Pathogenesis: All forms of beriberi are caused by a nutritional deficiency of thiamine. Thiamine is a critical vitamin that is needed for carbohydrate metabolism. Thiamine is the precursor for thiamine pyrophosphate (TPP). It is converted to TPP by the addition of one ATP molecule. TPP is needed as a cofactor for the proper function of many metabolic pathways. TPP helps transfer an aldehyde group from a donor to a beneficiary chemical structure. Three major energyproducing pathways are modulated by TPP: glycolysis, the Krebs cycle, and the pentose shunt (hexose monophosphate shunt). The hexose monophosphate shunt is important in producing other cofactors that play important biochemical roles for donation of hydrogen. The overall chemical state that occurs in patients with thiamine deficiency is a lack of ability to produce sufficient quantities of cellular ATP. This lack of the main source of energy for the cell results in the clinical findings. The nervous tissue and muscle tissue are particularly prone to damage from failure to produce sufficient ATP. It has been estimated that 3 to 6 weeks of a thiaminefree diet in an average human is sufficient to cause development of the initial signs and symptoms of beriberi.
Treatment: Therapy consists of supplementation of the patient’s diet with 50 mg/day intramuscularly of thiamine until the symptoms resolve. Treatment should also include other B-complex vitamins, because many patients who are deficient in one B vitamin also have low levels of the others. A nutritionist should be consulted to educate the patient on the need for a proper diet and how to achieve this. Alcoholics are prone to recurrence of beriberi and should be encouraged to participate in alcohol abstinence programs and to take a daily multivitamin supplement. The symptoms rapidly reverse on replacement of thiamine.
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