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Pyridoxine supplements may help patients with carpal tunnel syndrome

BMJ 1995; 310 doi: https://doi.org/10.1136/bmj.310.6993.1534b (Published 10 June 1995) Cite this as: BMJ 1995;310:1534
  1. Peter J Lewis
  1. Complementary physician Centre for the Study of Complementary Medicine, Southampton SO15 2DT

    EDITOR,—The standard treatment offered for the carpal tunnel syndrome is still a splint, a local injection of corticosteroid, or surgical decompression.1 Awareness of a simple and effective nutritional intervention—supplementation with pyridoxine (vitamin B-6)—remains low despite overwhelming evidence of its efficacy.

    Vitamin B-6 deficiency is a common finding in the carpal tunnel syndrome, and the total work up of patients with the syndrome “should include a nutritional evaluation and, in particular, a determination of B6 status.”2 Vitamin B-6 status can be determined by measurement of erythrocyte aspartate aminotransferase activity or plasma pyridoxal phosphate concentration. Several studies have shown that supplementation with pyridoxine (usually in doses of 50-200 mg a day) relieves the symptoms of the syndrome,3 and objective tests of median nerve conduction have shown that compression of the nerve is relieved.4 A therapeutic response may require supplementation for up to three months, with cure rates over this time in the order of 85%. Even Phalen, who originally described the carpal tunnel syndrome in 1952 and pioneered its surgical treatment, agrees that, in future, pyridoxine may be the treatment of choice.5

    Although supplementation with pyridoxine may occasionally cause a sensory neuropathy in doses as low as 200 mg daily over three years, this is usually a concern only in people taking 2000 mg or more. The neurotoxicity is believed to occur when the liver's capacity to phosphorylate pyridoxine to the active coenzyme pyridoxal phosphate is exceeded. The resulting high blood pyridoxine concentration could be directly neurotoxic or pyridoxine may compete for binding sites with pyridoxal phosphate, resulting in a relative deficiency of the active metabolite. Supplementation in the form of pyridoxal phosphate should therefore avoid this risk.

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