| Beriberi | |
|---|---|
| Classification and external resources | |
![]() A sufferer – turn of the 20th century in southeast Asia |
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| ICD-10 | E51.1 |
| ICD-9 | 265.0 |
| DiseasesDB | 14107 |
| eMedicine | ped/229 med/221 |
| MeSH | D001602 |
Beriberi (pronounced /bɛriˈbɛri/) is a nervous system ailment caused by a deficiency of thiamine (vitamin B1) in the diet. Thiamine is involved in the breakdown of energy molecules such as glucose and is also found on the membranes of neurons. Symptoms of beriberi include severe lethargy and fatigue, together with complications affecting the cardiovascular, nervous, muscular, and gastrointestinal systems.
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The origin of the term is obscure. One hypothesis is that it comes from a Sinhalese phrase meaning "I cannot, I cannot", the word being doubled for emphasis.[1]
Beriberi is a disease in which the body does not have enough thiamine (vitamin B1).
There are two major types of beriberi:
Beriberi is rare in the United States because most foods are now vitamin-enriched. If you eat a normal, healthy diet you should get enough thiamine. Today, beriberi occurs mostly in patients who abuse alcohol. Drinking heavily can lead to poor nutrition, and excess alcohol makes it harder for the body to absorb and store thiamine.
A rare condition known as genetic beriberi is passed down through families. People with genetic beriberi lose the ability to absorb thiamine from foods. This can happen slowly over time and symptoms occur when the person is an adult. However, because doctors may not consider beriberi in non-alcoholics, this diagnosis is often missed.
Beriberi can occur in breast-fed infants when the mother's body is lacking in thiamine. The condition can also affect infants who are fed unusual formulas that don't have enough thiamine.
Getting dialysis and taking high doses of diuretics raise your risk of beriberi.
Symptoms of dry beriberi:
Symptoms of wet beriberi:
Exams and Tests
A physical examination may show signs of congestive heart failure, which include:
A neurological exam may show signs of:
Blood tests will measure the amount of thiamine in the blood while urine tests will determine if thiamine is passing through the urine.
Treatment
The goal of treatment is to replace the thiamine your body is lacking. This is done with thiamine supplements. Thiamine supplements are given through a shot (injection) or taken by mouth.
Other vitamins may also be recommended.
Subsequent blood tests will determine if the thiamine supplements are being effective.
Beriberi is caused by a lack of thiamine (vitamin B1). Thiamine occurs naturally in unrefined cereals and fresh foods, particularly whole grain bread, fresh meat, legumes, green vegetables, fruit, milk, etc. Beriberi is therefore common in people whose diet excludes these particular types of nutrition e.g. as a result of famine.
Beriberi may be found in people whose diet consists mainly of polished white rice, which is very low in thiamine because the thiamin-bearing husk has been removed. It can also be seen in chronic alcoholics with an inadequate diet (Wernicke-Korsakoff syndrome), as well as being a rare side effect of gastric bypass surgery. If a baby is mainly fed on the milk of a mother who suffers from thiamin deficiency, then that child may develop beriberi as well.
The disease was often found in Asian countries (especially in the 19th century and before), due to those countries' reliance on white rice as a staple food.
Its symptoms include weight loss, emotional disturbances, impaired sensory perception (Wernicke's encephalopathy), 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 heart failure and death.
Treatment for beriberi is with thiamine hydrochloride, either in tablet form or injection. A rapid and dramatic recovery within hours can be made when this is administered to patients, and their health can be improved within an hour of starting treatment. In emergency situations where concentrated thiamin supplements are unavailable, feeding the patient with a thiamin-rich diet (e.g. whole grain brown bread) will lead to recovery, though at a much slower rate.
In Asia, where polished white rice was the common staple food of the middle class, beriberi resulting from lack of vitamin B was endemic. In 1884, Takaki Kanehiro, a British-trained Japanese medical doctor of the Japanese Navy, observed that beriberi was endemic among low-ranking crew who often ate nothing but rice, but not among crews of Western navies and officers who consumed a Western-style diet. Kanehiro initially believed that lack of protein was the chief cause of beriberi. With the support of the Japanese Navy, he experimented using crews of two battleships; one crew was fed only white rice, while the other was fed a diet of meat, fish, barley, rice, and beans. The group that ate only white rice documented 161 crew with beriberi and 25 deaths, while the latter group had only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that diet was the cause of beriberi. This was confirmed in 1897, when Christiaan Eijkman discovered that feeding unpolished rice instead of the polished variety to chickens helped to prevent beriberi in the chickens. 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.[2][3]
In 1901, Gerrit Grijns (May 28, 1865 – November 11, 1944), Dutch physician and assistant to Christiaan Eijkman in Netherlands Indies, correctly interpreted the disease as a deficiency syndrome.[4] Indeed, it was later shown that beriberi results from the deficiency of thiamine (vitamin B1).
Dr Edward Bright Vedder established (1910–13) an extract of rice bran as a treatment for beriberi.
Eijkman, a Dutch physician and pathologist, demonstrated that beriberi is caused by poor diet. His work led to the discovery of vitamins. Eijkman and Hopkins were awarded the 1929 Nobel Prize for Physiology or Medicine for the discovery.
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