Mary Wilson
Well-known member
Original Article
Male sexual health and dysfunction
pISSN: 2287-4208 / eISSN: 2287-4690 World J Mens Health 2021 Jul 39(3): 466-469 https://doi.org/10.5534/wjmh.210055
Eliyahu Kresch1 , Justin Achua1 , Russell Saltzman2 , Kajal Khodamoradi1 , Himanshu Arora1 , Emad Ibrahim1 , Oleksandr N. Kryvenko1,3,6 , Vania Wolff Almeida4 , Fakiha Firdaus1 ,
Joshua M. Hare2,5 , Ranjith Ramasamy1
Purpose:
A pilot study to describe histopathological features of penile tissue of patients who recovered from symptomatic COVID-19 infection and subsequently developed severe erectile dysfunction (ED).
Materials and Methods:
Penile tissue was collected from patients undergoing surgery for penile prosthesis for severe ED. Specimens were obtained from two men with a history of COVID-19 infection and two men with no history of infec- tion. Specimens were imaged with TEM and H&E staining. RT-PCR was performed from corpus cavernosum biopsies. The tissues collected were analyzed for endothelial Nitric Oxide Synthase (eNOS, a marker of endothelial function) and CO- VID-19 spike-protein expression. Endothelial progenitor cell (EPC) function was assessed from blood samples collected from COVID-19 (+) and COVID-19 (-) men.
Results:
TEM showed extracellular viral particles ~100 nm in diameter with peplomers (spikes) near penile vascular endo- thelial cells of the COVID-19 (+) patients and absence of viral particles in controls. PCR showed presence of viral RNA in COVID-19 (+) specimens. eNOS expression in the corpus cavernosum of COVID-19 (+) men was decreased compared to COVID-19 (-) men. Mean EPC levels from the COVID-19 (+) patients were substantially lower compared to mean EPCs from men with severe ED and no history of COVID-19.
Conclusions:
Our study is the first to demonstrate the presence of the COVID-19 virus in the penis long after the initial infec- tion in humans. Our results also suggest that widespread endothelial cell dysfunction from COVID-19 infection can contrib- ute to ED. Future studies will evaluate novel molecular mechanisms of how COVID-19 infection leads to ED.
https://wjmh.org/pdf/10.5534/wjmh.210055
Male sexual health and dysfunction
pISSN: 2287-4208 / eISSN: 2287-4690 World J Mens Health 2021 Jul 39(3): 466-469 https://doi.org/10.5534/wjmh.210055
Eliyahu Kresch1 , Justin Achua1 , Russell Saltzman2 , Kajal Khodamoradi1 , Himanshu Arora1 , Emad Ibrahim1 , Oleksandr N. Kryvenko1,3,6 , Vania Wolff Almeida4 , Fakiha Firdaus1 ,
Joshua M. Hare2,5 , Ranjith Ramasamy1
Purpose:
A pilot study to describe histopathological features of penile tissue of patients who recovered from symptomatic COVID-19 infection and subsequently developed severe erectile dysfunction (ED).
Materials and Methods:
Penile tissue was collected from patients undergoing surgery for penile prosthesis for severe ED. Specimens were obtained from two men with a history of COVID-19 infection and two men with no history of infec- tion. Specimens were imaged with TEM and H&E staining. RT-PCR was performed from corpus cavernosum biopsies. The tissues collected were analyzed for endothelial Nitric Oxide Synthase (eNOS, a marker of endothelial function) and CO- VID-19 spike-protein expression. Endothelial progenitor cell (EPC) function was assessed from blood samples collected from COVID-19 (+) and COVID-19 (-) men.
Results:
TEM showed extracellular viral particles ~100 nm in diameter with peplomers (spikes) near penile vascular endo- thelial cells of the COVID-19 (+) patients and absence of viral particles in controls. PCR showed presence of viral RNA in COVID-19 (+) specimens. eNOS expression in the corpus cavernosum of COVID-19 (+) men was decreased compared to COVID-19 (-) men. Mean EPC levels from the COVID-19 (+) patients were substantially lower compared to mean EPCs from men with severe ED and no history of COVID-19.
Conclusions:
Our study is the first to demonstrate the presence of the COVID-19 virus in the penis long after the initial infec- tion in humans. Our results also suggest that widespread endothelial cell dysfunction from COVID-19 infection can contrib- ute to ED. Future studies will evaluate novel molecular mechanisms of how COVID-19 infection leads to ED.
https://wjmh.org/pdf/10.5534/wjmh.210055