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10.1080/14647273.2020.1867902 http://scihub22266oqcxt.onion/10.1080/14647273.2020.1867902 33439057!ä!33439057 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hum+Fertil+(Camb) 2023 ; 26 (1): 182-185 Nephropedia Template TP {{tp|p=33439057|t=2023. COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms |pdf=|usr=}}{{33439057}} gab.com Text COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms JO: Hum Fertil (Camb) http://www.kidney.de/pget.php?&tw=1&pmid=33439057 #FOAvip 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. Twit Text FOAVip COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms ????Hum Fertil (Camb) http://www.kidney.de/pget.php?&tw=1&pmid=33439057 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33439057 #FOAvip English Wikipedia <ref>{{Cite pmid|33439057}}</ref> COVID-19 and hypogonadism: secondary immune responses rule-over endocrine mechanisms #MMPMID33439057 Sengupta P; Dutta S Hum Fertil (Camb) 2023[Feb]; 26 (1): 182-185 PMID33439057show ga 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. |*COVID-19[MESH] |*Hypogonadism[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Humans[MESH] |Immunity[MESH] |Male[MESH] |Peptidyl-Dipeptidase A/metabolism[MESH] |SARS-CoV-2/metabolism[MESH]COVID-19 and hypogonadism: secondary immune responses rule-over endocr(epmc).pdf DeepDyve Pubget Overpricing