OBJECTIVETo determine incidence and prevalence of diabetes mellitus (DM) after lung transplantation (LTx), identify risk factors for persistent DM after LTx, and determine its effect on survival.
RESEARCH DESIGN AND METHODSThis was a prospective, longitudinal study comparing DM status before and after LTx using oral glucose tolerance tests (OGTTs). DM prevalence and changes in metabolic control over time were determined. Risk factors for persistent DM and survival differences by DM status were assessed.
RESULTSBetween August 2010 and December 2012, 156 patients underwent LTx. DM prevalence after 3, 12, and 24 months was 47%, 44%, and 40%, respectively. A further 20%, 11%, and 7% had impaired glucose tolerance and/or impaired fasting glucose. Incidence of new-onset DM after transplant (NODAT) was 32%, 30%, and 24% after 3, 12, and 24 months. Nonfasting insulin levels and second phase insulin release fell 3 months after transplant (Tx) but returned to baseline by 2 years. The only risk factors for NODAT were 1-and 2-h glucose levels on pre-Tx OGTT (OR 1.73 [95% CI 1.19-2.50], P = 0.004, and 1.84 [1.22-2.77], P = 0.004, respectively). Survival was reduced in patients with DM at study end versus those without (estimated mean 979 days [95% CI 888-1,071] vs. 1,140 days [1,070-1,210], P = 0.023).
CONCLUSIONSMost patients had dysglycemia during the first year after LTx, and 32% developed NODAT. Hyperglycemia was caused both by b-cell dysfunction and by insulin resistance. Only pre-Tx OGTT glucose levels predicted persistent NODAT. As DM was common and associated with reduced survival, early detection and management of DM in LTx recipients are warranted.Diabetes mellitus (DM) is a common complication of solid organ transplantation and is associated with increased morbidity and mortality (1). It is especially common after lung transplantation (LTx), firstly because LTx recipients (LTR) require highdose immunosuppression with glucocorticoids in combination with calcineurin inhibitors and secondly because a significant minority of patients have cystic fibrosis (CF), which results both in lung damage necessitating LTx and in destruction of insulin-producing b-cells in the pancreas.