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New-Onset Post-Transplant Diabetes Mellitus after Allogeneic Hematopoietic Cell
Transplant Is Initiated by Insulin Resistance, Not Immunosuppressive
Authors Engelhardt BG, Savani U, Jung DK, Powers AC, Jagasia M, Chen H, Winnick JJ,
Tamboli RA, Crowe JE, Abumrad NN
Submitted By Submitted Externally on 4/8/2019
Status Published
Journal Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
Year 2019
Date Published 2/1/2019
Volume : Pages Not Specified : Not Specified
PubMed Reference 30738170
Abstract New-onset post-transplant diabetes mellitus (PTDM) occurs frequently after
allogeneic hematopoietic cell transplant (HCT). Although calcineurin inhibitors
and corticosteroids are assumed to be the cause for hyperglycemia, patients
developing PTDM have elevated fasting C-peptide levels before HCT and before
immunosuppressive medications. To determine if PTDM results from established
insulin resistance present before transplant, we performed oral glucose
tolerance tests (OGTTs) and measured whole body, peripheral, and hepatic insulin
sensitivity with euglycemic hyperinsulinemic clamps before and 90days after
HLA-identical sibling donor HCT in 20 patients without pretransplant diabetes.
HCT recipients were prospectively followed for the development of new-onset PTDM
defined as a weekly fasting blood glucose = 126mg/dL or random blood glucose =
200mg/dL. During the first 100 days all patients received calcineurin
inhibitors, and 11 individuals (55%) were prospectively diagnosed with new-onset
PTDM. PTDM diagnosis preceded corticosteroid treatment. During the pretransplant
OGTT, elevated fasting (87 mg/dL versus 101 mg/dL; P?=?.005) but not 2-hour
postprandial glucose levels predicted PTDM diagnosis (P = .648). In response to
insulin infusion during the euglycemic hyperinsulinemic clamp, patients
developing PTDM had lower whole body glucose utilization (P?=?.047) and
decreased peripheral/skeletal muscle uptake (P?=?.031) before and after
transplant, respectively, when compared with non-PTDM patients. Hepatic insulin
sensitivity did not differ. Survival was decreased in PTDM patients (2-year
estimate, 55% versus 100%; P = .039). Insulin resistance before HCT is a risk
factor for PTDM independent of immunosuppression. Fasting pretransplant glucose
levels identified PTDM susceptibility, and peripheral insulin resistance could
be targeted for prevention and treatment of PTDM after HCT.


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