Effect of Pyridoxine on Vitamin B6 Concentrations and Glutamic-Oxaloacetic Transaminase Activity in Whole Blood of Tuberculous Patients Receiving High-Dosage Isoniazid

Krishnamurthy, D V and Selkon, J B and Ramachandran, K and Devadatta, S and Mitchison, D A and Radhakrishna, S and Stott, H (1967) Effect of Pyridoxine on Vitamin B6 Concentrations and Glutamic-Oxaloacetic Transaminase Activity in Whole Blood of Tuberculous Patients Receiving High-Dosage Isoniazid. Bulletin of the World Health Organization, 36 (5). pp. 853-870. ISSN 00429686

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Abstract

An earlier report from the Tuberculosis Chemotherapy Centre, Madras, showed that, in tuberculous patients receiving high-dosage isoniazid (12.5-15.6 mg/kg body-weight), the concomitant administration of 6 mg of pyridoxine prevented peripheral neuropathy. In that study, biochemical determinations of B6 concentrations and GOT activity in whole blood had been routinely undertaken on all patients on admission to treatment, and at 6, 12, 24 and 52 weeks thereafter; in addition, extra determinations were undertaken for patients who developed peripheral neuropathy. The present paper reports the findings of these investigations, which are: (a) peripheral neuropathy developed predominantly among slow inactivators of isoniazid, and was associated with a substantial reduction in GOT activity but no apparent change in B6 concentration; (b) the reduction in GOT activity appeared to be due to deficiency of both the coenzyme (pyridoxal phosphate) and the apoenzyme; (c) the concomitant administration of pyridoxine (6 mg or 48 mg) with high-dosage isoniazid to 3 patients with peripheral neuropathy, 1 of whom had convulsions also, resulted in increased B6 concentrations and GOT activity, and no further convulsions; and(d) the concomitant administration of pyridoxine 6 mg daily, as a prophylactic, resulted in a significant increase in B6 concentrations and GOT activity and prevention of the neuropathy. These findings establish the existence of a definite association between the occurrence of isoniazid-induced toxicity and diminished pyridoxine function.

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