By A.L & Schwartz, Morton Latner
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Extra info for Advances in Clinical Chemistry Vol 23
By following several oral contraceptive users for 6 months after drug use was initiated, they were able to show that the greatest drop in plasma pyridoxal phosphate occurred in the first 3 months. Comparison of plasma pyridoxal phosphate using the standard tryptophan load test in 15 contraceptive users showed 11 users with raised urinary xanthurenic acid, but only four of these had reduced plasma coenzyme levels. In the same year, Davis and Smith (D9) reported on a study of 107women taking oral contraceptives for periods ranging from 1 month to 9 years (mean 36 months).
It would appear that the phosphorylated analog has binding affinities for apoenzymes similar to those of pyridoxal phosphate; hence, the degree of inhibition of vitamin B, enzyme-dependent reactions will vary with the degree of disassociation of the apoenzyme and coenzyme. This explains the complex, altered metabolism of the tryptophan-to-niacin pathway which Wolf (Wl) described. In addition, 4-deoxypyridoxine probably also inhibits the activity of pyridoxal kinase, thus reducing the production of pyridoxal phosphate (M15).
McKenzie et al. (M16) reported the case of a neonate, the child of a mother being treated for tuberculosis, who was commenced on 20 mg of isonicotinic acid hydrazide twice daily at birth, without supplemental pyridoxine. Multifocal clonic convulsions started on the thirteenth day and continued until pyridoxine therapy was commenced 4 days later. Previously, Morales and Lincoln (M17) had reported that 20 children on isonicotinic acid hydrazide showed no signs of deficiency when the dose was less than 10 mg/kg body weight daily.