Clinical deficiencies in vitamin B6 are rare. However, severe deficiency of vitamin B6 was reported in 1954 when infants were fed formula, which had been severely heated during manufacture. The heating caused the formation of pyridoxyllysine, which has anti-vitamin metabolic activity. The affected infants suffered seizures, which responded to B6 supplements (Coursin, 1954).
Other groups vulnerable to vitamin B6 deficiency and deficiency of other water-soluble vitamins, are those suffering from malabsorption, coeliac disease, chronic alcoholics and those undergoing dialysis for renal failure.
Clinical signs of deficiency are inflammation of the tongue, lesions of the lips and corners of the mouth; however, these symptoms are also seen in riboflavin deficiency. Peripheral neuropathy is found in thiamin as well as in pyridoxine deficiency. Finally, microcytic hypochromic (sideroblastic) anaemia associated with pyridoxine deficiency is caused by impaired synthesis of haem (Thurnham, 2000).
Evidence suggests that elevated homocysteine concentrations are a risk factor for cardiovascular disease. As several steps in the metabolism of homocysteine are vitamin B6-dependent, several workers have investigated the effects of vitamin
B6 nutrition on plasma homocysteine concentrations and its metabolites. However, fasting homocysteine concentrations are only weakly related to vitamin B6 status. It appears that reduced efficiency of the vitamin B6 dependent trans-sulphuration reactions are adequately countered by cellular remethylation capacity, and the steady state of plasma homocysteine is unaffected. That is, plasma homocysteine is much more strongly influenced by folate and vitamin B12 status than vitamin B6 status (Gregory, 2001).
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