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 Table of Contents  
EDITORIAL
Year : 2017  |  Volume : 4  |  Issue : 3  |  Page : 71-72

Shockwave therapy for erectile dysfunction: Is it really effective?


Department of Urology, National University Hospital, Singapore

Date of Web Publication28-Sep-2017

Correspondence Address:
King Chien Joe Lee
Department of Urology, National University Hospital, 1E Kent Ridge Road, NUHS Tower Block, Level 8, Singapore 119228
Singapore
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jina.jina_15_17

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How to cite this article:
Law YT, Lee KJ. Shockwave therapy for erectile dysfunction: Is it really effective?. J Integr Nephrol Androl 2017;4:71-2

How to cite this URL:
Law YT, Lee KJ. Shockwave therapy for erectile dysfunction: Is it really effective?. J Integr Nephrol Androl [serial online] 2017 [cited 2017 Dec 11];4:71-2. Available from: http://www.journal-ina.com/text.asp?2017/4/3/71/215739



Erectile dysfunction (ED) is defined as an inability to achieve or sustain an erection for satisfactory sexual performance. It has a prevalence of up to 52% and is influenced by age and other comorbidities such as diabetes, hypertension, and hypercholesterolemia.[1] Phosphodiesterase-5 inhibitors (PDE5-I) are effective pharmacological methods to treat ED; however, a proportion of patients (30%–40%) fails to respond.[2] Alternative treatments such as intracorporal injections and penile prostheses may be effective in PDE5-I nonresponders; however, potential complications often hinder long-term use. These methods attempt to improve erectile function but fail to treat the underlying pathophysiology of ED.

Low-intensity extracorporeal shock wave therapy (Li-ESWT) has recently gained favor in the treatment of ED and may modify the underlying pathophysiology of ED. The use of Li-ESWT in the treatment of ED was first inspired by cardiovascular studies which showed that in vitro and in vivo(porcine model) low-intensity Li-ESWT could enhance vascular endothelial growth factor and Flt-1 receptor expression, hence inducing neovascularization and improving myocardial ischemia.[3] Following that, the first animal study on ED using Li-ESWT which was performed 2007 showed that shockwave therapy may significantly reduce intracavernosal pressure/mean arterial pressure ratios through the induction of structural changes in penile tissue.[4] These ideas prompted by Vardi et al. to perform the first proof of concept human study using Li-ESWT to treat vasculogenic ED in 2010.[5] This small study of twenty patients demonstrated for the first time, the possibility of using Li-ESWT to treat ED. Since then, more human studies have reaffirmed the efficacy of Li-ESWT for ED, citing promising short-term results, improvements in cavernosal hemodynamics, and the potential to enable penile rehabilitation without drug therapy.[6],[7]

A smaller observational study of 50 patients by Bechara et al. showed that Li-ESWT could be efficacious and safe in 60% of patients who failed PDE5-I. Moreover, the improvement in response can be maintained for up to months in most patients.[8]

Recently, the first meta-analysis of Li-ESWT on men with ED was published by Clavijo et al.[9] This meta-analysis included 7 randomized controlled trials, with a total of 602 patients with vasculogenic ED. Results demonstrated a statistically significant improvement in the International Index of Erectile Function (IIEF-EF) scores in men who had undergone Li-ESWT as opposed to men who had undergone sham therapy. This meta-analysis showed a clinically significant average IIEF-EF score improvement after ESWT by 4.17 (P < 0.0001). Various treatment protocols were used in different studies, and the author recommended that future trials should start using 18,000 treatment shocks.

Although most publications do support the use of Li-ESWT in patients with vascular ED, recommendations still vary for patients with nonvascular ED such as postprostatectomy. To date, available literature cites mixed evidence on the use of Li-ESWT for patients with postradical prostatectomy ED. Chung et al.'s single-arm prospective study of 30 patients showed that patients with vasculogenic ED responded better to Li-ESWT than patients who had undergone radical prostatectomy (P < 0.05).[6] They cited that this may be due to underlying postoperative cavernosal nerve injury leading to greater expression of profibrotic factors, hence limiting the effects of Li-ESWT on cavernosal neovascularization and neuroregeneration.

A 2016 pilot study of 16 patients having ED postprostatectomy demonstrated that there was a median change in IIEF-5 scores by +3.5 (range: −1 to +8; P= 0.0049) at 1 month and +1 (range: −3 to –14; P= 0.046) at 12 months, respectively.[10] There were no severe side effects reported from this study, and the authors concluded that Li-ESWT may also have utility in improving erectile function after bilateral nerve-sparing radical prostatectomy. A drawback of the 2016 pilot study is that it lacks the use of erectogenic aids in the study population, the use of control groups, and small patient numbers. The difference in outcomes between the pilot study and the study by Chung et al. may perhaps be explained by the uncontrolled differences in time between surgery and application of Li-ESWT. A substantial lapse of time since surgery may have led to more significant penile fibrosis, implying that the use of Li-ESWT at an earlier stage postsurgery could have prevented fibrosis caused by long-term hypoxia from missing erections. More studies are needed to investigate if there are critical time points where Li-ESWT can be implemented for maximal benefit in patients.

In a study by Gruenwald et al.,[11] which evaluated the effects of Li-ESWT on 29 men with ED who failed PDE5-Is, of which 21 had diabetes, it was found that the 21 patients with diabetes did respond to Li-ESWT. Cavernosal blood flow and penile endothelial function, as measured by venous occlusion plethysmography of the penis, were both found to be significantly improved (P = 0.0001) in the men who responded to Li-ESWT.

To date, the mechanism of action of Li-ESWT in the management of ED is still incompletely elucidated. However, animal studies have provided various hypotheses. In 2013, Qiu et al. established that ESWT significantly restored erectile function in rates with streptozotocin-induced diabetes mellitus, similar to those exhibited by healthy controls.[12] These improvements were attributed to endothelial and smooth muscle regeneration in the penis mediated by recruitment of endogenous smooth muscle cells after Li-ESWT. A 2016 mice-model study by Assaly-Kaddoum et al.[13] then further suggested that Li-ESWT's improvements in erectile function may not be mediated through the usual mechanism dependent on nitric oxide and cyclic guanosine monophosphate but continued to reaffirm Li-ESWT's utility in improving erectile function. They suggested that the effects of Li-ESWT could be further potentiated by sildenafil treatment.

Human studies have demonstrated a statistically significant improvement in flow-mediated dilation in patients treated with Li-ESWT, indicating that animal studies may correlate well with human studies in terms of penile hemodynamics and endothelial function. More studies are required to elucidate the exact metabolic pathways behind the therapeutic changes associated with Li-ESWT.

Based on the current body of evidence of Li-ESWT, it is not difficult to see a paradigm shift in ED treatment. As with other therapies, stringent patient selection is crucial in maximizing the benefits of Li-ESWT, and more randomized controlled studies are needed to investigate outcomes of patients with vascular ED and nonvascular ED. We conclude that while the exact mechanism of action of how Li-ESWT improves ED is not fully clear, angiogenesis appears to be the key. This treatment option seeks to modify the underlying disease process of ED instead of merely augmenting erectile function.



 
  References Top

1.
Feldman HA, Goldstein I, Hatzichristou DG, Krane RJ, McKinlay JB. Impotence and its medical and psychosocial correlates: Results of the Massachusetts Male Aging Study. J Urol 1994;151:54-61.  Back to cited text no. 1
    
2.
Carson CC 3rd. Phosphodiesterase type 5 inhibitors: State of the therapeutic class. Urol Clin North Am 2007;34:507-15, vi.  Back to cited text no. 2
    
3.
Nishida T, Shimokawa H, Oi K, Tatewaki H, Uwatoku T, Abe K, et al. Extracorporeal cardiac shock wave therapy markedly ameliorates ischemia-induced myocardial dysfunction in pigs in vivo. Circulation 2004;110:3055-61.  Back to cited text no. 3
    
4.
Müller A, Akin-Olugbade Y, Deveci S, Donohue JF, Tal R, Kobylarz KA, et al. The impact of shock wave therapy at varied energy and dose levels on functional and structural changes in erectile tissue. Eur Urol 2008;53:635-42.  Back to cited text no. 4
    
5.
Vardi Y, Appel B, Jacob G, Massarwi O, Gruenwald I. Can low-intensity extracorporeal shockwave therapy improve erectile function? A 6-month follow-up pilot study in patients with organic erectile dysfunction. Eur Urol 2010;58:243-8.  Back to cited text no. 5
    
6.
Chung E, Cartmill R. Evaluation of clinical efficacy, safety and patient satisfaction rate after low-intensity extracorporeal shockwave therapy for the treatment of male erectile dysfunction: An Australian first open-label single-arm prospective clinical trial. BJU Int 2015;115 Suppl 5:46-9.  Back to cited text no. 6
    
7.
Olsen AB, Persiani M, Boie S, Hanna M, Lund L. Can low-intensity extracorporeal shockwave therapy improve erectile dysfunction? A prospective, randomized, double-blind, placebo-controlled study. Scand J Urol 2015;49:329-33.  Back to cited text no. 7
    
8.
Bechara A, Casabé A, De Bonis W, Ciciclia PG. Twelve-Month efficacy and safety of low-intensity shockwave therapy for erectile dysfunction in patients who do not respond to phosphodiesterase type 5 inhibitors. Sex Med 2016;4:e225-32.  Back to cited text no. 8
    
9.
Clavijo RI, Kohn TP, Kohn JR, Ramasamy R. Effects of low-intensity extracorporeal shockwave therapy on erectile dysfunction: A systematic review and meta-analysis. J Sex Med 2017;14:27-35.  Back to cited text no. 9
    
10.
Frey A, Sønksen J, Fode M. Low-intensity extracorporeal shockwave therapy in the treatment of postprostatectomy erectile dysfunction: A pilot study. Scand J Urol 2016;50:123-7.  Back to cited text no. 10
    
11.
Gruenwald I, Appel B, Vardi Y. Low-intensity extracorporeal shock wave therapy – A novel effective treatment for erectile dysfunction in severe ED patients who respond poorly to PDE5 inhibitor therapy. J Sex Med 2012;9:259-64.  Back to cited text no. 11
    
12.
Qiu X, Lin G, Xin Z, Ferretti L, Zhang H, Lue TF, et al. Effects of low-energy shockwave therapy on the erectile function and tissue of a diabetic rat model. J Sex Med 2013;10:738-46.  Back to cited text no. 12
    
13.
Assaly-Kaddoum R, Giuliano F, Laurin M, Gorny D, Kergoat M, Bernabé J, et al. Low intensity extracorporeal shockwave therapy improves erectile function in a model of type II diabetes independently of NO/cGMP pathway. J Urol 2016;196:950-6.  Back to cited text no. 13
    




 

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