PubMed HealthSearch

Biomedical subjects

M Kaji

Publications and source records attributed to M Kaji.

5 recordsLinked to original sources

Clinical results of a cross-over treatment with pyridoxine and placebo of the carpal tunnel syndrome.

Clinical evaluation was made of cross-over treatments by pyridoxine and a placebo of patient 22 having the carpal tunnel syndrome. Extraordinary monitoring of the specific activities of the erythrocyte glutamic oxaloacetic transaminase proved a severe vitamin B6 deficiency, which was partially corrected by the Recommended Dietary Allowance of 2 mg, and completely corrected by 100 mg. The severity of the syndrome diminished on the Recommended Dietary Allowances and the patient was asymptomatic at the higher dosage. On placebo, both the vitamin B6 deficiency and syndrome reappeared. Retreatment with 100 mg again corrected both the deficiency and syndrome. Measurements (total n = 19) of flexion of proximal interphalangeal joints of the index fingers by a goniometer, and of pinch by the Preston gauge revealed objective normalization. Scores of 17 symptoms revealed reductions at both the 2- (P less than 0.01) and 100-mg (P less than 0.001) dosages. Conduction through the carpal tunnels had improved by electromyography. These and previous data on a total of 22 patients showed the concomitant presence of a deficiency of vitamin B6 and the carpal tunnel syndrome; a causal relationship is apparent.

Adult

Biochemical evidence for a deficiency of vitamin B6 in the carpal tunnel syndrome based on a crossover clinical study.

In a patient with severe carpal tunnel syndrome and a significant deficiency of vitamin B(6), the evidence for the deficiency was an extraordinarily low basal specific activity of the glutamic-oxaloacetic transminase of the erythrocytes (EGOT). This enzyme was also deficient in pyridoxal phosphate. The patient was treated with the recommended dietary allowance of pyridoxine, 2 mg/day, for 11 weeks, then 100 mg/day for 12 weeks, a placebo for 9 weeks, and again pyridoxine at 100 mg/day for 11 weeks. Sixty-one monitorial assays of EGOT over 48 weeks supported the following interpretations. (i) His diet permitted the development of a debilitating carpal tunnel syndrome. (ii) Treatment with pyridoxine at 2 mg/day reduced the deficiency of EGOT activity from about 70% to 50%, maintained a deficiency of pyridoxal phosphate, and relieved but allowed a marginal syndrome. (iii) Treatment at 100 mg/day for 12 weeks nearly achieved a "ceiling" level of EGOT and eliminated the deficiency of pyridoxal phosphate. (iv) After placebo for 7 weeks, the deficiencies of EGOT activity and pyridoxal phosphate reappeared, and clinical symptoms become worse. (v) Retreatment at 100 mg/day reestablished a "ceiling" EGOT, with no deficiency of pyridoxal phosphate, and the patient was asymptomatic. These data also support the concept that a deficiency of vitamin B(6) is significant in the etiology of the carpal tunnel syndrome. Mechanistically, a state of deficiency of the coenzyme seems to lower the level of the apoenzyme; a state of no deficiency of the coenzyme regulates a ceiling level of the transaminase. The latter state is presumably desired for health.

Apoenzymes