Novel Penile Ultrasound Technique to Explain Mechanism of Erectile Dysfunction (ED) in Young Patients using Finasteride for Androgenic Alopecia

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February 2018 Volume 15, Issue 2, Supplement 1, Page S81

Novel Penile Ultrasound Technique to Explain Mechanism of Erectile Dysfunction (ED) in Young Patients using Finasteride for Androgenic Alopecia

R. Rubin, A. Winter, I. Goldstein

PlumX Metrics
DOI: https://doi.org/10.1016/j.jsxm.2017.11.194

Oblectives: Post-finasteride syndrome (PFS), has been reported in young men with persistent sexual/non-sexual symptoms despite stopping finasteride prescribed for androgenic alopecia. Since these men typically have normal penile Doppler hemodynamics they are often diagnosed as having psychogenic ED. Animal studies, however, reveal histologic erectile tissue fibrosis after exposure to finasteride. Novel penile ultrasound techniques were used to assess if a similar pathophysiology could explain the ED in young men with PFS.

Material and Methods: 27 men with PFS (mean age 31 years) met inclusion/exclusion criteria: potent prior to but ED since use of finasteride; <40 years old without obvious cardiovascular risk factors; underwent grayscale and color penile duplex Doppler ultrasound with a high frequency probe (Aixplorer 15.4 MHz transducer) during maximal pharmacologic erection. Grayscale imaging was performed using a standard protocol in axial B-mode at multiple gains, with various dynamic ranges, in multiple penile shaft locations to determine presence/absence of erectile tissue homogeneity or heterogeneity. Standard color Doppler parameters of peak systolic velocity (PSV) and end-diastolic velocity (EDV) were concomitantly assessed.

Results: Mean use of finasteride was 3.5 years (range 2 days–12 years). PFS symptoms included ED (100%); IIEF, EF domain scores were on average 14 (range 0–24). Other PFS symptoms included low libido (81%), orgasm dysfunction (66%), cognitive changes (55%), and mood changes (74%). Dihydrotestosterone (DHT) blood test values were low/lower tertile in 56%. 26/27 finasteride users (96%) demonstrated lack of homogeneity and hyperechoic/hypoechoic regions in erectile tissue. One patient (4%) had homogenous erectile tissue. Mean right/left PSV values were 30.3/29.8 cm/sec, with mean right/left EDV values 1.6/1.1 cm/sec during maximal pharmacologic smooth muscle relaxation.

Conclusions: Using novel ultrasound technology, 96% of men with PFS and ED demonstrated heterogeneity in their corporal tissue at maximal pharmacologic erection. This new protocol is able to show that PFS men complaining of ED may have an underlying biologic pathophysiology. Further we hypothesise that finasteride lowers DHT leading to corporal smooth muscle apoptosis and fibrosis similar to animal models, impairing tissue expandability leading to clinically reported venoocclusive dysfunction and ED

Disclosure: Work supported by industry: no. The presenter or any of the authors act as a consultant, employee (part time or full time) or shareholder of an industry.

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And? Any result?

Grayscale imaging was performed using a standard protocol in axial B-mode at multiple gains, with various dynamic ranges, in multiple penile shaft locations to determine presence/absence of erectile tissue homogeneity or heterogeneity. Standard color Doppler parameters of peak systolic velocity (PSV) and end-diastolic velocity (EDV) were concomitantly assessed. Mean use of finasteride was 3.5 years (range 2 days–12 years). PFS symptoms included ED (100%); IIEF, EF domain scores were on average 14 (range 0–24). Other PFS symptoms included low libido (81%), orgasm dysfunction (66%), cognitive changes (55%), and mood changes (74%). Dihydrotestosterone (DHT) blood test values were low/lower tertile in 56%. 26/27 finasteride users (96%) demonstrated lack of homogeneity and hyperechoic/hypoechoic regions in erectile tissue. One patient (4%) had homogenous erectile tissue. Mean right/left PSV values were 30.3/29.8 cm/sec, with mean right/left EDV values 1.6/1.1 cm/sec during maximal pharmacologic smooth muscle relaxation. Using novel ultrasound technology, 96% of men with PFS and ED demonstrated heterogeneity in their corporal tissue at maximal pharmacologic erection. This new protocol is able to show that PFS men complaining of ED may have an underlying biologic pathophysiology. Further we hypothesise that finasteride lowers DHT leading to corporal smooth muscle apoptosis and fibrosis similar to animal models, impairing tissue expandability leading to clinically reported venoocclusive dysfunction and ED

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As much as it sucks to hear confirmation that most of us probably have physical damage, it is good to hear confirmation that this is more than a psychological problem.

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So, it is possible that a shockwave therapy improves the situation??

What Goldstein finds I can also demonstrate from my basic ultrasound.

HEALTHY (16-6-2018) ― PFS (4-7-2018)

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It shows severe penile atrophy and apoptosis of the corpora cavernosa.
The images do not lie, only a stupid can deny that there is nothing.

“Further we hypothesise that finasteride lowers DHT leading to corporal smooth muscle apoptosis and fibrosis similar to animal models, impairing tissue expandability leading to clinically reported venoocclusive dysfunction and ED”

I’ve read this already in the rat studies before taking Fin, but this isn’t true for most of the people here right? Or do most PFS sufferers have chronic low dht? (sorry I havent read too many stories on here…)
This would mean high dht (and calciumintake) = no fibrosis
But if pfs sufferers have normal range dht something else would be to blame for this taking place?

Have youbtried shockwave therapy??

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So are we just screwed or can anything reverse some of this damage?

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Screwed.

I doubt that’s true. Chi for example had all sorts of penis rotation and oddities that resolved.

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So screwed means the only option left is a penile implant? What is when you have normal to high dht? In my opinion there has to be at least another factor than dht that caused this. Because here are many users who have normal to high dht. Including myself.

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I have DHT extreme 1750 pg/ml (250-990)! But it is as non-existent in my body

So will there be no treatments? Does anyone know what Dr. Goldstein things about the results?

@Demon it’s very unhelpful to state we are “screwed” when

a) there are some very desperate people visiting this forum who are on the edge of committing grave harm to themselves

b) there are accounts of people recovering from penile changes (@Chi , @Apr1989 )

If the study itself states that these changes are irreversible, by all means relay that. But that summary certainly does not state that. Have you actually read the whole study, or just this summary?

There’s a reason why a lot of people reporting recoveries advise not logging into these forums too often, and that is because sweeping negative assessments which some members are prone to are extremely unhelpful.

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Listen friend, I am in direct contact with Roberto Cosimo Melcangi (also Daniele Santi) he said verbatim that they are “too far away” and that a cure currently does not exist unfortunately.

The advice they gave and not to focus on this.

Did they say something regarding sage 217 I know that it will be probably only helpful/ beneficial to libido related issues and depression but who knows maybe also to some extent for nerve signaling dysfunctions like hemodynamics for penile tissue? Why can’t they(Melcangi, et cetera) do a statement here on this forum. Nothing against you personally but here are many people who make assumptions regarding the study which in the end tends to be not true

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I want to read summary.
Demon’s talk means ‘There is no cure for PFS in this time’ right?? And this is from Milano university??
But i have a question why these article come up this time? That study resulted in 2018 Feb.
Now is 2019 May!
Demon, you directly heard that results from Melcangi? When?
I just want to know…

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Irwin Goldstein’s study only shows that PFS patients have irreversible changes in penile tissue and he also said that the Syndrome is intractable. Yes, I repeat once again, I am in direct contact with Cosimo Melcangi and his team like Daniele Santi, who is my endocrinologist, and the Syndrome is incurable at the moment, there are no treatments, he also wrote it, black on white in my diagnosis. Everyone then is free to deceive himself as he sees fit. They both added not to take drugs or supplements to treat it or cure them because a possible side effect would be a serious mistake, as in my case. I made my PFS severe.

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