86-OR: Erectile Dysfunction in Men with Prediabetes and Type 2 Diabetes: The Diabetes Prevention Program Outcomes Study (DPPOS)

Abstract

Introduction: Erectile dysfunction (ED) is more common and less responsive to pharmacotherapy in men with T2D. Data in men with prediabetes (PreD) and risk profiles in those with T2D, are lacking. We determined the burden and risk factors for ED in men with PreD and with T2D enrolled in the DPPOS. Methods: Between 1996-1999, 3,234 adults with PreD were randomized to intensive lifestyle intervention, metformin, or placebo in the DPP. In 2001, metformin was continued for those originally randomized with modified lifestyle intervention offered to all. In 2016-2017, 568 (88%) of 648 male participants completed the International Index of Erectile Function (IIEF) . ED was defined as having low or very low confidence getting and keeping an erection and/or ED medication use. Backwards selection multivariable logistic regression models including DPP treatment estimated odds of ED for covariates significant in bivariate analysis in men with persistent PreD and T2D. Results: Overall, 218 (38%) men met ED criteria. Prevalence of ED was similar in men with PreD (41%) and T2D (37%) (p=0.4) . In all men, older age (p<0.001) , non-white race (p<0.001) and depression (defined by Beck Depression Inventory or antidepressant use) (p<0.01) were associated with ED. Among men with PreD, those assigned to intensive lifestyle intervention, but not metformin, had decreased odds of ED compared with the placebo group (OR=0.26, 95%CI=0.09, 0.77) . Among men with T2D, metabolic syndrome (MetS) , defined by NCEP ATP III criteria, was associated with increased odds of ED (OR=1.72, 95%CI=1.05, 2.83) . Conclusions: ED is highly prevalent in men with PreD and with T2D. In addition to demonstrated factors typically observed in the general population such as younger age and absence of depression, intensive lifestyle intervention was protective in men at increased risk for T2D. In men with T2D, ED was associated with MetS. Our findings suggest metabolic mechanisms contribute to the pathogenesis of ED in T2D. Disclosure Y.Blair: None. L.Doherty: None. M.Temprosa: None. H.Wessells: None. R.Pop-busui: Advisory Panel; Averitas Pharma, Inc., Boehringer Ingelheim International GmbH, Nevro Corp., Novo Nordisk, Reata Pharmaceuticals, Inc., Regenacy Pharmaceuticals, Inc. K.M.Gadde: Research Support; AstraZeneca, BioKier, Inc. P.Singh: None. A.V.Sarma: None. D.Research group: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (UDK048489, UDK048339, UDK048377, UDK048349, UDK048381, UDK048468, UDK048434, UDK048485, UDK048375, UDK048514, UDK048437, UDK048413, UDK048411, UDK048406, UDK048380, UDK048397, UDK048412, UDK048404, UDK048387, UDK048407, UDK048443, and UDK048400)