Summary: The effects of weight loss on erectile function and hormones have not been well studied. The aim of this study was to measure the degree to which sexual function and in particular erectile function and hormonal environment change after substantial weight loss, surgically and non‐surgically induced in the morbidly obese male in a prospective randomized long‐term controlled trial. Furthermore, how surgery makes a difference when treating morbidly obese men was envisaged in this context. We prospectively studied 20 morbidly obese men for 24 months, divided into two groups: group A included 10 patients who underwent life style modifications (exercise and diet) for 4 months and subsequently gastric bypass, and another 10 patients in group B were kept on weekly follow‐up. None of the men were taking phosphodiesterase type‐5 inhibitors. All patients underwent International Index of Erectile Function (IIEF)‐5 questionnaire, serum oestradiol, prolactin (PRL), luteinizing (LH) and follicle‐stimulating (FSH) hormones, free and total testosterone (FT and TT) at baseline (time 0), surgery – 4 months latter baseline (time 1) and final evaluation – 24 months (time 2). From times 0 to 1, group A presented a mean body mass index (BMI) reduction of 12.6 (p < 0.0001), whereas group B, 2.1 (p > 0.05). The BMI reductions between times 0 and 2 were 24.7 (p < 0.0001) and 0.7 (p > 0.05) for groups A and B respectively. BMI average between the two groups was similar at time 0 (p = 0.2142), and different at times 1 (p = 0.0033) and 2 (p < 0.0006). Increase in IIEF‐5 score (p = 0.0469), TT (p = 0.0349) and FSH levels (p = 0.0025), and reduction in PRL level (p < 0.0001) were observed in group A from times 0 to 2 and 1 to 2. There were no changes from times 0 to 1. Comparing groups A and B at time 2, IIEF‐5, TT and FT increased significantly in group A (p = 0.0224, 0.0043 and 0.0149 respectively). Surgery‐induced weight loss increased erectile function quality measured by IIEF‐5 questionnaire, increased TT, FT and FSH and reduced PRL levels. The hormonal impact verified could justify the improvement in erectile function. Lifestyle modifications impacted BMI without hormonal or sexual impact in morbidly obese. New studies are warranted in the field to support our data.

Obesity in men is associated with infertility in numerous studies, and the temporal trend for a decline in semen parameters parallels the increasing prevalence of obesity in the developed world. In addition to impaired semen quality, fertility among obese men may be affected by decreased libido and erectile dysfunction. This spectrum of expression of hypogonadism among obese men originates from multiple interacting factors including reduced levels of gonadotropins and testosterone, altered androgen-to-estrogen ratios, insulin resistance, and sleep apnea. No evidence-based treatment that increases the likelihood of pregnancy for the infertility associated with male obesity has been demonstrated to date. Interventions associated with improvement of intermediate outcomes that include the endocrine profile, semen parameters, and sexual function may be appropriately selected based on history, physical findings, as well as endocrine and metabolic evaluation. Among these interventions are weight loss through lifestyle change, relief from sleep apnea, use of aromatase inhibitors, gonadotropin administration, phosphodiesterase inhibitors, and insulin-sensitizing agents.

Intravesical bacillus Calmette–Guérin (BCG) immunotherapy is the standard of care in treating non–muscle-invasive bladder cancer, yet its mechanism of action remains elusive. Both innate and adaptive immune responses have been implicated in BCG activity. Although prior research has indirectly demonstrated the importance of T cells and shown a rise in CD4⁺ T cells in bladder tissue after BCG, T-cell subpopulations have not been fully characterized. We investigated the relationship between effector and regulatory T cells in an immune competent, clinically relevant rodent model of bladder cancer. Our data demonstrate that cancer progression in the N-methyl-N-nitrosourea (MNU) rat model of bladder cancer was characterized by a decline in the CD8/FoxP3 ratio, consistent with decreased adaptive immunity. In contrast, treatment with intravesical BCG led to a large, transient rise in the CD4⁺ T-cell population in the urothelium and was both more effective and immunogenic compared with intravesical chemotherapy. Whole-transcriptome expression profiling of posttreatment intravesical CD4⁺ and CD8⁺ T cells revealed minimal differences in gene expression after BCG treatment. Together, our results suggest that although BCG induces T-cell recruitment to the bladder, the T-cell phenotype does not markedly change, implying that combining T-cell–activating agents with BCG might improve clinical activity. Cancer Immunol Res; 5(7); 594–603. ©2017 AACR.