VITAMIN-B6 DEFICIENCY IN PATIENTS WITH A CLINICAL SYNDROME INCLUDING CARPAL-TUNNEL DEFECT - BIOCHEMICAL AND CLINICAL RESPONSE TO THERAPY WITH PYRIDOXINE

  • 1 January 1976
    • journal article
    • research article
    • Vol. 13  (4) , 743-757
Abstract
Ten individuals having a severe clinical status associated with the carpal tunnel syndrome were selected for treatment with pyridoxine. The status of vitamin B6, as pyridoxal phosphate, was determined by the specific activities of the glutamic oxaloacetic transaminase of the erythrocytes (EGOT). Before treatment the patients showed a deficiency of vitamin B6 as determined by a comparison of the specific activities of EGOT with those of a control group (P < 0.001) and a differential assay based upon the principle of unsaturation and saturation of a Coenzyme-Apoenzyme System (CAS), as applied to EGOT. These patients were treated with pyridoxine, and the specific activities of EGOT were determined after 2 and 4 wk. Not only was there a disappearance of the deficiency of pyridoxal phosphate, but the level of EGOT activity increased 55-68% during 2-4 wk, respectively. More apoenzyme was apparently biosynthesized, because the specific activities were significantly higher than before therapy (P < 0.0001/4 wk). Clinical evaluation showed a great improvement in their status, and anticipated surgery for some of the patients became unnecessary. Patients with a severe syndrome including the carpal tunnel defect probably have a deficiency of vitamin B6, and both the syndrome and the deficiency are relieved by therapy with pyridoxine.

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