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.

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Purpose: To evaluate the effect of short-acting 4.5% nasal testosterone gel (Natesto) on serum testosterone, gonadotropins, total motile sperm count, health related quality of life and sexual function. Materials and Methods: This was a single institution, open label, single arm trial conducted between November 2017 and September 2019 at the University of Miami. Men 18 to 55 years old diagnosed with symptomatic hypogonadism (total testosterone less than 300 ng/dl on 2 occasions) were included. Men with azoospermia, vasectomy or a total motile sperm count less than 5 million were excluded. Enrolled patients were treated with Natesto, a short-acting nasal testosterone (125 ml per nostril, 11.0 mg testosterone per dose, TID) for 6 months. Results: In total, 60 men were enrolled in the study. Of these, 44 and 33 patients were evaluated for testosterone at 3 and 6 months, respectively. A total of 31 patients (90.9%) reached a normal testosterone level (greater than 300 ng/dl) at 6 months. Follicle stimulating hormone and luteinizing hormone levels were maintained within the normal range in 81.8% and 72.7% of patients at 6 months, respectively. Total motile sperm count was maintained with total motile sperm count greater than 5 million over the treatment period in 88.4% of men at 3 months and 93.9% at 6 months. There were statistically significant improvements on International Index of Erectile Function sexual desire and overall satisfaction domains at 6 months. Conclusions: Natesto appears to increase testosterone while maintaining semen parameters in a majority of men. Natesto has the potential to be a safe and effective treatment for men with functional hypogonadism who wish to preserve semen parameters. Long-term studies beyond 6 months are needed before we can safely prescribe nasal testosterone gel for men interested in fertility.

Background Excess reactive oxygen species and reactive nitrogen species are implicated in male infertility and impaired spermatogenesis. Aim To investigate the effect of excess reactive nitrogen species and nitrosative stress on testicular function and the hypothalamic-pituitary-gonadal axis using the S-nitrosoglutathione reductase-null (Gsnor−/−) mouse model. Methods Testis size, pup number, and epididymal sperm concentration and motility of Gsnor−/− mice were compared with those of age-matched wild-type (WT) mice. Reproductive hormones testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone were compared in Gsnor−/− and WT mice. Immunofluorescence for Gsnor−/− and WT testis was performed for 3β-hydroxysteroid dehydrogenase and luteinizing hormone receptor (LHR) and compared. Human chorionic gonadotropin and gonadotropin-releasing hormone stimulation tests were performed to assess and compare testicular and pituitary functions of Gsnor−/− and WT mice. Outcomes Evaluation of fertility and reproductive hormones in Gsnor−/− vs WT mice. Response of Gsnor−/− and WT mice to human chorionic gonadotropin and gonadotropin-releasing hormone to evaluate LH and T production. Results Gsnor −/− mice had smaller litters (4.2 vs 8.0 pups per litter; P &lt; .01), smaller testes (0.08 vs 0.09 g; P &lt; .01), and decreased epididymal sperm concentration (69 vs 98 × 106; P &lt; .05) and motility (39% vs 65%; P &lt; .05) compared with WT mice. Serum T (44.8 vs 292.2 ng/dL; P &lt; .05) and LH (0.03 vs 0.74 ng/mL; P = .04) were lower in Gsnor−/− than in WT mice despite similar follicle-stimulating hormone levels (63.98 vs 77.93 ng/mL; P = .20). Immunofluorescence of Gsnor−/− and WT testes showed similar staining of 3β-hydroxysteroid dehydrogenase and LHR. Human chorionic gonadotropin stimulation of Gsnor−/− mice increased serum T (&gt;1,680 vs &gt;1,680 ng/dL) and gonadotropin-releasing hormone stimulation increased serum LH (6.3 vs 8.9 ng/mL; P = .20) similar to WT mice. Clinical Translation These findings provide novel insight to a possible mechanism of secondary hypogonadism from increased reactive nitrogen species and excess nitrosative stress. Strengths and Limitations Limitations of this study are its small samples and variability in hormone levels. Conclusion Deficiency of S-nitrosoglutathione reductase results in secondary hypogonadism, suggesting that excess nitrosative stress can affect LH production from the pituitary gland.

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