A late episode of post-transplant diabetes mellitus during active hepatitis C infection in a renal allograft recipient using tacrolimus

J.P. van Hooff, E.M. van Duijnhoven*, J.M.M. Boots, V.J. Goossens, N. Undre, M.H. Christiaans

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

A late episode of post-transplant diabetes mellitus during active hepatitis C infection in a renal allograft recipient using tacrolimus.

van Duijnhoven EM, Christiaans MH, Boots JM, Goossens VJ, Undre NA, van Hooff JP.

Department of Internal Medicine, University Hospital Maastricht, Maastricht, The Netherlands. EVD@SINT.AZM.NL

BACKGROUND: An association between hepatitis C virus and (post-transplant) diabetes mellitus has been reported. METHODS: 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. RESULTS: 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. CONCLUSION: 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. Copyright 2002 by the National Kidney Foundation, Inc.
Original languageEnglish
Pages (from-to)195-201
Number of pages7
JournalAmerican Journal of Kidney Diseases
Volume40
Issue number1
DOIs
Publication statusPublished - 1 Jan 2002

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