Posttransplant diabetes mellitus in liver transplant recipients: Risk factors, temporal relationship with hepatitis C virus allograft hepatitis, and impact on mortality

Background. Recent studies suggest an association between diabetes mellitus and hepatitis C virus (HCV) infection. Our aim was to determine (1) the pr evalence and determinants of new onset posttransplant diabetes mellitus (PT DM) in HCV (+) liver transplant (OLT) recipients, (2) the temporal relation ship between recurrent allograft hepatitis and the onset of PTDM, and (3) t he effects of antiviral therapy on glycemic control. Methods. Between January of 1991 and December of 1998, of 185 OLTs performe d in 176 adult patients, 47 HCV (+) cases and 111 HCV (-) controls were ana lyzed. We reviewed and analyzed the demographics, etiology of liver failure , pretransplant alcohol abuse, prevalence of diabetes mellitus, and clinica l characteristics of both groups. In HCV (+) patients, the development of r ecurrent allograft hepatitis and its therapy were also studied in detail. Results. The prevalence of pretransplant diabetes was similar in the two gr oups, whereas the prevalence of PTDM was significantly higher in HCV (+) th an in HCV (-) patients (64% vs. 28%, P=0.0001). By multivariate analysis, H CV infection (hazard ratio 2.5, P=0.001) and methylprednisolone boluses (ha zard ratio 1.09 per bolus,, P=0.02) were found to be independent risk facto rs for the development of PTDM. Development of PTDM was found to be an inde pendent risk factor for mortality (hazard ratio 3.67, P <0.0001). The cumul ative mortality in HCV (+) PTDM (+) versus HCV (+) PTDM (-) patients was 56 % vs. 14% (P=0.001). In HCV (+) patients with PTDM, we could identify two g roups based on the temporal relationship between the allograft hepatitis an d the onset of PTDM: 13 patients developed PTDM either before or in the abs ence of hepatitis (group A), and 12 concurrently with the diagnosis of hepa titis (group B). In gr. B, 11 of 12 patients received antiviral therapy. No rmalization of liver function tests with improvement in viremia was achieve d in 4 of 11 patients, who also demonstrated a marked improvement in their glycemic control. Conclusion. We found a high prevalence of PTDM in HCV (+) recipients. PTDM after OLT was associated with significantly increased mortality. HCV infect ion and methylprednisolone boluses were found to be independent risk factor s for the development of PTDM. In approximately half of the HCV (+) patient s with PTDM, the onset of PTDM was related to the recurrence of allograft h epatitis. Improvement in glycemic control was achieved in the patients who responded to antiviral therapy.