van Duijnhoven Elly M, Christiaans Maarten H L, Boots Johannes M M, Goossens Valère J, Undre Nasrullah A, van Hooff Johannes P
Department of Internal Medicine, University Hospital Maastricht, Maastricht, The Netherlands.
Am J Kidney Dis. 2002 Jul;40(1):195-201. doi: 10.1053/ajkd.2002.33930.
An association between hepatitis C virus and (post-transplant) diabetes mellitus has been reported.
We report a patient on tacrolimus-based immunosuppression who developed an episode of post-transplant diabetes mellitus (PTDM) 2 years after renal transplantation, after contracting a hepatitis C infection. Her glucose metabolism was evaluated regularly by intravenous glucose tolerance tests before and after the PTDM episode.
Before contracting hepatitis C, the patient's insulin resistance and insulin secretion were normal. After contracting hepatitis C, tacrolimus exposure increased, insulin resistance increased, and insulin secretion decreased markedly. Despite low tacrolimus exposure in the last 4 years, glucose metabolism did not recover completely. Although PTDM resolved and insulin resistance normalized, pancreatic beta cell secretion remained impaired by approximately 50% compared with the period before hepatitis C infection.
After an initial increase in insulin resistance, insulin secretion decreased markedly in a patient who contracted hepatitis C 12 to 22 months after renal transplantation. This change resulted in an episode of PTDM. Increased tacrolimus exposure secondary to reduced cytochrome P-450 metabolism as a result of impaired hepatocellular function at the time of the development of PTDM seems a likely explanation for the marked decrease in insulin secretion. Viral toxicity to the beta cell might be an additional explanation. The latter might be suspected from several reports about an association between diabetes mellitus and hepatitis C in patients who do not use drugs that interfere with glucose metabolism.
已有报告称丙型肝炎病毒与（移植后）糖尿病之间存在关联。
我们报告了一名接受基于他克莫司的免疫抑制治疗的患者，该患者在肾移植2年后感染丙型肝炎后发生了移植后糖尿病（PTDM）发作。在PTDM发作前后，通过静脉葡萄糖耐量试验定期评估她的糖代谢情况。
感染丙型肝炎之前，患者的胰岛素抵抗和胰岛素分泌正常。感染丙型肝炎后，他克莫司暴露增加，胰岛素抵抗增加，胰岛素分泌明显减少。尽管在过去4年中他克莫司暴露量较低，但糖代谢并未完全恢复。虽然PTDM得到缓解且胰岛素抵抗恢复正常，但与丙型肝炎感染前相比，胰腺β细胞分泌仍受损约50%。
在肾移植后12至22个月感染丙型肝炎的患者中，胰岛素抵抗最初增加后，胰岛素分泌明显减少。这种变化导致了PTDM发作。PTDM发生时，由于肝细胞功能受损导致细胞色素P - 450代谢减少，从而使他克莫司暴露增加，这似乎是胰岛素分泌明显减少的一个可能解释。病毒对β细胞的毒性可能是另一种解释。从一些关于未使用干扰糖代谢药物的患者中糖尿病与丙型肝炎之间关联的报告中可能会怀疑到后者。
