Vitamin B6 Deficiency
Vitamin B6 (pyridoxine) is necessary for tryptophan, 5-HIAA, alanine, nicotinic acid, and ALA synthetase synthesis. It is also used in mitochondrial iron reactions for energy production.
Deficiency results in anemia, peripheral neuropathy and hepatosplenomegaly.
The vitamin B6 antagonist deoxypyridoxine produces seborrheic dermatosis, glossitis, cheilosis, peripheral neuropathy, and lymphopenia. Vitamin B6 deficiency can cause convulsions in infants and anemia in adults (usually normocytic but occasionally microcytic).
B6 deficiency can be genetic - X-linked.
Drugs like INH induce deficiency by binding to B6.
Primary deficiency is rare, because most foods contain vitamin B6. An outbreak of convulsions in infants did follow the inadvertent destruction of vitamin B6 in infant formulas.
Secondary deficiency may result from malabsorption, alcoholism, oral contraceptive use, chemical inactivation by drugs (eg, isonicotinic acid hydrazide, cycloserine, hydralazine, penicillamine), excessive loss, and increased metabolic activity.
At present, there is no generally accepted test of vitamin B6 status.
The whole blood level of pyridoxal phosphate is a better indicator than the plasma level. Erythrocyte glutamic pyruvate and oxaloacetic transaminase activities are decreased in vitamin B6 deficiency, but these changes are not diagnostic because of the wide range of values in healthy persons.
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