vitamin B6
A primary, clinically overt deficiency of vitamin B6 is rare in humans, but subclinical conditioned deficiency states, paradoxically, are thought to be common. Three naturally occurring substances-pyridoxine, pyridoxal, and pyridoxamine-together with the phosphate forms of each possess vitamin B6 activity and are generically referred to as pyridoxine.
All are equally active metabolically, and all are converted in the tissues to the coenzyme form, pyridoxal 5-phosphate. This coenzyme participates as a cofactor for a large number of enzymes involved in transaminations, carboxylations, and deaminations in the metabolism of lipids and amino acids.
Vitamin B6 is present in virtually all foods; however, food processing may destroy pyridoxine and in the past was responsible for severe deficiency in infants fed poorly controlled dried milk preparations. Secondary hypovitaminosis B6 is produced most often by long-term use of any of a variety of drugs that act as pyridoxine antagonists. These include isoniazid (used to treat tuberculosis), estrogens, and penicillamine.
Pathology
Alcoholics are also prone to develop vitamin B6 deficiency because acetaldehyde, an alcohol metabolite, enhances pyridoxine degradation. Pregnancy is associated with increased demand. Thus, pyridoxine supplementation is required in these conditions.
A deficiency of vitamin B6 is associated with high levels of plasma homocysteine. The latter is a risk factor for atherosclerosis, but currently there is no evidence that vitamin B6 supplements reduce the risk of cardiovascular disease.
Clinical findings in vitamin B6-deficient patients resemble those seen in patients with riboflavin and niacin deficiency. Patients may have seborrheic dermatitis, cheilosis, glossitis, peripheral neuropathy, and sometimes convulsions.