Comparing risk of post infection erectile dysfunction following [SARS2] stratified by [LC], hospitalization status, and vasopressor, 2024, Grutman+

[SNT Gatchaman]

Comparing risk of post infection erectile dysfunction following SARS Coronavirus 2 stratified by acute and long COVID, hospitalization status, and vasopressor administration: a U.S. large claims database analysis
Grutman, Aurora J.; Gilliam, Kelli; Maremanda, Ankith P.; Able, Corey; Choi, Una; Alshak, Mark N.; Kohn, Taylor P.

No study has yet assessed the risk of developing erectile dysfunction (ED) after a diagnosis of long COVID, defined by the Centers for Disease Control and Prevention as the persistence or presence of new symptoms at least 4 weeks after initial SARS-CoV-2 infection, when compared to those diagnosed with acute COVID or cases in which more severe treatment is required.

To assess these risks, we queried the TriNetX COVID-19 Research Network from December 1st 2020 through June 2023. Men aged ≥ 18 diagnosed with long COVID were compared to those diagnosed with acute COVID and analyses were performed to compare men who were/were not hospitalized within 1 month of acute COVID diagnosis and men who did/did not need vasopressors. Cohorts were propensity score matched and compared for differences in new ED diagnosis and/or prescription of phosphodiesterase-5 inhibitors (PDE5i).

After propensity score matching, the long and acute COVID cohorts included 2839 men with an average age of 54.5±16.7 and 55.1±17.1 years respectively (p = 0.21). Men with long COVID were more likely to develop ED or be prescribed PDE5i (3.63%) when compared to men with only acute COVID infections (2.61%) [RR 1.39; 95% CI 1.04, 1.87]. There was no statistically significant risk of developing ED or being prescribed PDE5i for individuals who received vasopressors [RR 0.92; 95% CI 0.77,1.10] or were hospitalized [RR 0.93; 95% CI 0.82,1.06].

Link | PDF (Nature International Journal of Impotence Research)

 

[bobbler]

Of course the first question this brings to mind is how much funding is being given to biomedical research into this area vs 'treatments to cope'

compared to 'other' post-infective conditions?

And then I realise that viagra exists

 

[Milo]

I cannot see where the funding for this study came from. But the authors declare no conflicts of interest. Surely one of them has received funding from the pharma producing the blue pill at some time in their career, no?

 

[Hutan]

This forum thread may be of interest:
Use of sildenafil (viagra) to alter fatigue, functional status and impaired cerebral blood flow in ... CFS, 2020, Friedman (Pfizer)
There were hints of sildenafil helping with CFS symptoms, but problems with the study meant no conclusions could be drawn. Studies related to this could be useful.

 

[Hutan]

Phosphodiesterase-5 (PDE5) Inhibitors In the Management of Erectile Dysfunction

Sildenafil, vardenafil, tadalafil, and avanafil are classified as PDE5 inhibitors and are indicated for the treatment of men with ED. Sildenafil, the first PDE5 inhibitor, was introduced in 1998. More than 20 million men were treated with sildenafil in its first 6 years on the market.5 In 2003, vardenafil was approved, offering patients an alternative option. Tadalafil followed several months later and was also approved in 2003. Nicknamed the “weekend pill,” tadalafil’s 36-hour effectiveness offered patients more spontaneity.

In 2010, a 10-mg oral disintegrating tablet (ODT) formulation of vardenafil (Staxyn) was introduced; this ODT discreet formulation is considered more convenient to administer.

Several years after the introduction of tadalfil on the market, researchers toyed with the idea of a chronic, low-dose formulation to further enhance spontaneity. In 2008, Eli Lilly obtained FDA approval for the once-daily administration of tadalafil. In October 2011, tadalafil (Cialis) was also approved to treat benign prostatic hyperplasia (BPH) with or without ED. Avanafil (Stendra) was approved in April 2012, offering an onset of action as early as 15 minutes after administration and further expanding treatment options for men with ED.

Sildenafil and tadalafil are also used to treat pulmonary arterial hypertension (PAH) under the trade names Revatio (sildenafil 20-mg tablets and 10-mg/12.5-mL single-use vial injections) and Adcirca (tadalafil 20-mg tablets).

PHARMACOLOGY
During sexual arousal, nitric oxide (NO) is released from nerve terminals and endothelial cells in the corpus cavernosum. NO activates guanylate cyclase to convert guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP), triggering a cGMP-dependent cascade of events. The accumulation of cGMP leads to smooth-muscle relaxation in the corpus cavernosum and increased blood flow to the penis.

PDE5 is an enzyme found primarily in the smooth muscle of the corpus cavernosum that selectively cleaves and degrades cGMP to 5′-GMP. PDE5 inhibitors are similar in structure to cGMP; they competitively bind to PDE5 and inhibit cGMP hydrolysis, thus enhancing the effects of NO. This increase in cGMP in the smooth muscle cells is responsible for prolonging an erection.

PDE5 inhibitors lack a direct effect on corpus cavernosum smooth-muscle relaxation. Therefore, after administration, adequate sexual stimulation is necessary for an erection to occur.6,7