Background The short and long-term effects of COVID-19 on erectile function and penile vasculature remains poorly understood and is of particular importance as the virus has been found to be present within the penile tissue. Aim We determined the association of COVID-19 infection and subsequent diagnoses of erectile dysfunction. Methods We assessed the risk of ED in men with COVID-19 in the United States (US) using the TriNetX Research Network, a federated electronic medical records network of over 42 healthcare organizations and 66 million patients from the US. We identified adult men (≥ 18 years) with a recorded COVID-19 infection (ICD-10-CM B34.2, U07.1, U07.2, J12.81, J12.82, B97.29) since January 1, 2020, and compared them to an equivalent number of adult men who did not have COVID-19 over the same timeframe. Men with prior history or diagnosis of ED before January 1, 2020 were excluded. We accounted for confounding variables through propensity score matching for age, race, body mass index (BMI), and history of the following comorbid medical conditions: diabetes mellitus (E11), hypertension (I10), ischemic heart disease (I20-25) or hyperlipidemia (E78). Outcomes We assessed the association between COVID-19 and ED (N52) as a primary outcome through regression analysis with statistical significance assessed at p < .05. Results Prior to propensity score matching, men with COVID-19 were found to be older than men without COVID-19 (47.1 ± 21.4 vs 42.4 ± 24.3 years). Additionally, men with COVID-19 were noted to have increased prevalence of diabetes mellitus (DM) and hypertension (HTN) when compared to men without COVID-19 (13% DM and 27% HTN vs 7% DM and 22% HTN). After propensity score matching, we compared 230,517 men with COVID-19 to 232,645 men without COVID-19 and found that COVID-19 diagnosis was significantly associated with ED (OR 1.20, 95% CI 1.004 - 1.248, p = 0.04). Clinical Implications Our findings indicate that clinicians should consider evaluating erectile dysfunction among men with recent COVID-19 diagnoses and counsel them regarding the risk of developing erectile dysfunction. Strengths and Limitations Strengths include large sample size and adjustment for confounding variables. Limitations include reliance on a global federated dataset, retrospective study design, and lack of data regarding ED (mild vs moderate vs severe), COVID-19 infection severity, or history of prostate cancer and radiation, Conclusion There is an increased chance of new onset erectile dysfunction post-COVID-19 infection.

Vaccine hesitancy is a major public health obstacle to fighting the ongoing COVID‐19 epidemic. Due to studies that show COVID‐19 infection can affect sperm parameters and lead to orchitis, the public are concerned about the effect of the COVID vaccines on male reproduction. In this study, we investigated the association between COVID‐19 vaccination and risk of developing orchitis and/or epididymitis outcomes in a cohort of men using a large, US‐based, electronic health record database. After balancing for confounding variables, we found that receiving at least 1 COVID‐19 vaccine is associated with a decreased risk of developing orchitis and/or epididymitis.

Purpose: An unsafe hematocrit threshold for men receiving testosterone therapy (TT) has never been tested. This study seeks to determine whether secondary polycythemia among men receiving TT confers an increased risk of major adverse cardiovascular events (MACE) and venous thromboembolic events (VTE). Materials and Methods: Using a multi-institutional database of 74 million patients, we identified 2 cohorts of men with low testosterone (total testosterone <350 ng/dl) who received TT and subsequently either developed polycythemia (5,887) or did not (4,2784). Polycythemia was defined as hematocrit !52%. As a secondary objective, we identified 2 cohorts of hypogonadal men without polycythemia, who either did (26,880) or did not (27,430) receive TT. Our primary outcome was the incidence of MACE and VTE in the first year after starting TT. We conducted a Kaplan-Meier survival analysis to assess differences in MACE and VTE survival time, and measured associations following propensity score matching. Results: A total of 5,842 men who received TT and developed polycythemia were matched and compared to 5,842 men who did not develop polycythemia. Men with polycythemia had a higher risk of MACE/VTE (number of outcomes: 301, 5.15%) than men who had normal hematocrit (226, 3.87%) while on TT (OR 1.35, 95% CI 1.13e1.61, p <0.001). In hypogonadal men who received testosterone, no increased risk of MACE and VTE was identified as compared to hypogonadal men na€ ıve to TT. Conclusions: Developing polycythemia while on TT is an independent risk factor for MACE and VTE in the first year of therapy. Future research on the safety of TT should include hematocrit as an independent variable.

Purpose: We sought to compare testosterone formulations and determine the degree that hematocrit increases vary by testosterone therapy formulation. As head-to-head trials are rare, network meta-analysis of the contemporary studies is the only way to compare hematocrit changes by testosterone type, including topical gels and patches, injectables (both short-acting and long-acting) and oral tablets. Materials and Methods: We conducted a thorough search of listed publications in ScopusÒ, PubMedÒ, EmbaseÒ, Cochrane CENTRAL, and ClinicalTrials.gov. A total of 29 placebo-controlled randomized trials (3,393 men) met inclusion criteria for analysis of mean hematocrit change after testosterone therapy. Randomized controlled trial data for the following formulations of testosterone were pooled via network meta-analysis: gel, patch, oral testosterone undecanoate, intramuscular testosterone undecanoate, and intramuscular testosterone enanthate/cypionate. Results: All types of testosterone therapies result in statistically significant increases in mean hematocrit when compared with placebo. Meta-analysis revealed all formulations, including gel (3.0%, 95% CI 1.8e4.3), oral testosterone undecanoate (4.3%, 0.7e8.0), patch (1.4%, 0.2e2.6), intramuscular testosterone enanthate/cypionate (4.0%, 2.9e5.1), and intramuscular testosterone undecanoate (1.6%, 0.3e3.0) result in statistically significant increases in mean hematocrit when compared with placebo. When comparing all formulations against one another, intramuscular testosterone cypionate/enanthate were associated with a significantly higher increase in mean hematocrit compared to patch, but no differences in hematocrit between other formulations were detected. Conclusions: All types of testosterone are associated with increased hematocrit; however, the clinical concern of this increase remains questionable, warranting future studies. This is the first network meta-analysis to quantify mean hematocrit change and compare formulations, given the absence of head-to-head trials.

Purpose Male ageing is often associated with defective sperm DNA remodeling mechanisms that result in poorly packaged chromatin and a decreased ability to repair DNA strand breaks. However, the impact of advanced paternal age on DNA fragmentation remains inconclusive. The aim of the present systematic review was to investigate the impact of advancing paternal age (APA) on DNA fragmentation. Materials and Methods We conducted a thorough search of listed publications in Scopus, PubMed, and EMBASE, in accordance with the PRISMA guidelines. Results We identified 3,120 articles, of which nineteen were selected for qualitative analysis, resulting in a sample of 40,668 men. Of the 19 articles evaluating the impact of APA on DFI% (DNA fragmentation Index) included, 4 were on Normozoospermic and subfertile men, 3 on normozoospermic, Oligoasthenoteratozoospermic and Teratozoospermic, 6 on fertile and infertile men, 4 on just infertile men, and 2 evaluated a general population. Seventeen of the ninrnteen studies demonstrated APA's effect and impact on DFI%. Conclusions Although there was no universal definition for APA, the present review suggests that older age is associated with increased DFI. In elderly men with normal semen parameters, further studies should be performed to assess the clinical implications of DFI, as a conventional semen analysis can often fail to detect an etiology for infertility.

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