There is no mention of serum testosterone levels for males infected by COVID-19 in the National Institute of Health COVID-19 Treatment Guidelines. [1]
There is no mention of serum testosterone levels for males infected by COVID-19 in the Infectious Diseases Society of America COVID-19 Treatment Guidelines. [2]
The American Urological Association has published articles relating to COVID-19. However, there is no mention of COVID-19 and serum testosterone in their clinical guidelines. [3]
A review article assessing whether testosterone could worsen COVID-19 outcomes in men concluded that testosterone, in comparison to estrogen, may predispose men to widespread COVID-19 infection. Low serum levels of testosterone may predispose men, especially elderly men, to poor prognosis or death. [4]
A review article assessing gender differences in COVID-19 concluded that different levels of angiotensin-converting enzyme 2 (ACE2) in men and women, the effects of testosterone on ACE2 levels, and the fact that the ACE2 gene is located on the X-chromosome could contribute to men having a higher risk of developing severe COVID-19. [5]
A review article assessing the role of sex hormones in COVID-19 concluded that testosterone might reduce the need for assisted ventilation through its anticatabolic effect on respiratory muscles and could be considered in developing treatment strategies for patients with COVID-19. [6]
A review article assessing male reproductive health during COVID-19 concluded that testicular function in COVID-19 patients may need to be studied due to potential negative association on testosterone levels and overall reproductive health. Treatment with phosphodiesterase-5 (PDE5) inhibitors might be beneficial for both COVID-19 and erectile dysfunction in these patients. [7]
A review article assessing sex differences in severity and mortality in COVID-19 found that coronavirus genetic material was detected in the semen samples of infected males. Analysis of RNA sequencing data showed that both angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) were highly expressed in the testis compared to the ovary, supporting that coronavirus may enter the human testis. The researchers concluded that there is male-biased severity and mortality in different countries. However, sex-biased pathogenesis is not understood properly and could be multifactorial. [8]
A review article assessing sex-derived attributes contributing to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mortality found that a greater COVID-19 fatality rate in men could be a consequence of several biological differences between the sexes, and may be hypothesized as a result of suppressed immune responses due to testosterone. [9]