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Thiamine deficiency
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"Beri beri" redirects here. For the African ethnic group, see Kanuri people.
Thiamine deficiency[1]
Synonyms
Beriberi, vitamin B1 deficiency, thiamine-deficiency syndrome[1][2]
A person with beriberi during the beginning of the 20th century in Southeast Asia.
Specialty
Neurology, cardiology, pediatrics
Symptoms
Wet: Fast heart rate, shortness of breath, leg swelling[1]
Dry: Numbness, confusion, trouble moving the legs, pain[1]
Types
Wet, dry, gastrointestinal[3]
Causes
Not enough thiamine[1]
Risk factors
Diet of mostly white rice, alcoholism, dialysis, chronic diarrhea, diuretics[1][4]
Prevention
Food fortification[1]
Treatment
Thiamine supplementation[1]
Frequency
Rare (US)[1]
[edit on Wikidata]
Thiamine deficiency, also known as beriberi, is a condition that occurs due to not enough thiamine (vitamin B1).[1] There are two main types: wet beriberi, and dry beriberi.[1] Wet beriberi results in a fast heart rate, shortness of breath, and leg swelling.[1] Dry beriberi results in numbness of the hands and feet, confusion, trouble moving the legs, and pain.[1] A form with loss of appetite and constipation may also occur.[3]
Risk factors include a diet of mostly white rice, alcoholism, dialysis, chronic diarrhea, and taking high doses of diuretics.[1][4] Rarely it may be due to a genetic condition which results in difficulties absorbing thiamine found in food.[1] Wernicke encephalopathy and Korsakoff syndrome are forms of dry beriberi.[4] Diagnosis is based on symptoms, low levels of thiamine in the urine, high blood lactate, and improvement with treatment.[5]
Treatment is by thiamine supplementation, either by mouth or by injection.[1] With treatment symptoms generally resolve in a couple of weeks.[5] The disease may be prevented at the population level through the fortification of food.[1]
Thiamine deficiency is rare in the United States.[1] It remains relatively common in sub-Saharan Africa.[2] Outbreaks have been seen in refugee camps.[4] Thiamine deficiency has been described for thousands of years in Asia and become more common in the late 1800s with the increased processing of rice.[6]
Contents
[hide]
1 Signs and symptoms
1.1 Dry beriberi
1.1.1 Brain disease
1.2 Wet beriberi
1.3 Gastrointestinal beriberi
1.4 Infants
2 Cause
2.1 Genetics
3 Pathophysiology
4 Diagnosis
5 Treatment
6 Epidemiology
7 History
7.1 Etymology
8 Other animals
8.1 Poultry
8.2 Ruminants
8.3 Snakes
8.4 Wild birds and fish
9 References
10 External links
Signs and symptoms[edit]
Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception, weakness and pain in the limbs, and periods of irregular heart rate. Edema (swelling of bodily tissues) is common. It may increase the amount of lactic acid and pyruvic acid within the blood. In advanced cases, the disease may cause high-output cardiac failure and death.
Symptoms may occur concurrently with those of Wernicke's encephalopathy, a primarily neurological thiamine-deficiency related condition.
Beriberi is divided into four categories as follows. The first three are historical and the fourth, gastrointestinal beriberi, was recognized in 2004:
Dry beriberi specially affects the peripheral nervous system
Wet beriberi specially affects the cardiovascular system and other bodily systems
Infantile beriberi affects the babies of malnourished mothers
Gastrointestinal beriberi affects the digestive system and other bodily systems
Dry beriberi[edit]
Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves. It is also referred to as endemic neuritis. It is characterized by:
Difficulty in walking
Tingling or loss of sensation (numbness) in hands and feet
Loss of tendon reflexes[7]
Loss of muscle function or paralysis of the lower legs
Mental confusion/speech difficulties
Pain
Involuntary eye movements (nystagmus)
Vomiting.
A selective impairment of the large proprioceptive sensory fibers without motor impairment can occur and present as a prominent sensory ataxia, which is a loss of balance and coordination due to loss of the proprioceptive inputs from the periphery and loss of position sense.[8]
Brain disease[edit]
Wernicke's encephalopathy (WE), Korsakoff's syndrome (alcohol amnestic disorder), Wernicke–Korsakoff syndrome are forms of dry beriberi.[4]
Wernicke's encephalopathy is the most frequently encountered manifestation of thiamine deficiency in Western society,[9][10] though it may also occur in patients with impaired nutrition from other causes, such as gastrointestinal disease,[9] those with HIV-AIDS, and with the injudicious administration of parenteral glucose or hyperalimentation without adequate B-vitamin supplementation.[11] This is a striking neuro-psychiatric disorder characterized by paralysis of eye movements, abnormal stance and gait, and markedly deranged mental function.[12]
Korsakoff's syndrome is, in general, considered to occur with deterioration of brain function in patients initially diagnosed with WE.[13] This is an amnestic-confabulatory syndrome characterized by retrograde and anterograde amnesia, impairment of conceptual functions, and decreased spontaneity and initiative.[14]
Alcoholics may have thiamine deficiency because of the following:
Inadequate nutritional intake: Alcoholics tend to intake less than the recommended amount of thiamine.
Decreased uptake of thiamine from the GI tract: Active transport of thiamine into enterocytes is disturbed during acute alcohol exposure.
Liver thiamine stores are reduced due to hepatic steatosis or fibrosis.[15]
Impaired thiamine utilization: Magnesium, which is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption. The inefficient utilization of any thiamine that does reach the cells will further exacerbate the thiamine deficiency.
Ethanol per se inhibits thiamine transport in the gastrointestinal system and blocks phosphorylation of thiamine to its cofactor form (ThDP).[16]
Following improved nutrition and the removal of alcohol consumption, some impairments linked with thiamine deficiency are reversed, in particular poor brain functionality, although in more severe cases, Wernicke–Korsakoff syndrome leaves permanent damage. (See delirium tremens.)
Wet beriberi[edit]
Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous. Wet beriberi is characterized by:
Increased heart rate
Vasodilation leading to decreased systemic vascular resistance, and high output cardiac failure[17]
Elevated jugular venous pressure[18]
Dyspnea (shortness of breath) on exertion
Paroxysmal nocturnal dyspnea
Peripheral edema[18] (swelling of lower legs)
Gastrointestinal beriberi[edit]
Gastrointestinal beriberi causes abdominal pain. Gastrointestinal beriberi is characterized by:
Abdominal pain
Nausea
Vomiting
Lactic acidosis[19][20]
Infants[edit]
Infantile beriberi usually occurs between two and six months of age in children whose mothers have inadequate thiamine intake. It may present as either wet or dry beriberi.[2]
In the acute form, the baby develops dyspnea and cyanosis and soon dies of heart failure. These symptoms may be described in infantile beriberi:
Hoarseness, where the child makes moves to moan but emits no sound or just faint moans[21] caused by nerve paralysis[7]
Weight loss, becoming thinner and then marasmic as the disease progresses[21]
Vomiting[21]
Diarrhea[21]
Pale skin[7]
Edema[7][21]
Ill temper[7]
Alterations of the cardiovascular system, especially tachycardia (rapid heart rate)[7]
Convulsions occasionally observed in the terminal stages[21]
Cause[edit]
Beriberi may also be caused by shortcomings other than inadequate intake: diseases or operations on the digestive tract, alcoholism,[18] dialysis, genetic deficiencies, etc. All these causes mainly affect the central nervous system, and provoke the development of what is known as Wernicke's disease or Wernicke's encephalopathy.
Wernicke's disease is one of the most prevalent neurological or neuropsychiatric diseases.[22] In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases.[23] Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12.5% or more. Mortality caused by Wernicke's disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries.[24][25] The number of people with Wernicke's disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases.
Genetics[edit]
Genetic diseases of thiamine transport are rare but serious. Thiamine responsive megaloblastic anemia (TRMA) with diabetes mellitus and sensorineural deafness[26] is an autosomal recessive disorder caused by mutations in the gene SLC19A2,[27] a high affinity thiamine transporter. TRMA patients do not show signs of systemic thiamine deficiency, suggesting redundancy in the thiamine transport system. This has led to the discovery of a second high-affinity thiamine transporter, SLC19A3.[28][29] Leigh disease (subacute necrotising encephalomyelopathy) is an inherited disorder that affects mostly infants in the first years of life and is invariably fatal. Pathological similarities between Leigh disease and WE led to the hypothesis that the cause was a defect in thiamine metabolism. One of the most consistent findings has been an abnormality of the activation of the pyruvate dehydrogenase complex.[30]
Mutations in the SLC19A3 gene have been linked to Biotin-Thiamine Responsive Basal Ganglia Disease[31] which is treated with pharmacological doses of thiamine and biotin, another B vitamin.
Other disorders in which a putative role for thiamine has been implicated include subacute necrotising encephalomyelopathy, opsoclonic cerebellopathy (a paraneoplastic syndrome), and Nigerian seasonal ataxia. In addition, several inherited disorders of ThDP-dependent enzymes have been reported,[32] which may respond to thiamine treatment.[14]
Pathophysiology[edit]
Thiamine in the human body has a half-life of 18 days and is quickly exhausted, particularly when metabolic demands exceed intake. A derivative of thiamine, thiamine pyrophosphate (TPP), is a cofactor involved in the citric acid cycle, as well as connecting the breakdown of sugars with the citric acid cycle. The citric acid cycle is a central metabolic pathway involved in the regulation of carbohydrate, lipid, and amino acid metabolism, and its disruption due to thiamine deficiency inhibits the production of many molecules including the neurotransmitters glutamic acid and GABA.[33] Additionally thiamine may also be directly involved in neuromodulation.[34]
Diagnosis[edit]
Oxidation of thiamine derivatives to fluorescent thiochromes by potassium ferricyanide under alkaline conditions
A positive diagnosis test for thiamine deficiency can be ascertained by measuring the activity of the enzyme transketolase in erythrocytes (Erythrocyte Transketolase Activation Assay). Thiamine, as well as its phosphate derivatives, can also be detected directly in whole blood, tissues, foods, animal feed, and pharmaceutical preparations following the conversion of thiamine to fluorescent thiochrome derivatives (Thiochrome Assay) and separation by high-performance liquid chromatography (HPLC).[35][36][37] In recent reports, a number of Capillary Electrophoresis (CE) techniques and in-capillary enzyme reaction methods have emerged as potential alternative techniques for the determination and monitoring of thiamine in samples.[38] The normal thiamine concentration in EDTA-blood is about 20-100 µg/l.
Treatment[edit]
Many people with beriberi can be treated with thiamine alone.[39] Given thiamine intravenously (and later orally), rapid and dramatic [18] recovery can occur within hours. In situations where concentrated thiamine supplements are unavailable, feeding the person with a thiamine-rich diet (e.g. whole grain brown bread) will lead to recovery, though at a much slower rate.[citation needed]
Following thiamine treatment, rapid improvement occurs, in general, within 24 hours.[40] Improvements of peripheral neuropathy may require several months of thiamine treatment.[41]
Epidemiology[edit]
Historically, beriberi was associated with a diet including much polished rice (white rice); when the relationship between polishing rice and the disease was discovered, it became possible to prevent and treat the deficiency condition, for example with inexpensive rice bran. Beriberi caused by inadequate nutritional intake is rare today in developed countries[citation needed] because of quality of food and the fact that many foods are fortified with vitamins.[citation needed] No reliable statistics are given for beriberi in developed countries in the 19th century or earlier; neither are statistics available before the last century in countries in extreme poverty.[citation needed]
Beriberi is a recurrent nutritional disease in detention houses, even in this century. In 1999, an outbreak of beriberi occurred in a detention center in Taiwan.[42] High rates of illness and death in overcrowded Haitian jails were traced in 2007 to the traditional practice of washing rice before cooking.[43] In the Ivory Coast, among a group of prisoners with heavy punishment, 64% were affected by beriberi. Before beginning treatment, prisoners exhibited symptoms of dry or wet beriberi with neurological signs (swarming[specify]: 41%), cardiovascular signs (dyspnoea: 42%, thoracic pain: 35%), and edemas of the lower limbs (51%). With treatment the rate of healing was about 97%.[44]
Populations under extreme stress may be at higher risk for beriberi. Displaced populations, such as refugees from war, are susceptible to micronutritional deficiency, including beriberi.[45] The severe nutritional deprivation caused by famine also can cause beriberis, although symptoms may be overlooked in clinical assessment or masked by other famine-related problems.[46] An extreme weight-loss diet can, rarely, induce a famine-like state and the accompanying beriberi.[18]
History[edit]
Sun Simiao (581–682 AD) was the first person in medical history to document the diagnosis, treatment, and prevention of Beriberi (leg edema due to vitamin B1 deficiency), a deficiency disease caused by lack of vitamin B1. For this, he prescribed combinations of herbs rich in vitamin B1 and unpolished rice (the outer layer of rice and other grains rich in B vitamins)[47][48][49][50]
In the late 19th century, beriberi was studied by Takaki Kanehiro, a British-trained Japanese medical doctor of the Japanese Navy.[51] Beriberi was a serious problem in the Japanese navy: Sailors fell ill an average of four times a year in the period 1878 to 1881, and 35% were cases of beriberi.[51] In 1883, Kanehiro learned of a very high incidence of beriberi among cadets on a training mission from Japan to Hawaii, via New Zealand and South America. The voyage lasted more than nine months and resulted in 169 cases of sickness and 25 deaths on a ship of 376 men. With the support of the Japanese Navy, he conducted an experiment in which another ship was deployed on the same route, except that its crew was fed a diet of meat, fish, barley, rice, and beans. At the end of the voyage, this crew had only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that diet was the cause.[51] In 1884, Kanehiro observed that beriberi was common among low-ranking crew who were often provided free rice and thus ate little else, but not among crews of Western navies, nor among Japanese officers who consumed a more varied diet.
In 1897, Christiaan Eijkman, a Dutch physician and pathologist, demonstrated that beriberi is caused by poor diet, and discovered that feeding unpolished rice (instead of the polished variety) to chickens helped to prevent beriberi. The following year, Sir Frederick Hopkins postulated that some foods contained "accessory factors"—in addition to proteins, carbohydrates, fats, and salt—that were necessary for the functions of the human body.[52][53] In 1901, Gerrit Grijns (May 28, 1865 – November 11, 1944), a Dutch physician and assistant to Christiaan Eijkman in the Netherlands, correctly interpreted the disease as a deficiency syndrome,[54] and between 1910 and 1913, Edward Bright Vedder established that an extract of rice bran is a treatment for beriberi.[citation needed] In 1929, Eijkman and Hopkins were awarded the Nobel Prize for Physiology or Medicine for their discoveries.
Etymology[edit]
According to the Oxford English Dictionary, the term "beriberi" comes from a Sinhalese phrase meaning "weak, weak" or "I cannot, I cannot", the word being duplicated for emphasis.[55][56][57][58]
According to Jacobus Bontius (Jacob de Bondt; 1591–1631), a Dutch physician who encountered the disease while working in Java in 1630, In the first known description of beriberi (or, beri-beri), he wrote: "A certain very troublesome affliction, which attacks men, is called by the inhabitants beriberi (which means sheep). I believe those, whom this same disease attacks, with their knees shaking and the legs raised up, walk like sheep. It is a kind of paralysis, or rather tremor: for it penetrates the motion and sensation of the hands and feet indeed sometimes of the whole body."[59]
Other animals[edit]
Poultry[edit]
As most feedstuffs used in poultry diets contain enough quantities of vitamins to meet the requirements in this species, deficiencies in this vitamin do not occur with commercial diets. This was, at least, the opinion in the 1960s.[60]
Mature chickens show signs 3 weeks after being fed a deficient diet. In young chicks, it can appear before 2 weeks of age.
Onset is sudden in young chicks. There is anorexia and an unsteady gait. Later on, there are locomotor signs, beginning with an apparent paralysis of the flexor of the toes. The characteristic position is called "stargazing", meaning a chick "sitting on its hocks and the head in opisthotonos".
Response to administration of the vitamin is rather quick, occurring a few hours later.[61][62]
Differential diagnosis include riboflavin deficiency and avian encephalomyelitis. In riboflavin deficiency, the "curled toes" is a characteristic symptom. Muscle tremor is typical of avian encephalomyelitis. A therapeutic diagnosis can be tried by supplementing thiamine only in the affected bird. If the animals do not respond in a few hours, thiamine deficiency can be excluded.
Ruminants[edit]
Polioencephalomalacia (PEM) is the most common thiamine deficiency disorder in young ruminant and nonruminant animals. Symptoms of PEM include a profuse, but transient, diarrhea, listlessness, circling movements, star gazing or opisthotonus (head drawn back over neck), and muscle tremors.[63] The most common cause is high-carbohydrate feeds, leading to the overgrowth of thiaminase-producing bacteria, but dietary ingestion of thiaminase (e.g., in bracken fern), or inhibition of thiamine absorption by high sulfur intake are also possible.[64] Another cause of PEM is Clostridium sporogenes or Bacillus aneurinolyticus infection. These bacteria produce thiaminases that will cause an acute thiamine deficiency in the affected animal.[65]
Snakes[edit]
Snakes that consume a diet largely composed of goldfish and feeder minnows are susceptible to developing thiamine deficiency. This is often a problem observed in captivity when keeping garter and ribbon snakes that are fed a goldfish-exclusive diet, as these fish contain thiaminase, an enzyme that breaks down thiamine.[66]
Wild birds and fish[edit]
Thiamine deficiency has been identified as the cause of a paralytic disease affecting wild birds in the Baltic Sea area dating back to 1982.[67] In this condition, there is difficulty in keeping the wings folded along the side of the body when resting, loss of the ability to fly and voice, with eventual paralysis of the wings and legs and death. It affects primarily 0.5–1 kg sized birds such as the herring gull (Larus argentatus), common starling (Sturnus vulgaris) and common eider (Somateria mollissima). Researches noted, "Because the investigated species occupy a wide range of ecological niches and positions in the food web, we are open to the possibility that other animal classes may suffer from thiamine deficiency as well."[67]p. 12006
In the counties of Blekinge and Skåne (south-most Sweden) mass deaths of especially herring gull but also other species has been observed since the early 2000s. More recently, species of other classes seems to be affected. High mortality of salmon (Salmo salar) in the river Mörrumsån is reported, and the last years mammals like Eurasian Elk (Alces alces) has suffered death in unusual high number. Lack of thiamine is the common denominator where analysis is done. The County Administrative Board of Blekinge did in April 2012 find the situation so alarming that they asked the Swedish government to set up a closer investigation.[68]
References[edit]
^ Jump up to: a b c d e f g h i j k l m n o p q r "Beriberi". Genetic and Rare Diseases Information Center (GARD) – an NCATS Program. 2015. Retrieved 11 November 2017.
^ Jump up to: a b c Adamolekun, B; Hiffler, L (24 October 2017). "A diagnosis and treatment gap for thiamine deficiency disorders in sub-Saharan Africa?". Annals of the New York Academy of Sciences. doi:10.1111/nyas.13509. PMID 29064578.
^ Jump up to: a b Ferri, Fred F. (2017). Ferri's Clinical Advisor 2018 E-Book: 5 Books in 1. Elsevier Health Sciences. p. 1368. ISBN 9780323529570.
^ Jump up to: a b c d e "Nutrition and Growth Guidelines | Domestic Guidelines - Immigrant and Refugee Health". CDC. March 2012. Retrieved 11 November 2017.
^ Jump up to: a b Swaiman, Kenneth F.; Ashwal, Stephen; Ferriero, Donna M.; Schor, Nina F.; Finkel, Richard S.; Gropman, Andrea L.; Pearl, Phillip L.; Shevell, Michael (2017). Swaiman's Pediatric Neurology E-Book: Principles and Practice. Elsevier Health Sciences. p. e929. ISBN 9780323374811.
Jump up ^ Lanska, DJ (2010). "Chapter 30: historical aspects of the major neurological vitamin deficiency disorders: the water-soluble B vitamins". Handbook of clinical neurology. 95: 445–76. doi:10.1016/S0072-9752(08)02130-1. PMID 19892133.
^ Jump up to: a b c d e f Katsura, E.; Oiso, T. (1976). Beaton, G.H.; Bengoa, J.M., eds. "Chapter 9. Beriberi" (PDF). World Health Organization Monograph Series No. 62: Nutrition in Preventive Medicine. Geneva: World Health Organization.
Jump up ^ Spinazzi, Marco; Angelini, Corrado; Patrini, Cesare (2010). "Subacute sensory ataxia and optic neuropathy with thiamine deficiency". Nature Reviews Neurology. 6 (5): 288–93. doi:10.1038/nrneurol.2010.16. PMID 20308997.
^ Jump up to: a b Kril JJ (1996). "Neuropathology of thiamine deficiency disorders". Metab Brain Dis. 11 (1): 9–17. doi:10.1007/BF02080928. PMID 8815394.
Jump up ^ For an interesting discussion on thiamine fortification of foods, specifically targetting beer, see "Wernicke's encephalopathy and thiamine fortification of food: time for a new direction?". Medical Journal of Australia.
Jump up ^ Butterworth RF, Gaudreau C, Vincelette J, et al. (1991). "Thiamine deficiency and wernicke's encephalopathy in AIDS". Metab Brain Dis. 6 (4): 207–12. doi:10.1007/BF00996920. PMID 1812394.
Jump up ^ Harper C. (1979). "Wernicke's encephalopathy, a more common disease than realised (a neuropathological study of 51 cases)". J Neurol Neurosurg Psychiatry. 42 (3): 226–231. doi:10.1136/jnnp.42.3.226. PMC 490724  . PMID 438830.
Jump up ^ McCollum EV A History of Nutrition. Cambridge, MA: Riverside Press, Houghton Mifflin; 1957.
^ Jump up to: a b Butterworth RF. Thiamin. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern Nutrition in Health and Disease, 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006.
Jump up ^ Butterworth RF (1993). "Pathophysiologic mechanisms responsible for the reversible (thiamine-responsive) and irreversible (thiamine non-responsive) neurological symptoms of Wernicke's encephalopathy". Drug Alcohol Rev. 12 (3): 315–22. doi:10.1080/09595239300185371. PMID 16840290.
Jump up ^ Rindi G, Imarisio L, Patrini C (1986). "Effects of acute and chronic ethanol administration on regional thiamin pyrophosphokinase activity of the rat brain". Biochem Pharmacol. 35 (22): 3903–8. doi:10.1016/0006-2952(86)90002-X. PMID 3022743.
Jump up ^ Anand, I. S.; Florea, V. G. (2001). "High Output Cardiac Failure". Current Treatment Options in Cardiovascular Medicine. 3 (2): 151–159. doi:10.1007/s11936-001-0070-1. PMID 11242561.
^ Jump up to: a b c d e McIntyre, Neil; Stanley, Nigel N. (1971). "Cardiac Beriberi: Two Modes of Presentation". BMJ. 3 (5774): 567–9. doi:10.1136/bmj.3.5774.567. PMC 1798841  . PMID 5571454.
Jump up ^ Donnino M (2004). "Gastrointestinal Beriberi: A Previously Unrecognized Syndrome". Ann Intern Med. 141: 898–899. doi:10.7326/0003-4819-141-11-200412070-00035.
Jump up ^ Duca, J., Lum, C., & Lo, A. (2015). Elevated Lactate Secondary to Gastrointestinal Beriberi. J GEN INTERN MED Journal of General Internal Medicine
^ Jump up to: a b c d e f Latham, Michael C. (1997). "Chapter 16. Beriberi and thiamine deficiency". Human nutrition in the developing world (Food and Nutrition Series – No. 29). Rome: Food and Agriculture Organization of the United Nations (FAO). ISSN 1014-3181.
Jump up ^ Cernicchiaro, Luis (2007), Enfermedad de Wernicke (o Encefalopatía de Wernicke). Monitoring an acute and recovered case for twelve years. [Wernicke´s Disease (or Wernicke´s Encephalopathy)] (in Spanish)
Jump up ^ Salen, Philip N (1 March 2013). Kulkarni, Rick, ed. "Wernicke Encephalopathy". Medscape.
Jump up ^ Harper, CG; Giles, M; Finlay-Jones, R (April 1986). "Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy". J Neurol Neurosurg Psychiatry. 49 (4): 341–5. doi:10.1136/jnnp.49.4.341. PMC 1028756  . PMID 3701343.
Jump up ^ Harper, C (March 1979). "Wernicke's encephalopathy: a more common disease than realised. A neuropathological study of 51 cases". J Neurol Neurosurg Psychiatry. 42 (3): 226–31. doi:10.1136/jnnp.42.3.226. PMC 490724  . PMID 438830.
Jump up ^ Slater, PV (1978). "Thiamine Responsive Megaloblastic Anemia with severe diabetes mellitus and sensorineural deafness (TRMA)". The Australian nurses' journal. 7 (11): 40–3. PMID 249270.
Jump up ^ Kopriva, V; Bilkovic, R; Licko, T (Dec 1977). "Tumours of the small intestine (author's transl)". Ceskoslovenska gastroenterologie a vyziva. 31 (8): 549–53. ISSN 0009-0565. PMID 603941.
Jump up ^ Beissel, J (Dec 1977). "The role of right catheterization in valvular prosthesis surveillance (author's transl)". Annales de cardiologie et d'angéiologie. 26 (6): 587–9. ISSN 0003-3928. PMID 606152.
Jump up ^ Online Mendelian Inheritance in Man (OMIM) 249270
Jump up ^ Butterworth RF. Pyruvate dehydrogenase deficiency disorders. In: McCandless DW, ed. Cerebral Energy Metabolism and Metabolic Encephalopathy. Plenum Publishing Corp.; 1985.
Jump up ^ Biotin-Thiamine-Responsive Basal Ganglia Disease - GeneReviews® - NCBI Bookshelf
Jump up ^ Blass JP. Inborn errors of pyruvate metabolism. In: Stanbury JB, Wyngaarden JB, Frederckson DS et al., eds. Metabolic Basis of Inherited Disease. 5th ed. New York: McGraw-Hill, 1983.
Jump up ^ Sechi, G; Serra, A (May 2007). "Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management". Lancet Neurology. 6 (5): 442–55. doi:10.1016/S1474-4422(07)70104-7. PMID 17434099.
Jump up ^ Hirsch, JA; Parrott, J (2012). "New considerations on the neuromodulatory role of thiamine". Pharmacology. 89 (1–2): 111–6. doi:10.1159/000336339. PMID 22398704.
Jump up ^ Bettendorff L, Peeters M, Jouan C, Wins P, Schoffeniels E (1991). "Determination of thiamin and its phosphate esters in cultured neurons and astrocytes using an ion-pair reversed-phase high-performance liquid chromatographic method". Anal. Biochem. 198 (1): 52–59. doi:10.1016/0003-2697(91)90505-N. PMID 1789432.
Jump up ^ Losa R, Sierra MI, Fernández A, Blanco D, Buesa J (2005). "Determination of thiamine and its phosphorylated forms in human plasma, erythrocytes and urine by HPLC and fluorescence detection: a preliminary study on cancer patients". J Pharm Biomed Anal. 37 (5): 1025–1029. doi:10.1016/j.jpba.2004.08.038. PMID 15862682.
Jump up ^ Lu J, Frank E (May 2008). "Rapid HPLC measurement of thiamine and its phosphate esters in whole blood". Clin Chem. 54 (5): 901–906. doi:10.1373/clinchem.2007.099077. PMID 18356241.
Jump up ^ Shabangi M, Sutton J (2005). "Separation of thiamin and its phosphate esters by capillary zone electrophoresis and its application to the analysis of water-soluble vitamins". Journal of Pharmaceutical and Biomedical Analysis. 38 (1): 66–71. doi:10.1016/j.jpba.2004.11.061. PMID 15907621.
Jump up ^ Nguyen-Khoa, Dieu-Thu Beriberi (Thiamine Deficiency) Treatment & Management. Mescape
Jump up ^ Tanphaichitr V. Thiamin. In: Shils ME, Olsen JA, Shike M et al., editors. Modern Nutrition in Health and Disease. 9th ed. Baltimore: Lippincott Williams & Wilkins; 1999
Jump up ^ Maurice V, Adams RD, Collins GH. The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition. 2nd ed. Philadelphia: FA Davis, 1989.
Jump up ^ Chen KT, Twu SJ, Chiou ST, Pan WH, Chang HJ, Serdula MK (2003). "Outbreak of beriberi among illegal mainland Chinese immigrants at a detention center in Taiwan". Public Health Rep. 118: 59–64. doi:10.1093/phr/118.1.59. PMC 1497506  . PMID 12604765.
Jump up ^ Sprague, Jeb; Alexandra, Eunida (17 January 2007). "Haiti: Mysterious Prison Ailment Traced to U.S. Rice". Inter Press Service.
Jump up ^ Aké-Tano, O.; Konan, E. Y.; Tetchi, E. O.; Ekou, F. K.; Ekra, D.; Coulibaly, A.; Dagnan, N. S. (2011). "Le béribéri, maladie nutritionnelle récurrente en milieu carcéral en Côte-d'Ivoire". Bulletin de la Société de pathologie exotique. 104 (5): 347–351. doi:10.1007/s13149-011-0136-6.
Jump up ^ Prinzo, Z. Weise; de Benoist, B. (2009). "Meeting the challenges of micronutrient deficiencies in emergency-affected populations" (PDF). Proceedings of the Nutrition Society. 61 (2): 251–7. doi:10.1079/PNS2002151. PMID 12133207.
Jump up ^ Golden, Mike (May 1997). "Diagnosing Beriberi in Emergency Situations". Field Exchange (1): 18.
Jump up ^ http://www.pss.org.sg/whats-happening/e-bulletin/issue-no-30/lessons-sun-si-miao-chinese-patron-deity-physicians#.WWTQI2gxXMI
Jump up ^ http://www.shen-nong.com/eng/history/suitang.html
Jump up ^ http://www.itmonline.org/arts/sunsimiao.htm
Jump up ^ King Sun Simiao of the medicine twenty-nine Achivement
^ Jump up to: a b c Itokawa, Yoshinori (1976). "Kanehiro Takaki (1849–1920): A Biographical Sketch". Journal of Nutrition. 106 (5): 581–8. PMID 772183.
Jump up ^ Challem, Jack (1997). "The Past, Present and Future of Vitamins". Archived from the original on 8 June 2010. [unreliable medical source?]
Jump up ^ Christiaan Eijkman, Beriberi and Vitamin B1, Nobelprize.org, Nobel Media AB, retrieved 8 July 2013
Jump up ^ Grijns, G. (1901). "Over polyneuritis gallinarum". Geneeskundig Tijdschrift voor Nederlandsch-Indie. 43: 3–110.
Jump up ^ Oxford English Dictionary: "Beri-beri ... a Cingalese word, f. beri weakness, the reduplication being intensive ...", page 203, 1937
Jump up ^ A Sinhalese-English Dictionary, Rev. Charles Carter: "බැරි බැරි.රෝගය, a. the diseaseberi beri, a form of neuritis accompanied by dropsy &c ...", page 448, 1924
Jump up ^ Beriberi, Information about Beriberi. faqs.org
Jump up ^ "Beriberi". Online Etymology Dictionary. Retrieved 8 July 2013.
Jump up ^ Berg, Jeremy M; Tymoczko, John L; Stryer, Lubert (2002). "The Disruption of Pyruvate Metabolism Is the Cause of Beriberi and Poisoning by Mercury and Arsenic". Biochemistry (5th ed.). ISBN 978-0-7167-3051-4.
Jump up ^ Merck Veterinary Manual, ed 1967, pp 1440-1441.
Jump up ^ R.E. Austic and M.L. Scott, Nutritional deficiency diseases, in Diseases of poultry, ed. by M.S. Hofstad, Iowa State University Press, Ames, Iowa, USA ISBN 0-8138-0430-2, p. 50.
Jump up ^ The disease is described more carefully here: merckvetmanual.com
Jump up ^ National Research Council. 1996. Nutrient Requirements of Beef Cattle, Seventh Revised Ed. Washington, D.C.: National Academy Press.
Jump up ^ Polioencephalomalacia: Introduction, Merck Veterinary Manual
Jump up ^ Polioencephalomacia: Introduction, "ACES Publications"
Jump up ^ https://www.researchgate.net/publication/264981292_Update_on_Common_Nutritional_Disorders_of_Captive_Reptiles
^ Jump up to: a b Balk, L; Hägerroth, PA; Akerman, G; Hanson, M; Tjärnlund, U; Hansson, T; Hallgrimsson, GT; Zebühr, Y; Broman, D; Mörner, T.; Sundberg, H.; et al. (2009). "Wild birds of declining European species are dying from a thiamine deficiency syndrome". Proc Natl Acad Sci U S A. 106 (29): 12001–12006. doi:10.1073/pnas.0902903106. PMC 2715476  . PMID 19597145.
Jump up ^ Blekinge län, Länsstyrelsen (2013). "2012-04-15 500-1380-13 Förhöjd dödlighet hos fågel, lax og älg" (PDF).
External links[edit]
Classification
V · T · D
ICD-10: E51.1
ICD-9-CM: 265.0
MeSH: D001602
DiseasesDB: 14107
External resources
MedlinePlus: 000339
eMedicine: ped/229 med/221

Wikimedia Commons has media related to Beriberi.
[hide]
v
t
e
Malnutrition or nutrition disorders (E40–E68, 260–269)
Malnutrition
Protein-energy
malnutrition
Kwashiorkor
Marasmus
Catabolysis
Vitamin deficiency
B vitamins
B1: Beriberi / Wernicke–Korsakoff syndrome (Wernicke's encephalopathy
Korsakoff's syndrome)
B2: Riboflavin deficiency
B3: Pellagra (Niacin deficiency)
B6: Pyridoxine deficiency
B7: Biotin deficiency
B9: Folate deficiency
B12: Vitamin B12 deficiency
Other
vitamins
A: Vitamin A deficiency/Bitot's spots
C: Scurvy
D: Vitamin D deficiency/Rickets/Osteomalacia
E: Vitamin E deficiency
K: Vitamin K deficiency
Mineral
deficiency
Sodium
Potassium
Magnesium
Calcium
Iron
Zinc
Manganese
Copper
Iodine
Chromium
Molybdenum
Selenium (Keshan disease)
Overnutrition
Overweight
Obesity
Childhood obesity
Obesity hypoventilation syndrome
Abdominal obesity
Vitamin poisoning
Hypervitaminosis A
Hypervitaminosis D
Hypervitaminosis E
Mineral overload
see inborn errors of metal metabolism, toxicity
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