COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms.
Hum Fertil (Camb)
; : 1-6, 2021 Jan 13.
Artículo
en Inglés
| MEDLINE | ID: covidwho-20242660
ABSTRACT
Men show higher vulnerability to severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection (COVID-19) and present with depleted testosterone levels. Reports pertaining to high luteinizing hormone (LH), while diminished levels of in COVID-19 patients negate the hypothalamic-pituitary-testicular (HPT) axis mediated lowering of testosterone. Although not evidenced, high testicular expression of angiotensin-converting enzymes-2 (ACE2), that aids viral entry into cells, may suggest direct viral-testicular invasion. However, secondary inflammation and oxidative stress (OS), owing to SARS-CoV-2 infection, are more likely to impair steroidogenesis. Moreover, blockage of ACE2 aided angiotensin II into angiotensin (1-7) conversion may also affect testosterone synthesis. SARS-CoV-2, by mimicking adrenocorticotrophic (ACTH) hormones, may trigger host antibodies against the ACTH molecules to suppress host stress response. This commentary concisely presents the possible mechanisms by which SARS-CoV-2 infection may affect testosterone levels, which possibly result in compromised male reproductive health.
Texto completo:
Disponible
Colección:
Bases de datos internacionales
Base de datos:
MEDLINE
Idioma:
Inglés
Revista:
Hum Fertil (Camb)
Asunto de la revista:
Medicina Reproductiva
Año:
2021
Tipo del documento:
Artículo
País de afiliación:
14647273.2020.1867902
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