Vitamin B₆ - Deficiencies

Deficiencies

The classic clinical syndrome for B₆ deficiency is a seborrhoeic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy.

While severe vitamin B₆ deficiency results in dermatologic and neurologic changes, less severe cases present with metabolic lesions associated with insufficient activities of the coenzyme pyridoxal phosphate. The most prominent of the lesions is due to impaired tryptophan-niacin conversion. This can be detected based on urinary excretion of xanthurenic acid after an oral tryptophan load. Vitamin B₆ deficiency can also result in impaired transsulfuration of methionine to cysteine. The pyridoxal phosphate-dependent transaminases and glycogen phosphorylase provide the vitamin with its role in gluconeogenesis, so deprivation of vitamin B₆ results in impaired glucose tolerance.

A deficiency of vitamin B₆ alone is relatively uncommon and often occurs in association with other vitamins of the B complex. The elderly and alcoholics have an increased risk of vitamin B₆ deficiency, as well as other micronutrient deficiencies. Renal patients undergoing dialysis may experience vitamin B₆ deficiency. Also, patients with liver disease, rheumatoid arthritis, women with type 1 diabetes, and those infected with HIV also appear to be at risk, despite adequate dietary intakes. The availability of vitamin B₆ to the body can be affected by certain drugs such as anticonvulsants and corticosteroids. The drug isoniazid (used in the treatment of tuberculosis), and cycloserine, penicillamine, and hydrocortisone all interfere with vitamin B₆ metabolism. These drugs may form a complex with vitamin B₆ that is inhibitory for pyridoxal kinase, or they may positively displace PLP from binding sites.