Schmidt P, Zazgornik J, Kopsa H, Balcke P, Pils P, Bayer P M
Wien Klin Wochenschr. 1977 Dec 23;89(24):819-21.
Regular 4-weekly follow-up controls of serum lactate dehydrogenase activity in 23 renal transplant recipients revealed a constant rise in serum LDH activity during the early postoperative months. During the first post-transplant month serum LDH activity increased from 150.0 +/- 48.2 mE/ml to 195.5 +/- 84.8 mE/ml, serum enzyme activity being highest (329.1 +/- 143.2 mE/ml) 6 months after surgery. Since serum creatinine levels remained relatively constant, it seems unlikely that renal rejection played a major pathogenic role in the production of increased LDH activity. Since the pattern of lactate dehydrogenase isoenzymes was ithin normal limits, the pathogenesis of increased LDH serum activity following renal transplantation is not yet clear. Possible causes such as liver damage due to hepatitis B, macrocytosis induced by immunosuppressive therapy and myopathy to steroids are discussed.
对23名肾移植受者进行定期的每4周一次的血清乳酸脱氢酶活性随访监测，结果显示术后早期血清乳酸脱氢酶活性持续升高。移植后的第一个月，血清乳酸脱氢酶活性从150.0±48.2 mE/ml升至195.5±84.8 mE/ml，术后6个月时血清酶活性最高（329.1±143.2 mE/ml）。由于血清肌酐水平保持相对稳定，肾排斥反应似乎不太可能在乳酸脱氢酶活性升高的产生中起主要致病作用。由于乳酸脱氢酶同工酶模式在正常范围内，肾移植后血清乳酸脱氢酶活性升高的发病机制尚不清楚。文中讨论了可能的原因，如乙型肝炎导致的肝损伤、免疫抑制治疗引起的大细胞性贫血以及对类固醇的肌病反应。
