Ellis J M, Folkers K, Levy M, Shizukuishi S, Lewandowski J, Nishii S, Schubert H A, Ulrich R
Proc Natl Acad Sci U S A. 1982 Dec;79(23):7494-8. doi: 10.1073/pnas.79.23.7494.
The specific activities and percentage deficiencies of the glutamic oxaloacetic transaminase of erythrocytes (EGOT) were determined for patients with carpal tunnel syndrome (CTS) diagnosed by clinical examination and electrical conduction data; the EGOT data revealed a severe deficiency of vitamin B-6. After double-blind treatment with pyridoxine and placebo, two physicians identified those receiving pyridoxine (clinically improved) and those receiving placebo (did not improve) without error, P less than 0.0078. Correcting a deficiency of the coenzyme at receptors of existing molecules of the apoenzyme appears to take place within days; correction of the deficiency in the number of molecules of the transaminase takes place over 10-12 weeks. The clinical response, appraised by the diminution of the symptoms of CTS, was correlated only with the restored levels of the transaminase which presumably results from a translational long-term increase in the number of molecules of EGOT by a mechanism activated by correcting a deficiency of pyridoxal 5'-phosphate. Apparent Km values of EGOT were identical for groups of patients with CTS and others without CTS but with identical specific activities, indicating that CTS is a primary deficiency of vitamin B-6 rather than one of a dependency state. Clinical improvement of the syndrome with pyridoxine therapy may frequently obviate hand surgery.
通过临床检查和电传导数据确诊为腕管综合征（CTS）的患者，测定了其红细胞谷草转氨酶（EGOT）的比活性和百分缺陷率；EGOT数据显示维生素B-6严重缺乏。在使用吡哆醇和安慰剂进行双盲治疗后，两位医生准确无误地识别出接受吡哆醇治疗（临床症状改善）和接受安慰剂治疗（症状未改善）的患者，P值小于0.0078。在现有脱辅酶分子的受体处纠正辅酶缺乏似乎在数天内即可发生；转氨酶分子数量的缺乏纠正则需要10至12周。通过CTS症状减轻来评估的临床反应，仅与转氨酶水平的恢复相关，这可能是由于通过纠正磷酸吡哆醛缺乏而激活的机制使EGOT分子数量长期翻译性增加所致。CTS患者组和其他无CTS但比活性相同的患者组的EGOT表观Km值相同，表明CTS是维生素B-6的原发性缺乏而非依赖性状态之一。吡哆醇治疗该综合征的临床改善可能常常可避免手部手术。
