Alcoholism thiamin deficiency

In chronic alcoholics, thiamine deficiency may manifest as Wernicke-Korsakoff syndrome, which Is characterized by a constellation of unusual neurologic disturbances. Including amnesia, apathy, and nystagmus. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Cessation of prolonged heavy alcohol abuse may be followed by alcohol withdrawal or life-threatening alcohol withdrawal delirium. Typical withdrawal symptoms are autonomic hyperactivity, increased hand tremor, insomnia and anxiety, and are treated with benzodizepines and thiamine. Alcoholism is the most common cause of thiamine deficiency and can lead in its extreme form to the Wernicke s syndrome that can be effectively treated by high doses of thiamine. 

Thiamin deficiency can result in three distinct syndromes a chronic peripheral neuritis, beriberi, which may or may not be associated with heart ilure and edema acute pernicious (fulminating) beriberi (shoshin beriberi), in which heart failure and metabolic abnormalities predominate, without peripheral neuritis and Wernicke s encephalopathy with KorsakofPs psychosis, which is associated especially with alcohol and dmg abuse. The central role of thiamin diphosphate in... 

Thiamine deficiency results in early decreases in activity of the mitochondrial enzyme a-ketoglutarate dehydrogenase in brain. Wernicke s encephalopathy, also known as the Wernicke-Korsakoff syndrome is a neuropsychiatric disorder characterized by ophthalmoplegia, ataxia and memory loss. Wernicke s encephalopathy is encountered in chronic alcoholism, in patients with HIV-AIDS and in other disorders associated with grossly impaired nutritional status. The condition results from thiamine deficiency. 

Neuropathy can result from deficiency of vitamins or hormones. Alcoholics often obtain a large proportion of their caloric needs from ethanol, and hence become thiamine-deficient. Alcoholic neuropathy results from a combination of thiamine deficiency, which impairs... 

Koike, H., Iijima, M., Sugiura, M. et al. Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Ann. Neurol. 54 19-29,2003. 

Thiamine deficiency is commonly seen in alcoholics, who may develop a complex of symptoms associated with Wernicke peripheral neuropathy and Korsakoff psychosis. Alcohol interferes with thiamine absorption from the intestine. Symptoms include ... 

Delirium tremens (the D.T.s ) resulting from alcohol withdrawal is slightly different in that it is usually preceded by the shakes, convulsions and occasionally by alcoholic hallucinosis - characterized by accusatory auditory hallucinations. As observed 60 years ago by Maurice Victor, an expert on alcohol problems, delirium tremens usually does not appear until day 3 or 4 following abrupt withdrawal from alcohol. The patient is generally malnourished and grossly deficient in vitamin Bj (thiamine) as the result of a diet consisting of little but alcohol. This deficiency ftirther compromises mental function. 

Nutritional Deficiency-Related Dementias. We have already mentioned that chronic alcoholics are subject to thiamine deficiency that can cause dementia. It usually occurs only after heavy, prolonged abuse of alcohol. In developed countries, the other key nutritional concern is vitamin deficiency. Vitamin deficiency can surprisingly strike even those with a healthy diet. Such people are missing a vital protein, intrinsic factor, which would enable them to absorb it from their digestive tract. 

Thiamine deficiency may also develop In alcoholics due to poor nutrition and poor absorption of thiamine In the gastrointestinal tract. 

Inadequate nutrition and conditions which are complicated by malabsorption may lead to thiamine deficiency. Beriberi, a diet-deficiency disease, is especially prevalent in those parts of the East where the diet consists mainly of polished rice. The disease is characterized by neuritis but may also lead to serious heart failure. Recovery is prompt when adequate amounts of vitamin B1 are restored to the diet. Severe deficiency as can occur in alcoholics may lead to Wernicke s encephalopathy, often accompanied by Korsakoff s syndrome. Care should be taken with intravenous substitution with thiamine in these cases to prevent serious complications like vascular collapse with hypotension, respiratory distress or an-gioedema. 

The spectrum of cognitive deficits associated with chronic alcohol use extends to the extreme of Wernicke s encephalopathy and Korsakoff s psychosis. Wernicke s encephalopathy is an acute neurologic syndrome caused by thiamine deficiency. Symptoms include mental confusion, ophthalmoplegia, and ataxia. Many of these symptoms reverse with administration of thiamine however about 50% of patients are left with some degree of ataxia. Left untreated, Wernicke s encephalopathy can progress to stupor, coma, and death. Approximately 80% to 90% of alcoholics treated for Wernicke s encephalopathy are left with Korsakoff s psychosis, a syndrome of impaired learning and recent memory produced by lesions of the medial dorsal nuclei of the thalamus. 

It is indicated in wet beriberi, dry beriberi, Wernicke s encephalopathy, prophylaxis of thiamine deficiency, hyperemesis gravidarum, Korsakoff s syndrome, chronic alcoholics, multiple neuritis, toxic and confusional states, delirium tremens and anorexia nervosa. 

Wernicke-Korsakoff syndrome is a relatively uncommon but important entity characterized by paralysis of the external eye muscles, ataxia, and a confused state that can progress to coma and death. It is associated with thiamin deficiency but is rarely seen in the absence of alcoholism. Because of the importance of thiamine in this pathologic condition and the absence of toxicity associated with thiamine administration, all patients suspected of having Wernicke-Korsakoff syndrome (including virtually all patients who present to the emergency department with altered consciousness, seizures, or both) should receive thiamine therapy. Often, the ocular signs, ataxia, and confusion improve promptly upon administration of thiamine. However, most patients are left with a chronic disabling memory disorder known as Korsakoff s psychosis. 

TAs one might predict, mutations in the genes for the subunits of the PDH complex, or a dietaiy thiamine deficiency, can have severe consequences. Thiamine-deficient animals are unable to oxidize pyruvate normally. This is of particular importance to the brain, which usually obtains all its energy from the aerobic oxidation of glucose in a pathway that necessarily includes the oxidation of pyruvate. Beriberi, a disease that results from thiamine deficiency, is characterized by loss of neural function. This disease occurs primarily in populations that rely on a diet consisting mainly of white (polished) rice, which lacks the hulls in which most of the thiamine of rice is found. People who habitually consume large amounts of alcohol can also develop thiamine deficiency, because much of their dietaiy intake consists of the vitamin-free empty calories of distilled spirits. An elevated level of pyruvate in the blood is often an indicator of defects in pyruvate oxidation due to one of these causes. ... 

In one form of thiamine deficiency, Wernicke s syndrome may be noted. Therein is paralysis, or weakness of the muscles that causes motion of the eyeball. Oosely associated with thiamine deficiency are dietary problems of alcoholism. The psychotic disturbances of alcoholism, including delirium tremens, frequently respond to thiamine and other B complex vitamins. Injections of thiamine often produce dramatic improvements in persons suffering from beriberi. Beriberi sometimes occurs in infants who are breast-fed by mothers who suffer a thiamine deficiency. Beriberi remains of concern in the Orient where polished rice is a dietary staple. 

Although now largely eradicated, beriberi remains a problem in some parts of the world among people whose diet is especially high in carbohydrates. A different condition, affecting the central rather than peripheral nervous system, the Wemicke-Korsakoff syndrome, is also due to thiamin deficiency. It occurs in developed countries, especially among alcoholics and narcotic addicts. 

Synthetic allithiamin derivatives, such as thiamin propyl and tetrahydro-furfuryl disulfides, have been used for the prevention and treatment of thiamin deficiency. Because they are lipid soluble, and are not subject to the normal control of thiamin absorption by saturation of the intestinal transport system, they have potential benefits in the treatment of thiamin-deficient alcoholics, whose absorption of thiamin is impaired. 

The absorption of thiamin is impaired in alcoholics, leading to thiamin deficiency (Section 6.4.4). In vitro, tissue preparations show normal uptake of the vitamin into the mucosal cells in the presence of ethanol, but impaired transport to the serosal compartment. The sodium-potassium-dependent ATPase of the basolateral membrane responsible for the active efQux of thiamin into the serosal fluid is inhibited by ethanol (Hoyumpa et al., 1977). 

Homewood J and Bond NW (1999) Thiamin deficiency and Korsakoff s syndrome failure to find memory impairments following nonalcoholic Wernicke s encephalopathy. Alcohol 19, 75-84. 

Vitamin Bj Vitamin Bj was discovered in 1926 by Jansen and Do-NATH, who synthesized it in its crystalline form from rice bran. It was initially called aneurine due to its antipolyneuropathic effect. Because it contains sulphur, Windaus correctly renamed it thiamine in 1932, a term by which it is still known today. The stixicture of this vitamin was described by Williams and Grewe in 1936. It is made up of pyrimidine and thiazole. Thiamine occurs in nature as free thiamine and in the form of thiamine monophosphate, diphosphate and triphosphate. A maximum amount of 8 — 15 mg is absorbed daily in the proximal portion of the small intestine. In the case of oversupply, thiamine is neither stored nor intestinally absorbed. A regular intake, with a daily requirement of about 1 mg, is necessary. The major coenzyme is thiamine pyrophosphate (TPP). Thiamine deficiency may be caused by malnutrition, impaired absorption, alcoholism, antithiamines or a lack of magnesium. Magnesium is an important cofactor for the coenzyme thiamine pyrophosphate. 

An alcohol-related thiamine deficiency, Wemicke-Korsakojf Syndrome, is caused by inadequate intake of thiamine as well as impaired absorption and storage, and is the common cause of dementia. 

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