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Review
. 2020 Apr;11(4):779-801.
doi: 10.1007/s13300-020-00790-5. Epub 2020 Feb 24.

Post-Transplantation Diabetes Mellitus

Syed Haris Ahmed  1 , Kathryn Biddle  2 , Titus Augustine  3 , Shazli Azmi  3
Affiliations
Review

Post-Transplantation Diabetes Mellitus

Syed Haris Ahmed et al. Diabetes Ther. 2020 Apr.

Abstract

Solid organ transplantation (SOT) is an established therapeutic option for chronic disease resulting from end-stage organ dysfunction. Long-term use of immunosuppression is associated with post-transplantation diabetes mellitus (PTDM), placing patients at increased risk of infections, cardiovascular disease and mortality. The incidence rates for PTDM have varied from 10 to 40% between different studies. Diagnostic criteria have evolved over the years, as a greater understating of PTDM has been reached. There are differences in pathophysiology and clinical course of type 2 diabetes and PTDM. Hence, managing this condition can be a challenge for a diabetes physician, as there are several factors to consider when tailoring therapy for post-transplant patients to achieve better glycaemic as well as long-term transplant outcomes. This article is a detailed review of PTDM, examining the pathogenesis, diagnostic criteria and management in light of the current evidence. The therapeutic options are discussed in the context of their safety and potential drug-drug interactions with immunosuppressive agents.

Keywords: Calcineurin inhibitors; Diabetes mellitus; Graft failure; Macrovascular; Microvascular; Mortality; Post-transplantation; Rejection; Steroids; mTOR inhibitors.

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Figures

Fig. 1
Fig. 1
Cumulative 5-year incidence of PTDM in heart, liver, lung and kidney transplant patients after the adoption of the OGTT as the gold standard for diagnosis
Fig. 2
Fig. 2
Risk factors for PTDM. HCV hepatitis C virus, PCKD polycystic kidney disease, CNI calcineurin inhibitor, mTOR mammalian target of rapamycin, CMV cytomegalovirus
Fig. 3
Fig. 3
mTORi and CNI affect the insulin signalling cascade. IRS2 insulin receptor substrate, PDK1 phosphoinositide-dependent protein kinase, PI3K phosphatidylinositol 3 kinase, cAMP cyclic adenosine monophosphate, NFAT transcription factors nuclear factor of activated T-cells, CREB cAMP response element binding protein, CNI calcineurin inhibitor, mTOR mammalian target of rapamycin, GLP1 glucagon-like peptide-1
Fig. 4
Fig. 4
Flow diagram depicting proposed glycaemic management after transplant surgery
See this image and copyright information in PMC

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