In a patient with severe carpal tunnel syndrome and a significant deficiency of vitamin B6, the evidence for the deficiency was an extraordinarily low basal specific activity of the glutamic-oxaloacetic transaminase 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 followin nterpretations. (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 a so support the concept that a deficiency of vitamin B6 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.An exceptional study has been made of our 22nd patient who had a severe carpal tunnel syndrome. This study was cooperative and effectively combined both the biochemical and the clinical aspects. We describe herein the biochemical aspects which constitute evidence for an association of a deficiency of vitamin B6 with the carpal tunnel syndrome as based on a crossover clinical study. The companion and detailed clinical aspects will be described elsewhere.Ellis et al.(1) cooperatively found a deficiency of vitamin B6, as pyridoxal phosphate, in a group of 10 patients who had a clinical status associated with the carpal tunnel syndrome. These patients showed a significant (P < 0.001) deficiency of vitamin B6, as determined by the basal specific activities of the glutamic-oxaloacetic transaminase (L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1) of the erythrocytes (EGOT) in comparison with those of a control group. The detection and quantitation of the deficiency of pyridoxal phosphate was based upon the principle of unsaturation and saturation of a coenzyme-apoenzyme system-for example, EGOT. These 10 patients were treated with pyridoxine. Disappearance of the deficiency of pyridoxal phosphate was observed and, notably, the level of EGOT activity increased by 55-68% during 2-4 weeks, respectively. Apparently, more apoenzyme had been biosynthesized, because the specific acti...
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