Background: Post-transplant diabetes mellitus is a significant risk factor for cardiovascular disease in solid organ transplantation.
The main underlying pathophysiological mechanism of PTDM is pancreatic beta cell dysfunction in the context
of insulin resistance, but the relative importance of each of these important components of glycemic metabolism is
under intense debate.
Methods: We searched MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials to January 15, 2015. We
selected systematic reviews and meta-analyses and randomized clinical trials. When no such reports were found for a
given topic or drug, observational studies were included in the assessment.
Results: There are agents with known diabetogenic effects: corticosteroids, calcineurin inhibitors including tacrolimus
and cyclosporine, as well as the mammalian target of rapamycin inhibitors (sirolimus and everolimus). The association
between the use of induction agents and PTDM is very scarce. No diabetogenic effects have been found with the use of
azathioprine, mycophenolate mofetil and its derivatives.
Conclusion: Immunosuppression is the major modifiable risk factor for development of PTDM but risk versus benefit
analysis is required to balance risk of developing PTDM versus rejection. Caution is advisable in immunosuppressant adjustments
in the event that PTDM develops based on current evidence. Physicians should choose and use immunosuppression
regimens shown to have the best outcome for patient and graft survival, irrespective of PTDM risk.