Malnutrition thiamin deficiency

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. 

A thorough nutrition-focused history and physical examination is the most valuable means of screening patients for vitamin deficiency or toxicity (Table 135-9). It is uncommon to see a single vitamin deficiency usually multiple vitamin deficiencies occur with general malnutrition. Single vitamin deficiencies do occur, however. Thiamine deficiency may result in lactic acidosis and encephalopathy, whereas pernicious anemia due to vitamin B12 deficiency has been reported with increasing frequency, especially in the elderly. Recently, the incidence of vitamin D deficiency has increased in children. Laboratory assessment may be useful to confirm the clinical suspicion of a deficiency state. The first indication of a deficiency is usually a fall in circulating serum concentrations of the vitamin or its coenzyme. 

In Western societies, gross thiamine deficiency is most often associated with alcoholism. The mechanism for active absorption of thiamine is strongly and directly inhibited by alcohol. Subclinical deficiency of thiamine from malnutrition or anorexia may be common in the general population and is usually associated with multiple vitamin deficiencies. 

Malnutrition is a serious complication of chronic alcoholism, especially thiamine deficiency, which can result in neurological impairments therefore, thiamine must be administered intravenously. This is not the first intervention. 

Wernicke s encephalopathy is most commonly associated with alcoholism. It has been suggested that there may be a synergistic effect of alcoholism and thiamine deficiency, where a brain affected by alcoholism may be more susceptible to injury caused by thiamine deficiency (Homewood and Bond, 1999). However, WE may be found in any clinical state associated with malnutrition or thiamine deficiency... 

Water-soluble vitamins removed by hemodialysis (HD) contribute to malnutrition and vitamin deficiency syndromes. Patients receiving HD often require replacement of water-soluble vitamins to prevent adverse effects. The vitamins that may require replacement are ascorbic acid, thiamine, biotin, folic acid, riboflavin, and pyridoxine. Patients receiving HD should receive a multivitamin B complex with vitamin C supplement, but should not take supplements that include fat-soluble vitamins, such as vitamins A, E, or K, which can accumulate in patients with renal failure. 

Neal RA. Vitamin deficiencies Thiamin. Hansen RG and Munro HN. 129. 1970. Nashville, GSMHA and National Institute of Health. Proc. Workshop on Problems of Assessment and Alleviation of Malnutrition in the US. 

Alcohol provides calories but does not provide vitamins. This is one of the leading causes of malnutrition. Metabolizing alcohol involves an enzyme (alcohol dehydrogenase) with thiamine pyrophosphate (TPP) as a cofactor. The cofactor, in turn, is a metabolite of vitamin Bj, leading to severe deficiencies. 

Deficiencies of various nutrients, primarily vitamins, impair cognition. The link is strongest for vitamin Bj2, thiamine, and niacin. Yet even for these, the role of mild subclinical or multiple deficiencies in the genesis of mental dysfunction is unclear. Most information in this field is based on animal studies often poorly applicable to the human condition or on clinical pathology complicated by advanced age, alcoholism, and intercurrent disease. There is a need for well controlled, double-blind, prospective trials to elucidate the cognitive effects of malnutrition. 

The vitamin B complex contains a number of factors which are closely associated in their distribution in nature and have related functions in intermediate metabolism. Of the eleven factors which are available in pure form, five have been shown to be constituents of coenzymes, namely, thiamine, riboflavin, niacinamide, pyridoxine, and pantothenic acid. It seems likely that other B vitamins may be found to function in a similar manner. Two members of the B complex, choline and inositol, appear to have lipotropic activity, and two others, folic acid and vitamin B12, have antianemic properties. Deficiency of vitamins of the B complex is one of the most frequently encountered syndromes of malnutrition in man. 

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