Vol. 6, Issue 2, Part A (2024)

Background: High expression of ACE2 and TMPRSS2 in testes suggests men's vulnerability to SARS-CoV-2 infection, leading to orchitis, oxidative damage, inflammation, and immunological responses that disrupt the hypothalamic-pituitary-gonadal axis and impaired gonadal steroidogenesis, potentially causing hypogonadism, sexual dysfunction, and infertility.

Objectives: To determine the frequency of testosterone deficiency in post-COVID patients and its association with the severity of COVID-19 disease.

Methods: In this cross-sectional study we enrolled 48 post-COVID male patients aged 18-69 years and equal number of age, BMI, and WC matched participants as healthy control. After using a questionnaire to enlist participants, we measured total testosterone, luteinizing hormone (LH), folicle stimulating hormone (FSH), SHBG, and albumin, then computed free (cFT) and bioavailable testosterone. Testosterone deficiency was defined as TT < 264 ng/ml and/or cFT < 220 pmol/L.

Results: Frequency of testosterone deficiency 12 (25%) was significantly (P=0.028) higher in the post-COVID group compared to only 4 (8.3%) in the healthy control group. The recovered COVID-19 patients had significantly lower total (P=0.034), calculated free (p<0.001) and bioavailable testosterone (p<0.001), and higher SHBG (p<0.001) levels in comparison to the healthy individuals. In contrast to post-COVID patients with normal testosterone levels, patients with deficient testosterone had significantly greater rates of central obesity (P=0.040), and sexual dysfunction (P=0.011) as well as hospitalizations requiring oxygen therapy (P=0.007) and COVID-19 disease severity (P=0.004). In regression analysis, COVID-19 was a significant predictor of testosterone deficiency [OR=4.295 (P=0.034, 95% CI= 1.115, 16.548)], and moderate to severe COVID-19 disease increased the odds of testosterone deficiency by approximately 10 times [OR=9.950 (p=0.017, 95% CI= 1.513, 65.454)] in post-COVID group.

Conclusion: Post-COVID male patients were found to have a higher prevalence of testosterone deficiency in comparison to matched control participants. COVID-19 severity was the most significant predictor of low testosterone levels in recovered COVID-19 patients.