Thiamin deficiency effect

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. 

Straightforward thiamine deficiency in man, beri-beri, is characterized by accumulation of pyruvic and lactic acids in the blood and brain, and impairment of cardiovascular, nervous, and gastrointestinal function (DIO, G17, P4, Yl). Neurological lesions characterize thiamine deficiency in growing rats (B40), guinea pigs (M6), mice (M13), chicks, and pigeons (B30). The effects of thiamine deficiency on the central nervous system of animals have been reviewed (DIO). 

Til. Role of the Vitamin Thiamine People with beriberi, a disease caused by thiamine deficiency, have elevated levels of blood pyruvate and a-ketoglutarate, especially after consuming a meal rich in glucose. How are these effects related to a deficiency of thiamine ... 

Individuals on long-term diuretic therapy may also experience elevated levels of homocysteine, an amino acid regulated by folate. High homocysteine levels increase the risk of heart disease. Thiamin, or vitamin Bj, depletion is another possible side effect of loop diuretics. Individuals with thiamin deficiencies are at risk for fatigue, heart enlargement, muscle cramps, heart rate irregularities, and impaired mental function. 

Apart from children with thiamin-responsive maple symp urine disease (Section 6.3.1.4) and thiamin-responsive megaloblastic anemia (Section 6.2), there are no established pharmacological uses of thiamin other than the treatment of deficiency. Because of the neurological involvement in thiamin deficiency, the vitamin has been used in nerve tonics, although there is no evidence that it has any effect except in cases of deficiency. 

Butterworth RF (2006) Metabolic Encephalopathies. In Siegel GJ, Albers RW, Brady ST, Price DL (eds) Basic neurochemistry, 7th edn. Elsevier, London, pp 593-602 Butterworth RF, Besnard AM (1990) Thiamine-dependent enzyme changes in temporal cortex of patients with Alzheimer s disease. Metab Brain Dis 5(4) 179-184 Butterworth RF, GaudreauC, Vincelette J, Bouigault AM, LamotheF, Nutini AM (1991) Thiamine deficiency and Wernicke s encephalopathy in AIDS. Metab Brain Dis 6(4) 207-212 Butterworth RF, Heroux M (1989) Effect of pyrithiamine treatment and subsequent thiamine rehabilitation on regional cerebral amino acids and thiamine-dependent enzymes. J Neurochem 52(4) 1079-1084... 

Harata N, Iwasaki Y (1995) Evidence for early blood-brain btirrier breakdown in experimental thiamine deficiency in the mouse. Metab Brain Dis 10(2) 159-174 Harper CG (1983) The incidence of Wernicke s encephalopathy in Australia A neuropathological study of 131 cases. J Neurol Neurosurg Psychiatry 46 593-598 Harper CG, Butterworth RF (1997) Nutritional and metabolic disorders. In Graham DI, Lantos PL (eds) Greenfield s neuropathology. Arnold, London, pp 601-655 Hayton SM, Kriss T, Wase A, Muller DP (2006) Effects on neural function of repleting vitamin E-deflcient rats with alpha-tocopherol. J Neurophysiol 95(4) 2553-2559 Hayton SM, MuUer DP (2004) Vitamin E in neural and visual function. Ann N Y Acad Sd 1031 263-270... 

Langlais PJ, Anderson G, Guo SX, Bondy SC (1997) Increased cerebral free radical production during thiamine deficiency. Metab Brain Dis 12(2) 137-143 Langlais PJ, Mair RG (1990) Protective effects of the glutamate antagonist MK-801 on pyrithiamine-induced lesions and amino acid changes in rat brain. J Neurosd 10(5) 1664-1674... 

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. 

---