw a close connection between the monsoon humidity and the emergence of beriberi. Likewise, the governments did not want to limit the lucrative rice trade. It was not until the 1940s that the Indian public began to delve into public nutrition issues. Beriberi became a major issue in newspapers and media. It was not until the 1960s that the mass occurrence was reduced and, with a few exceptions, hardly occurred in the 1980s.

Pioneering role of Takaki Kanehiro

Takaki Kanehiro

The Japanese naval doctor Kanehiro Takaki carried out investigations into the development of the disease on ships of the Imperial Navy in the 1880s. In 1884 two warships were sent on a comparable nine-month voyage across New Zealand to South America and back to Japan. On the ship Tsukuba , the sailors received a mixed diet with meat, fish, barley, rice and beans. On the battleship Ryūjō only white rice was served. Of the 376 crew members of the Ryūjō, 161 fell ill with beriberi and 25 fatally. Only 14 men of the tsukuba fell ill and none died; the 14 had secretly denied some of the extra food. Takaki suspected a lack of nitrogenous foods as the cause; in the Japanese navy the board food was adapted accordingly and beriberi was dramatically reduced.

In the Japanese army, however, the thesis of the infectious disease attributed to the German school (represented by Mori Ōgai ) in Japan was still widespread, which in the Russo-Japanese War in 1905 led to 27,000 deaths from beriberi. 47,000 soldiers were killed in action.

Discovery and synthesis of thiamine

Structure of thiamine
Christiaan Eijkman

Outside of the Japanese armed forces, however, nothing had changed. In 1886 a group of experts with the Dutch doctor Christiaan Eijkman was sent to the then Dutch colony of Indonesia to research the disease. Between 1890 and 1897 he observed deficiency symptoms in chickens that had been fed only polished rice from table waste. Eijkman, as a supporter of the germ theory, was initially convinced of a bacterial cause of the disease or toxic components in the table waste. His assistant Gerrit Grijns found that the symptoms disappeared after feeding unpeeled rice or green peas and meat. Both extracted a so-called "anti-polyneuritis factor" with water and ethanol from rice husks. Eijkman himself was long convinced that he had a “pharmacological antidote” against the “Beri-Beri microbes” or their toxins present in rice endosperm (white rice) ; In contrast, Grijns preferred the thesis that white rice lacks a special substance that is important for the metabolism of the nervous system . Inspired by these observations, the Polish biochemist Casimir Funk began his research on beriberi in London. In 1911 he isolated an amine from unpeeled or unpolished rice grains that contained at least some of the "silver skin" (between the outer shell and the core) as an "anti-beri-beri factor", the deficiency of which he mistakenly blamed for the development of the disease. In fact, the substance was ineffective in treating beriberi. He must have found the niacin , the deficiency of which leads to pellagra . Nevertheless, this and other work led him to introduce the term “vital amine” in 1912 for a whole group of these vital substances, from which the term vitamins was ultimately derived.

1926 thiamine was the first B vitamin of Barend Coenraad Petrus Jansen and Willem Frederik Donath isolated from the sheath of the rice grain and of these "aneurine" (for a nti neur itisches Vitam in named). They overlooked the sulfur atom in the molecule and published a wrong formula, which caused confusion for years. According to other sources, Suzuki Umetaro was the first in Japan in 1910 to isolate the substance - under the name of "aberic acid" - and to receive a patent for it . In 1929, Eijkman was awarded the Nobel Prize in Physiology or Medicine (together with Frederick G. Hopkins , a pioneer in vitamin research) for his discoveries . The synthesis of thiamine was first carried out in 1936 by Robert R. Williams .

Recent cases

Infant beriberi occurs when breastfeeding by mothers with a thiamine deficiency. An incident in Israel became known in which beriberi was found in infants in 2003. The babies were fed a substitute milk made from soy protein . Due to a manufacturing error, this food was made without the addition of vitamin B1. Three infants died and several others suffered serious health problems.

Even after 1905, outbreaks of beriberi were partly explained by moldy rice and the resulting citreoviridine poisoning. From 2006 to 2008 there was an outbreak of beriberia in Maranhão (Brazil) with 40 deaths. A connection with the consumption of poor quality rice by subsistence farmers is assumed. The influence of mold growth, which was determined by some researchers, was not generally confirmed.

In 2008, ten beriberi cases were registered in an Indian population in Roraima (Brazil) on the occasion of a vaccination campaign. Three of the patients had already died. A retrospective study attempted to identify additional cases in the region and possible causes of the disease. 90 other people were identified who had been treated for symptoms of beriberi. Male sex and alcohol consumption were found to be risk factors. Therapy with thiamine was successful in all cases.

In July 2009 the wet disease broke out in some soldiers from the African Union Mission to Somalia in Mogadishu. Due to the distrust of the local environment, they only consumed the unilateral troop catering. The beriberis symptoms could be eliminated in a very short time with injected thiamine doses.

See also

literature

  • Ludwig Weissbecker: Vitamin B 1 -avitaminosis (beriberi). In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition, ibid. 1961, pp. 1090-1092.

Web links

Individual evidence

  1. Berthold Koletzko: Kinder- und Jugendmedizin , Springer-Verlag, 13th edition, p. 160
  2. WHO 1999, p. 9 and p. 47 (PDF)
  3. ^ Vitamins ( Memento from October 19, 2008 in the Internet Archive ) in Meyers Online Lexicon
  4. Klaus Pietrzik, Ines Golly, Dieter Loew: Manual vitamins: for prevention, treatment and advice; 94 tables . ISBN 3-437-55361-5 , pp. 47 ( limited preview in Google Book search).
  5. a b c d e f g h i j k l m n o p q r David Arnold: British India and the “Beriberi Problem”, 1798–1942 . In: Medical History . tape 54 , no. 3 , July 1, 2010, p. 295-314 , PMID 20592882 , PMC 2889456 (free full text).
  6. a b c J. W. Bennett, M. Klich: Mycotoxins. In: Clin Microbiol Rev. 2003 July; 16 (3), pp. 497-516, literally: The yellow rice toxins (citrinin, citreoviridin, luteoskyrin, rugulosin, rubroskyrin, and related compounds) are believed to have exacerbated Shoshin-kakke, a particularly malignant form of beriberi seen in Japan in the early 20th century (222)
  7. Kenneth John Carpenter: Beriberi, White Rice, and Vitamin B: A Disease, a Cause, and a Cure . University of California Press, 2000
  8. a b Helena Cristina Alves Vieira Lima, Eucilene Alves Santana Porto, José Ricardo Pio Marins, Rejane Maria Alves, Rosângela Rosa Machado: Outbreak of beriberi in the state of Maranhão, Brazil: revisiting the mycotoxin aetiologic hypothesis . In: Tropical Doctor . tape 40 , no. 2 , April 1, 2010, ISSN  0049-4755 , p. 95-97 , doi : 10.1258 / td.2009.090439 , PMID 20305104 ( sagepub.com [accessed September 25, 2015]).
  9. a b M. Peraica, B. Radić, A. Lucić, M. Pavlović: Toxic effects of mycotoxins in humans . In: Bulletin of the World Health Organization . tape 77 , no. 9 , January 1, 1999, ISSN  0042-9686 , p. 754-766 , PMID 10534900 , PMC 2557730 (free full text).
  10. ^ A b John T. Watson, Hassan El Bushra, Emmaculate J. Lebo, Godfrey Bwire, James Kiyengo: Outbreak of Beriberi among African Union Troops in Mogadishu, Somalia . In: PLoS ONE . tape 6 , no. 12 , December 21, 2011, p. e28345 , doi : 10.1371 / journal.pone.0028345 , PMID 22205947 , PMC 3244391 (free full text).
  11. Pediatric Beriberi. medscape.com, April 16, 2012, accessed June 3, 2012 .
  12. Barbara I. Tshisuaka: Beriberi. In: Werner E. Gerabek , Bernhard D. Haage, Gundolf Keil , Wolfgang Wegner (eds.): Enzyklopädie Medizingeschichte. De Gruyter, Berlin / New York 2005, ISBN 3-11-015714-4 , p. 167 f .; here: p. 167.
  13. Beriberi. faqs.org, accessed June 3, 2012 .
  14. ^ William Hunter: An essay on the diseases incident to Indian seamen, or lascars, on long voyages , Calcutta, The Honorable Company's Press, 1804, pp. 77-141., Cited in Arnold 2010
  15. Alexander R. Bay: Beriberi in Modern Japan: The Making of a National Disease . University Rochester Press, 2012
  16. ^ Morris Low: Building a Modern Japan: Science, Technology, and Medicine in the Meiji Era and Beyond . Palgrave Macmillan, 2005, ISBN 1-4039-6832-2 .
  17. ^ A b Yoshinori Itokawa: Kanehiro Takaki (1849-1920) A Biographical Sketch . In: The Journal of Nutrition . tape 106 , no. 5 , 1976, ISSN  1541-6100 , pp. 581-588 ( online at jn.nutrition.org [accessed June 3, 2012]).
  18. A late resumption of the 'German School', an alternative interpretation of beriberi as mold poisoning can be found with the nutrition journalist Udo Pollmer as well as Ramsay Tainsh, most recently in Ramsay Tainsh: Beriberi and Mycotoxicosis: An historical account. In: International Journal of Environmental Studies. Volume 19, Issue 3 & 4 September 1982, pp. 205-207, but this contradicts the medical literature on the subject
  19. A. Hawk: The great disease enemy, Kak'ke (beriberi) and the Imperial Japanese Army . In: Mil Med . tape 171 , no. 4 , 2006, p. 333-339 , PMID 16673750 ( online ( memento of April 2, 2010 in the Internet Archive )).
  20. a b c The Nobel Prize in Physiology or Medicine 1929. nobelprize.org, accessed June 3, 2012 .
  21. ^ A b Kenneth J. Carpenter, Barbara Sutherland: Eijkman's Contribution to the Discovery of Vitamins. In: Journal of Nutrition. Vol. 125 No. February 2, 1995, pp. 155-163.
  22. ^ Otto Westphal , Theodor Wieland , Heinrich Huebschmann: life regulator. Of hormones, vitamins, ferments and other active ingredients. Societäts-Verlag, Frankfurt am Main 1941 (= Frankfurter Bücher. Research and Life. Volume 1), pp. 48–50 ( Das Silberhäutchen ).
  23. Michael J. Lentze, Franz J. Schulte, Jürgen Schaub, Jürgen Spranger: Pädiatrie. Basics and Practice 3rd, completely revised and expanded edition. Springer, Heidelberg 2007, ISBN 978-3-540-71895-6 , p. 25.
  24. Petra Ahne, Petra Wache, Lilo Berg: Artificial milk with risk, baby food - the German company Humana made massive mistakes in the production of kosher soy milk. As a result, two children died in Israel. In: Berliner Zeitung , November 12, 2003.
  25. Matheus P. Cerroni, Jean CS Barrado, Aglaer A. Nobrega, Alysson BM Lins, Iolanda P. da Silva, Robson R. Mangueira, Rômulo H. da Cruz, Sandra MF Mendes, Jeremy Sobel: Outbreak of Beriberi in an Indian Population of the Upper Amazon Region, Roraima State, Brazil, 2008. In: Am J Trop Med Hyg. , 2010 Nov 5, 83 (5), pp. 1093-1097. doi: 10.4269 / ajtmh.2010.10-0345 . PMC 2963975 (free full text).