Thiamin Wernicke-Korsakoff syndrome

Keywords Vitamins Thiamine Wernicke-Korsakoff syndrome Pyridoxine Niacin Folic acid Antioxidants... 

Thiamin has a very low toxicity (oral LD5o of thiaminchloride hydrochloride in mice 3-15 g/kg body weight). The vitamin is used therapeutically to cure polyneuropathy, beri-beii (clinically manifest thiamin deficiency), and Wernicke-Korsakoff Syndrome ( Wernicke encephalopathy and Korsakoff psychosis). In mild polyneuropathy, 10-20 mg/d water-soluble or 5-10 mg/d lipid-soluble thiamin are given orally. In more severe cases, 20-50 mg/d water-soluble or 10-20 mg/d lipid-soluble thiamin are administered orally. Patients suffering from beri-beri or from early stages of Wernicke-Korsakoff Syndrome receive 50-100 mg of thiamin two times a day for several days subcutaneously or intravenously until symptoms are alleviated. Afterwards, the vitamin is administered orally for several weeks. 

B, Thiamin Coenzyme in pyruvate and a-ketoglutarate, dehydrogenases, and transketolase poorly defined function in nerve conduction Peripheral nerve damage (beriberi) or central nervous system lesions (Wernicke-Korsakoff syndrome)... 

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. 

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. 

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. 

Thiamine (vitamin B1 ) Essential vitamin required for synthesis of the coenzyme thiamine pyrophosphate Administered to patients suspected of having alcoholism (those exhibiting acute alcohol intoxication or alcohol withdrawal syndrome) to prevent Wernicke-Korsakoff syndrome Administered parenterally Toxicity None Interactions None... 

Wernicke-Korsakoff syndrome In the United States, thiamine defi-... 

Vitamin B1 (thiamine) has the active form, thiamine pyrophosphate. It is a cofactor of enzymes catalyzing the conversion of pyruvate to acetyl CoA, a-ketoglutarate to succinyl CoA, and the transketolase reactions in the pentose phosphate pathway. A deficiency of thiamine causes beriberi, with symptoms of tachycardia, vomiting, and convulsions. In Wernicke-Korsakoff syndrome (most common in alcoholics), individuals suffer from apa thy, loss of memory, and eye movements. There is no known toxicity for this vitamin. 

Wernicke-Korsakoff syndrome, stemming from thiamine deficiency and characterized by confusion, ataxia, and ocular abnormalities (nystagmus and lateral rectus muscle palsy). 

Studies in thiamin-deficient animals revealed the presence of Alzheimer-like amyloid plaques in the brain. Although there is no evidence of similar plaque formation in the brains of patients with the Wernicke-Korsakoff syndrome, this has led to trials of thiamin for treatment of Alzheimer s disease... 

Blass JP and Gibson GE (1977) Abnormality of a thiamine-requiring enzyme in patients with Wernicke-Korsakoff syndrome. New England Journal of Medicine 297, 1367-70. 

Ma JJ and Truswell AS (1995) Wernicke-Korsakoff syndrome in Sydney hospitals before and after thiamine enrichment of flour. Medical Journal of Australia 163, 531-4. 

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 Wernicke-Korsakoff syndrome, is also due to thiamin deficiency. It occurs in developed countries, especially among alcoholics and narcotic addicts. 

Thiamine is a nutritional supplement used during periods of deficiency known as beriberi and its manifestations such as Wernicke-Korsakoff syndrome. Thiamine needs increase during diseases of the small intestine, malabsorption, congenital metabolic dysfunction, liver disease, alcoholism, and during pregnancy and lactation. Supplementation of thiamine for treatment of Alzheimer s disease, congestive heart failure, and cataracts has been investigated however, evidence is unclear as to its benefits at this time. 

Rodriguez-Martin JL, Qizilbash N, and Lopez-Arrieta JM (2001) Thiamine for Alzheimer s disease. Cochrane Database of Systematic Reviews 2 CD001498. Thomson AD (2000) Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol Alcoholism 35(Suppl 1) 2-7. 

Vitamin B complex is the collective term for a number of water-soluble vitamins found particularly in dairy products, cereals and liver.Vitamin B (thiamine) is used by mouth for dietary supplement purposes and by injection in emergency treatment of Wernicke-Korsakoff syndrome. Vitamin B2 (riboflavin) is a constituent of the coenzyme FAD (flavine adenine dinucleotide) and FMN (flavine mononucleotide) and is therefore important in cellular respiration. Vitamin Be (pyridoxine) is a coenzyme for decarboxylases and transamination, and is concerned with many metabolic processes. Overdose causes peripheral neuropathy. It may be used medically for vomiting and radiation sickness and for premenstrual tension. Pyridoxine has a negative interaction with the therapeutic use of levodopa in parkinsonism by enhancing levodopa decarboxylation to dopamine in the periphery, which does not then reach the brain. The antitubercular drug isoniazid interferes with pyridoxine, and causes a deficiency leading to peripheral neuritis that may need to be corrected with dietary supplements. Vitamin B ... 

The patient is experiencing symptoms of the withdrawal syndrome from physical dependency on ethanol. Since seizures are possible, it would not be appropriate to attempt sedation with a phenothiazine such as chlorpromazine. Thiamine is usually administered to counteract the symptoms of Wernicke-Korsakoff syndrome but will not alleviate withdrawal symptoms. Neither buspirone nor naltrexone has value in the immediate management of alcohol withdrawal states. The patient is indeed suffering from delirium tremens. The answer is (B). 

Thiamine (B ), a vitamin, intravenously to a client diagnosed with Wernicke-Korsakoff syndrome. 

Wernicke Korsakoff syndrome (WKS) is the neurological disorder most clearly linked to thiamine deficiency in humans. WK develops in a subset of chronic alcoholics, who are vitamin deficient because so many calories are consumed as alcohol instead of normal diet, and a diet rich in carbohydrates increases the metabolic demand for thiamine. Thiamine dependent enzymes were diminished in the brains of patients who died with WKS, but not in alcoholic controls (Butterworth et al., 1993). Transketolase in fibroblasts from those patients who develop WKS syndrome binds TPP more avidly than the control lines. The Km was nearly ten times higher in patients with WKS. Thus, these patients have an abnormahty of transketolase that would be clinically unimportant if the diet was adequate (Blass and Gibson, 1977, 1979). The latter demonstrate a predisposing biochemical mutation to a neurological diseases that is only revealed by inadequate diet. 

Butterworth, R.F., Kril, J.J., and Harper, C.G. (1993). Thiamine-dependent enzyme changes in the brains of alcoholics relationship to the Wernicke-Korsakoff syndrome. Alcohol. Clin. Exp. Res. 17 1084-1088. 

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