"Beri Beri" redirects here. For the African ethnic group, please see Kanuri people
Beriberi refers to a cluster of symptoms caused primarily by a nutritional deficit in Vitamin
B1. Beriberi has conventionally been divided into three separate entities, relating to
the body system mainly involved or age of patient. Beriberi is one of several thiamine-deficiency
related conditions which may occur concurrently, including Wernicke's encephalopathy, Korsakoff's
syndrome, and Wernicke-Korsakoff syndrome. Historically, Beriberi has been endemic in
regions dependent on what is variously referred to as polished, white, or de-husked rice.
This type of rice has its husk removed in order to extend its lifespan, but also has
the unintended side-effect of removing the primary source of thiamine.
Pathophysiology Thiamine in the human body has a half-life
of 18 days and is quickly exhausted, particularly when metabolic demands exceed intake. Thiamine
is involved in a variety of glucose metabolism-related and neurological functions. After modification
in the body to a diphosphate form, thiamine is involved in a vast array of functions:
Carbohydrate metabolism Production of the neurotransmitters glutamic
acid and GABA, through the citric acid cycle Lipid metabolism, necessary for myelin production
Amino acid metabolism Neuromodulation.
Neurons are very sensitive to ionic and metabolic changes produced in their immediate environment,
which initially affect metabolism, electrical activity and performance, but then can lead
to cell death. Signs and symptoms
Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception,
weakness and pain in the limbs, and periods of irregular heart rate. Edema 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 three historical
classifications: Dry beriberi specially affects peripheral
nervous system Wet beriberi specially affects the cardiovascular
system and other bodily systems Infantile beriberi affects also the children
of malnourished mothers. Dry beriberi
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 in hands and
feet Loss of tendon reflexes
Loss of muscle function or paralysis of the lower legs
Mental confusion/speech difficulties Pain
Involuntary eye movements 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.
Wet beriberi 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 Elevated jugular venous pressure
Dyspnea on exertion Paroxysmal nocturnal dyspnea
Peripheral oedema Infantile beriberi
Infantile beriberi usually occurs between two and six months of age in children whose
mothers have inadequate thiamine intake. In the acute form, the baby develops dyspnea
and cyanosis and soon dies of heart failure. The following symptoms may be described in
infantile beriberi: Hoarseness, where the child makes moves to
moan but emits no sound or just faint moans, caused by nerve paralysis
Weight loss, becoming thinner and then marasmic as the disease progresses
Vomiting Diarrhea
Occasionally convulsions were observed in the terminal stages
Pale skin Edema
Ill temper Alterations of the cardiovascular system,
especially tachycardia. Epidemiology
Inadequate nutrition Beriberi caused by inadequate nutritional
intake is rare today in developed countries because of quality of food and the fact that
many foods are fortified with vitamins. There are no reliable statistics for beriberi in
developed countries in the 19th century or earlier; neither are statistics available
before the last century in countries in extreme poverty.
Beriberi is a recurrent nutritional disease in detention houses even in this century.
High rates of illness and death in overcrowded Haitian jails was traced in 2007 to the traditional
practice of washing rice before cooking. 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, cardiovascular signs,
and oedemas of the lower limbs. The rate of healing was about 97%.
Populations under extreme stress may be at higher risk for beriberi. Displaced populations,
such as war refugees, are susceptible to micronutritional deficiency, including beriberi. The severe
nutritional deprivation caused by famine will also cause beriberi, although symptoms may
be overlooked in clinical assessment or masked by other famine-related problems. Extreme
dieting can also rarely induce a famine-like state and the accompanying beriberi.
Wernicke's encephalopathy Beriberi may also be caused by shortcomings
other than inadequate intake: diseases or operations on the digestive tract, alcoholism,
dialysis, genetic deficiencies, etc. All these causes mainly affecting the central nervous
system, and provoking 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. In autopsy series, features of Wernicke lesions
are observed in approximately 2% of general cases. 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. The rate of sufferers 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 persons can experience fetal damage and
subsequent diseases. History
Etymology The origin of the term 'beriber' comes from
a Sinhalese phrase meaning "weak, weak" or "I cannot, I cannot", the word being duplicated
for emphasis. In 1630, a Dutch physician named Jacobus Bontius
encountered the disease while working in Java. In the first known description of beriberi,
he wrote: "A certain very troublesome affliction, which attacks men, is called by the inhabitants
beriberi. 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." Identification
In the late 1800s, beriberi was studied by Takaki Kanehiro, a British-trained Japanese
medical doctor of the Japanese Navy. 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. 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 9 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 suffered
only 14 cases of beriberi and no deaths. This convinced Kanehiro and the Japanese Navy that
diet was the cause. In 1884, Kanehiro observed that beriberi was endemic among low-ranking
crew who often were provided nothing but rice, but not among crews of Western navies and
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 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. In 1901, Gerrit Grijns,
a Dutch physician and assistant to Christiaan Eijkman in the Netherlands, correctly interpreted
the disease as a deficiency syndrome, and between 1910 and 1913, Edward Bright Vedder
established that an extract of rice bran is a treatment for beriberi. Nonetheless, as
late as 1911, the Encyclopaedia Britannica Eleventh Edition described it as ""believed...to
be caused by an infective agent of a parasitic nature". In 1929, Eijkman and Hopkins were
awarded the Nobel Prize for Physiology or Medicine for their discoveries.
Treatment Many patients of beriberi can be treated with
thiamine alone, but many causes necessarily lead to multiple deficiencies of vitamins
and minerals such as hyperemesis gravidarum or gastric bypass.
Initially, is managed intravenously with thiamine. This supplementation should be earlier than
glucose supply that would cause the worsening of the disease. Supplementation can be monitored
using blood tests. Rapid and dramatic recovery can occur within hours of administration.
In situations where concentrated thiamine supplements are unavailable, feeding the patient
with a thiamine-rich diet will lead to recovery, though at a much slower rate.
See also Wernicke's encephalopathy
Wernicke-Korsakoff syndrome Korsakoff's syndrome
References
Bibliography Angstadt, John D.; Bodziner, Richard A.. "Peripheral
Polyneuropathy from Thiamine Deficiency following Laparoscopic Roux-en-Y Gastric Bypass". Obesity
Surgery 15: 890–2. doi:10.1381/0960892054222759. PMID 15978166.
Bay, Alexander R.. Beriberi in Japan: The Making of a National Disease. Rochester, New
York: University of Rochester Press. ISBN 9781580464277. Hawk, Alan. "The Great Disease Enemy, Kak'ke
and the Imperial Japanese Army". Military Medicine 171: 333–9. PMID 16673750.
Mouly, S.; Khuong, MA; Cabie, A; Saimot, AG; Coulad, JP. "Beri-Beri and thiamine deficiency
in HIV infection". AIDS 10: 931–2. doi:10.1097/00002030-199607000-00024. PMID 8828758.
Shivalkar, B; Engelmann, I; Carp, L; De Raedt, H; Daelemans, R. "Shoshin syndrome: Two case
reports representing opposite ends of the same disease spectrum". Acta cardiologica
53: 195–9. PMID 9842404. External links
www.wrongdiagnosis.com : beriberi Beriberi is a disease in which the body does
not have enough thiamine or vitamin B1. Beriberi is also a nutritional disorder and it is characterized
by impairment of the nerves and heart. There are two major types of this disease: Wet beriberi
and Dry beriberi. Wet Beriberi affects the cardiovascular system. Dry beriberi and WernickepKorsakoff
syndrome affect the nervous system. Beriberi disease is rare in the United States
because most of their food is enriched with vitamins. Beriberi is usually originated with
people who abuse alcohol, drinking heavily can to poor nutrition and the excess of alcohol
makes the body difficult to absorb thiamine. There is a genetic beriberi, which is a very
rare condition. This is inherited. People with a genetic beriberi tend to lose the ability
to absorb thiamine from foods. This can happen slowly over time and symptoms occur when the
person is in the adulthood. Beriberi disease can also occur in breast-fed infants. This
is because the mother’s body is lacking thiamine.
The symptoms for dry beriberi include: Difficulty walking
Loss of feeling in hands and feet Loss of muscle function or paralysis of the
lower legs Mental confusion/speech difficulties
Pain Strange eye movements
Tingling Vomiting
The symptoms for wet beriberi: Awakening at night short of breath
Increased heart rate Shortness of breath with activity
Swelling of the lower legs In order to treat this disease, there are
some exams and test: A physical examination may show the signs of congestive heart failure.
Congestive heart failure is a condition in which the heart is no longer to pump out enough
oxygen rich in blood. This physical examination includes:
Difficulty breathing with neck veins that stick out
Enlarged heart Fluid in the lungs
Rapid heartbeat Swelling in both lower legs
There is also neurological exam this shows the signs of: • Changes in the walk • Coordination
problems • Decreased reflexes • Drooping of the eyelids
As other typical test, blood tests and urine tests may have to be done. Blood tests are
for measuring the amount of thiamine in the blood. Urine tests are to see if thiamine
is passing through urine. There is treatment for beriberi disease. This
is to replace the thiamine your body is lacking. This is done with supplement of thiamine.
In order to give thiamine supplements, a shot/ injection, or it can be taken by mouth.
Beriberi is most common in: Far Eastern countries, where their daily diet is boiled white rice.
United States, consuming a lot of alcohol causes this. Basically beriberi is most common
in parts where people don’t consume foods with vitamins especially high in thiamine.
An example would be, uncooked fish.