Do anti-CD25 monoclonal antibodies potentiate posttransplant diabetes mellitus?

Abstract

Anti-CD25 monoclonal antibodies (MAbs) are directed against the IL-2 (CD-25) receptor, which is associated with the pathogenesis of diabetes mellitus (DM). Measuring CD25 on peripheral blood lymphocytes could be a new immunologic marker to identify patients with prediabetes.

Objective: The study aimed to analyze whether administration of anti-CD25 MAbs was an independent risk factor for posttransplant diabetes mellitus (PTDM) in kidney transplant (KT) patients at 3 months after transplantation.

Patients and methods: Seventy-four stable, nondiabetic KT patients were included in the study. The overall sex distribution was 70% men and mean overall age, 52 +/- 10 years. Thirty-eight subjects where treated with anti-CD25 antibodies (basiliximab). The diagnosis of PTDM was made if patients required insulin or oral antidiabetic drugs and/or had glycemia >200 mg/dL at 120 minutes after an oral glucose tolerance test (75 g glucose). We determined the age, weight, body mass index, acute rejection, chronic hepatitis C virus (HCV) infection, and type of calcineurin inhibitor.

Results: Thirty-four percent of patients developed PTDM. Patients treated with anti-CD25 antibodies were older (P = .022) and showed a greater incidence of PTDM (P = .041). The logistic regression analysis (dependent variable: PTDM; independent variables: age, anti-CD25, tacrolimus vs cyclosporine) showed that treatment with anti-CD25 is an independent risk factor for PTDM (P = .041; OR 3.28; CI 95% 1.04-10.31).

Conclusion: Patients treated with anti-CD25 MAbs showed greater incidence of PTDM.