Non-surgical treatment of Peyronie's disease (PD) has come a long way since it was first described in 1743. A myriad of treatment options are currently available, including oral, intralesional and external energy therapies. The purpose of this article is to review the contemporary literature on non-surgical therapies for PD, and where possible, focus on randomized, placebo-controlled trials, as well as review the latest guidelines for the management of PD from the International Committee on Sexual Medicine, which conveyed its findings in July 2009. At this time, it appears that a combination of oral agents and/or intralesional injection with traction therapy may provide a synergy between the chemical effects of the drugs and the mechanical effects of traction. Until a reliable treatment emerges, it does appear that some of the non-surgical treatments discussed can be used to stabilize the scarring process and may result in some reduction of deformity with improved sexual function.
In 1743, Francois de la Peyronie described, and was the first to offer treatment for induratio penis plastica, which subsequently became known as Peyronie's disease (PD).1 PD is most simply referred to as a fibrotic wound-healing disorder of the tunica albuginea. It is both a physically and psychologically devastating disorder that causes penile deformity, curvature, hinging, narrowing, shortening and painful erections. Despite a myriad of treatment options, PD remains a considerable therapeutic dilemma due to several factors including an incomplete understanding of its etiopathophysiology and the relative paucity of randomized, placebo-controlled trials. A general explanation of this disorder, which has gained acceptance, is that PD is a disorder in which genetically susceptible individuals experience a localized response to endogenous factors such as tumor growth factor (TGF)-β, which are released in response to repeated microtrauma. This can lead to biological transformation of cells within the tunica albuginea, cell cycle dysregulation, genotypic changes and increased expression of cytokines and free radicals. This inflammatory response leads to unregulated extracellular matrix deposition including fibronectin and collagen, and ultimately plaque formation, which does not appear to undergo proper scar remodeling, leaving an inelastic segment in the involved tunica albuginea.2,3,4,5,6,7,8 Del Carlo et al.9 investigated the role of matrix metalloproteinases (MMPs), the major identified antifibrotic enzymes, and tissue inhibitors of matrix metalloproteinases (TIMPs) in the pathogenesis of PD, using harvested plaque from human PD patients. PD tissue samples were found to have reduced or absent levels of MMP 1, 8 and 13, when compared with patient-matched perilesional tunica. PD fibroblasts were then cultured with soluble MMP and tissue inhibitors of matrix metalloproteinases after treatment with either TGF-1 or interleukin-1. They found that interleukin-1 stimulation increased the production of MMP 1, 2, 8, 9, 10 and 13 in PD fibroblasts, whereas TGF-1 increased the production of only MMP 10 and decreased the production of MMP-13, but markedly increased the production of all tissue inhibitors of matrix metalloproteinases. These findings suggest that PD fibroblasts may be manipulated to encourage scar remodeling in the final phase of wound healing and may be an avenue for future research.
Several non-surgical options are currently being employed in the treatment of PD, which may reduce or stabilize objective measures such as penile curvature and also improve subjective measures such as sexual function, pain and partner satisfaction. PD data outcomes are difficult to interpret without a validated questionnaire, and this is further complicated by a reported spontaneous improvement rate of 13–39%.10,11,12,13 The purpose of this article is to review the contemporary literature on non-surgical therapies for PD, and where possible, focus on randomized, placebo-controlled trials. The recently published guidelines on PD treatment by the International Consultation on Sexual Medicine (ICSM) are noted.14
Pentoxifylline (PTX) has been shown in vitro to attenuate both collagen fiber deposition and elastogenesis through an alpha 1 antitrypsin-related mechanism in normal tunica albuginea-derived fibroblasts exposed to TGF-β1, suggesting a possible role for PTX in the management of PD.15,16 PTX is a nonspecific phosphodiesterase inhibitor, with combined anti-inflammatory and antifibrogenic properties by downregulating TGF-β and increasing fibrinolytic activity. In the only double-blind placebo-controlled study of the efficacy and safety of PTX, 228 patients with early chronic PD, Safarinejad et al.17 demonstrated improvement in penile curvature and plaque volume, when compared with placebo. The study population comprised mostly of patients who had failed previous oral therapies, including potassium aminobenzoate, carnitine, colchicine, tamoxifen and vitamin E, or a combination thereof. When treated with PTX, ventral, dorsal and lateral curvature decreased by 40, 22.2 and 20%, respectively, in a total of 36.9% patients. Curvature was measured using dynamic penile duplex ultrasound before and after an intracavernous injection with 20 μg of prostaglandin E1. Within the placebo group, ventral, dorsal and lateral curvature was shown to increase by 26.9, 31.4 and 22.2%, respectively. Treatment satisfaction was assessed using the Erectile Dysfunction Inventory of Treatment Satisfaction (EDITS) questionnaire.18 Mean EDITS scores after 6 months of treatment were significantly higher, when compared with placebo, 64.2 versus 38.3, respectively. Patients in the treatment group experienced more nausea, vomiting, dyspepsia and diarrhea.17 This was a single-center study, and further randomized, placebo-controlled trials are necessary to optimize treatment regimens and confirm these results.
Potassium aminobenzoate (Potaba)
Zarafonetis and Horrax19 were the first to describe the use of potassium aminobenzoate (Potaba, Glenwood, LLC, Englewood, NJ, USA) for the treatment of PD. It appears to have both an anti-inflammatory and an anti-fibrotic effect due to stabilization of the tissue serotonin–monoamine oxidase activity and a direct inhibitory effect on fibroblast glycosaminoglycan secretion.19,20 Weidner et al.21 performed a randomized, placebo-controlled trial of potassium aminobenzoate, in which subjects were given 3 g orally, four times a day for 1 year. A significant reduction in plaque size was demonstrated in the treatment group. This, however, was not correlated with a decrease in penile curvature. A 2005 follow-up study, also by Weidner et al.,22 included 103 patients with disease duration of no greater than 12 months. Patients were therapy naïve and could not have calcified plaques. This was a randomized, double blind, placebo-controlled trial, which showed that the use of potassium amionobenzoate might protect against the progression of penile curvature. The study also suggests that penile deviation may be prevented with the use of potassium aminobenzoate in patients with Peyronie's plaque without penile deviation. In the 13 patients with an initial straight penis, zero patients developed a deviation while taking potassium para-aminobenzoate. However, six out of eight patients (75%) receiving placebo developed a new penile curvature. There were no relevant differences between potassium aminobenzoate and placebo, with regard to improvement of pre-existing penile deviation.
Colchicine inhibits fibrosis and collagen deposition primarily by inhibiting neutrophil microtubules.23 Colchicine has been used both as a primary oral therapy for PD, as well as in combination with other modalities. Kadioglu et al.24 treated 60 patients in the acute phase of PD (mean duration 5.7 months±4.3 months), using 1 mg of colchicine twice daily, with a mean follow-up of 11 months. They found significant improvement of pain in 95% of men; however, although 30% of patients reported improved curvature, 22% of patients reported worsened curvature. Akkus et al.25 administered an escalating dose of colchicine in a non-randomized, non-placebo-controlled fashion to 19 patients with PD over a 3–5-month period. Of these patients, 36% noted a reduction in curvature and 63% reported an improvement in the palpable plaque. Of the patients who were experiencing painful erections at the time of treatment initiation, 78% had resolution of this symptom. Safarinejad26 performed a randomized, placebo-controlled trial of colchicine in 2004, with 84 men with PD. Mean disease duration was 15 months (range 6–42 months) and 73.8% had failed before medical therapy potassium aminobenzoate, vitamin E and/or tamoxifen. Colchicine was no better than placebo in improving pain, curvature or plaque size as measured by ultrasound. This is the only randomized trial looking at the effects of colchicine as a monotherapy. Side-effect profile includes gastrointestinal distress, diarrhea and aplastic anemia.
Tamoxifen is a selective estrogen receptor modulator that has both agonist and antagonist effects on target tissues depending on tissue-specific estrogen receptor expression. In addition, tamoxifen is reported to affect the release of TGF from fibroblasts and blocks TGF-receptors, thus potentially reducing fibrogenesis.27,28 A study in 1999 by Teloken et al.29 failed to show any statistically significant difference between tamoxifen and placebo. This study included 25 patients who were given tamoxifen 20 mg twice daily for 3 months. There was no demonstrable improvement in pain, curvature or plaque size.
Carnitine is a naturally occurring metabolic intermediate. Carnitine facilitates the entry of long chain fatty acids into muscle mitochondria, which are then used as an energy substrate. Carnitine is hypothesized to inhibit acetyl coenzyme-A, which may help in the repair of damaged cells.30 Safarinejad et al.,31 in a double-blind, placebo-controlled trial, compared L-carnitine, L-carnitine plus vitamin E, and vitamin E alone with placebo. A total of 236 men with PD were randomized amongst the four groups for a total of 6 months. The study failed to demonstrate improvement in pain, curvature or plaque size in any group.
Vitamin E is one of the oldest described oral treatments for the treatment of PD, and there does appear to be a biochemical mechanism to support its use.32 Vitamin E, a fat-soluble vitamin metabolized in the liver, excreted in bile is an antioxidant that is thought to limit oxidative stress of reactive oxygen species known to be increased during the acute and proliferative phases of wound healing.33 Increased free radical expression and a prolonged inflammatory phase of wound healing has been demonstrated in PD.4,33 In 1983, Pryor and Farell34 conducted a double-blind, placebo-controlled crossover study evaluating vitamin E for the treatment of PD in 40 patients. No significant improvements were noted in plaque size or penile curvature. In 2007, Safarinejad et al.35 compared the effects of vitamin E with L-carnitine, separately or in combination with placebo, and found no significant difference in the improvement in pain, curvature or plaque size. The study involved 236 patients with early chronic PD, which was defined as pain during erection, penile curvature not interfering with vaginal penetration, palpable scar which is not painful, hyperechoic lesions, total plaque area less than 2 cm2, and absence of calcification. Patients had received two or more previous treatments for PD, including potassium aminobenzoate, tamoxifen, colchicine, systemic steroids and intralesional verapamil. Gelbard et al.12 compared vitamin E therapy to the natural history of PD in 97 patients with disease duration ranging from 3 months to 8 years; no significant differences were found between the two groups in terms of curvature, pain or the ability to have intercourse. To date, no placebo-controlled trials using vitamin E have demonstrated any clinical benefit in the treatment of PD, and there is some evidence that vitamin E may also increase the risk of cerebrovascular events.36
Procarbazine is an oral alkylating agent primarily used as a component of chemotherapy regimens for Hodgkin's lymphoma, as well as primary CNS lymphoma and high-grade gliomas.37 A study by Bystrom38 in 1976 showed positive results, although this has not been re-demonstrated in further studies. Morgan and Pryor39 reported in 1978, 91% of patients failing to improve, or becoming worse. Procarbazine is a known cytotoxic agent with significant side-effect profile including hepatotoxicity, myelosuppression, central nervous system effects and gastrointestinal disturbances.40
Oral therapy conclusion
Overall, there appears to be no oral therapy that has been shown to reliably reduce penile deformity in a clinically meaningful way. The recently published ICSM guidelines on PD by Ralph et al.14 state that ‘There is evidence that there is no benefit with respect to deformity reduction with any oral therapy, including vitamin E, potassium aminobenzoate, colchicine, tamoxifen, and carnitine.’ Refer to Table 1 for a summary of oral treatments for PD.
Calcium channel blockers
Verapamil is a calcium channel blocker that, in vitro, has been shown to inhibit local extracellular matrix production by fibroblasts, reduce fibroblast proliferation, increase local collagenase activity and alter the cytokine milieu of fibroblasts.41,42 In 1994, Levine et al.43 were the first to introduce intralesional verapamil for PD. This was the first of the three published non-randomized trials by this group. The first study evaluated the response to dose escalation for efficacy and toxicity in 14 men. No adverse effects were noted, and subjectively, there was significant measured improvement in plaque-associated penile narrowing (100%) and curvature (42%). Objectively, a decreased-plaque volume of greater than 50% was noted in 30% of the subjects. Plaque softening was noted in all patients, whereas 83% noticed that plaque-related changes in erectile function had arrested or improved.43 The second trial of 38 men demonstrated in patients with early-stage disease defined as PD for less than 1 year, a rapid reduction of pain after a mean of 2.5 injections in 97% of men, improvement in sexual function, reduction in deformity and a mean reduction of 21° in 65% of men completing the protocol. In late-stage disease, defined as PD for greater than 1 year, intralesional verapamil decreased curvature in 44% of the men, with a mean reduction in curvature of 23°,44 suggesting that there was efficacy in men with more mature disease. The third trial was the largest published single-center study of intralesional verapamil.45 This was a prospective non-randomized study of 140 patients with mean duration of disease of 17.7 months, and 77.5% of patients had received previous therapy including vitamin E, potassium aminobenzoate or colchicine. All patients received a standardized dose of 10-mg verapamil (5 mg 2 ml−1) diluted to 10 ml total volume with injectable saline. The solution was distributed throughout the plaque. Each set of injections was administered at a prescribed interval of 2 weeks for a total of 12 treatment sessions. Of the patients who completed therapy, 121 were evaluated with a second duplex ultrasound, which revealed that curvature decreased in 73 (60%, mean decrease in curvature from baseline of 30°, range 5°–90°), increased in 10 (8%, mean increase of 26°, range 5°–45°) and remained unchanged in 38 (31%).45 In these three studies, subjects received 12 bi-weekly injections over 6 months. The rationale is that scar remodeling occurs at ‘glacial speed.’ Therefore, repeated treatment over time would encourage better results. This is in contradistinction to the study by Bennett et al.,46 in which 94 subjects received 10 mg of intralesional verapamil biweekly, but for only six injections over 3 months. These authors concluded that intralesional verapamil in this regimen resulted in curve improvement in 22% and stabilization of curvature in 60%. This group of investigators previously reported that 48% of patients had curvature progression in a no-treatment natural history observation study.47 The first randomized, single-blind trial of intralesional verapamil was published in 1998 by Rehman et al.48 Significant improvements were noted in terms of erection quality and plaque volume. A trend towards improvement in curvature was also noted in this rather small study. In 2009, Shirazi et al.49 performed a randomized, single-blind, placebo-controlled trial, comparing intralesional verapamil with saline. The study included 80 patients who received 10 mg of intralesional verapamil for only six bi-weekly injections. The study failed to demonstrate any significant differences/improvements in penile deformity, pain, plaque softening or sexual function between the two groups. Recently nicardipine, a calcium channel blocker, was compared with saline injection as a potential treatment for PD. Soh et al.50 assigned 74 patients randomly to nicardipine or saline injection. Subjects were administered a total of six bi-weekly injections. Objective outcomes included change in International Index of Erectile Function (IIEF)-5 score, an international pain scale, plaque size and penile curvature as measured by photographs of a pharmacologically induced erection. The study demonstrated significant improvement in IIEF-5 score and in plaque size only in the nicardipine group. Reduction in penile curvature was seen in both the nicardipine and saline groups. The article, however, does not provide specific values for degrees or percentage of curve reduction. No severe side effects were observed in the treatment group.50
Duncan et al.51 reported in 1991 that interferon (IFN) α, β and γ decrease the rate of proliferation of fibroblasts in Peyronie's plaques in vitro, reduce the production of extracellular collagen, and increase the activity of collagenase. Initial studies performed by Wegner et al.52,53 demonstrated low rates of improvement using IFN-α2b, but a high incidence of side effects, including myalgias and fever. In 2006, Hellstrom et al.54 reported in a multicenter, placebo-controlled trial of 117 men with PD for more than 12 months, who underwent six bi-weekly injections of either IFN-α2b or saline for a total of 12 weeks. Average curvature in the treatment group improved 13° versus 4° in the placebo arm. Pain resolution was noted in 67% of the treatment patients versus 28% for the placebo. This study has gained significant attention, as it was the first placebo-controlled trial of intralesional injection therapy for PD, which offered evidence of treatment benefit. Yet, later in 2006, Inal et al.55 compared intralesional IFN-α2b injections with and without vitamin E versus vitamin E alone in 30 men. Mean duration of disease was 10.8 months (range 6–18), and all patients were treatment-naive before entry into the study. Curvature was measured during duplex ultrasound of a pharmacologically induced erection. The study showed no statistically significant difference in penile curvature, when compared with the initial measurements of the individual groups or among the three groups.
Collagenase is an enzyme, which catalyzes the breakdown of collagen, the primary component of the dense fibrotic PD plaque and, therefore, appears to be a sensible injectable agent to lyse the collagen types I and III found in PD plaques. Gelbard et al.56,57 were the first to study clostridial collagenase in vitro for the treatment of PD in 1982. Jordan58 assessed the efficacy and safety of intralesional clostridial collagenase injection therapy in a non-controlled trial with 25 men with PD. Mean duration of PD was 39.2 months, average penile deviation was 53° and no alternative treatment could be used within 1 month before study entry. Patients were treated with three injections of clostridial collagenase 10 000 untis per 0.25 ml per injection administered over 7–10 days. A repeat treatment (i.e., three injections of collagenase 10 000 untis per 0.25 ml per injection) was administered over 7–10 days at 3 months. Angle of deformity was measured under vacuum-induced erection at baseline, 3, 6 and 9 months, and demonstrated a positive treatment response as defined by a decrease in curvature of 25% from baseline in 57%. Positive treatment results peaked at 3 months and declined progressively at 9 months. The study author attributed this to a loss of successful patients to follow up while non-responders remained in the study pool. Collagenase therapy was generally safe and well tolerated. Adverse events occurred in 20 (80%) patients, with edema, penile pain and ecchymosis as the most common. A double-blind, placebo-controlled trial by Gelbard et al.59 in 1993, composed of 49 men, showed a statistically significant improvement in vacuum-induced curvature in the treatment group when compared with placebo; however, maximal improvement ranged from 15° to 20° and was only seen in the patients with curvature of less than 30° and plaques of less than 2 cm in length. Currently, this agent is in a large scale, multicenter, multination, randomized, placebo-controlled trial,60 which may become the first FDA-approved treatment for PD.
Corticosteroids have been used for the treatment of PD due to their anti-inflammatory effects.61 Several non-randomized studies have reported decrease in plaque size and penile pain, whereas others have shown no difference from the natural history of the disease.62,63 In 1980, Williams and Green64 showed in a prospective study spanning 1 year, improvement in 3% of patients. Triamcinolone was administered every 6 weeks for 36 weeks; 33% reported subjective improvement in pain and plaque size. Most recently in 2010, Dickstein et al.65 reported improvement in penile pain associated with erections after subcutaneous steroid injection. A total of 16 patients received 50 mg subcutaneous non-intralesional injections of triamcinolone every 4–6 weeks. All 16 patients reported improvement in pain with mean pre- and post-treatment pain scores of 6.6 ±2.1 and 0.5±0.5, respectively. Mean pain-free duration was 23.8 months (range 3–5 months). There were no reported adverse events in this trial. Future studies may be required to validate these findings. Previously reported adverse events include tissue atrophy, thinning of skin and immunosuppression.
Orgotein is a pharmaceutical version of copper/zinc superoxide dismutases that possesses anti-inflammatory properties. Through its actions, superoxide radicals are converted to more benign peroxide and oxygen molecules, potentially reducing inflammation, which would otherwise lead to fibrosis. Orgotein was originally shown in 1981 to improve penile pain, curvature and plaque size by two independent studies.66,67 These studies, however, lacked appropriate controls and had flawed experimental design. To date, no randomized, placebo-controlled, double-blind trials have been published that identify a statistically significant effect of this therapy. Reported adverse effects include pain, swelling, stiffness, dysesthesias and skin rashes. Due to off-label reports of toxicity, orgotein is not available in the United States.68
Intralesional therapy conclusion
The ICSM guidelines regarding intralesional therapy states there are, ‘No objective measures of therapeutic benefit,’ non-controlled for intralesional steroids. On collagenase, the ICSM guidelines states, ‘Several small trials showed limited benefit. It is currently being studied in a phase 3 trial.’ ‘Verapamil appears to make scientific sense but there are no large scale placebo controlled trials.’ On IFN, the ICSM guidelines states, ‘One placebo-controlled trial showed an outcome benefit with interferon over saline.’ On steroids, the ICSM guidelines states, ‘No objective measures of therapeutic benefit.’14 There are no ICSM guidelines regarding the use of intralesional orgotein. Refer to Table 2 for a summary on intralesional therapy.
External energy therapies
Iontophoresis involves the transport of ions through tissue by means of an electric current. Stancik et al.69 recently demonstrated the decreased expression of basic fibroblast growth factor (bFGF) mRNA and bFGF protein expression in excised Peyronie's plaques after having undergone electromotive drug therapy with dexamethasone, verapamil and lidocaine when compared with therapy naïve plaques. This study also showed an overexpression of TGF-β protein and the TGF-β receptor in those treated using electromotive drug therapy. In 2007, Levine and co-workers70 reported in a randomized, double-blind, placebo-controlled trial of 42 men with PD, which compared verapamil with saline and showed similarly measured curve reduction in both groups. The total number of patients experiencing significant improvement (20° or greater) was seven patients (30%) in the treatment group and four (21%) in the saline group. Although a greater percentage of patients treated with verapamil had improved curvature, the results were not statistically significant. The authors concluded that the positive response may be due to the electric current, which has been noted in other fields such as dermatology to induce wound healing.71 Di Stasi et al.72 in 2005 compared patient's receiving verapamil and dexamethasone using iontophoresis versus 2% lidocaine iontophoresis in a prospective, randomized, double-blind, placebo-controlled study of 96 patients. In the treatment group, plaque volume decreased, mean measured-erect penile curvature was reduced from 43° to 21° as measured by photographs and duplex ultrasound during full pharmacologically induced erection. No significant changes were noted in the lidocaine group.
The ICSM guidelines state, ‘Several controlled trials had evidence of reduced deformity following iontophoresis treatment using verapamil and dexamethasone’.14
Penile electroshock wave therapy (ESWT)
Local penile ESWT has been suggested to be of benefit for the treatment of PD. Various hypotheses about its mechanism of action exist, including direct damage to the plaque, resulting in an inflammatory reaction with increased macrophage activity leading to plaque lysis, improved vascularity resulting in plaque resorption, and the creation of contralateral scarring of the penis resulting in ‘false’ straightening.73 Hauck et al.74 randomized 43 men to ESWT or oral placebo for 6 months. No significant effect was noted in terms of curvature, plaque size or subjective improvement in sexual function or rigidity. Palmieri et al.75 randomized 100 patients to ESWT or placebo shocks, which were delivered via a nonfunctioning transducer. This is the only published placebo-controlled trial of ESWT. Four weekly treatments of 2000 shocks were administered to the treatment group. They reported a disappearance of pain in 53% in the treatment group versus 7% in the placebo group. At 24 weeks follow-up, there was no significant difference in plaque size or curvature in the ESWT group, but the placebo group showed a statistically significant increase in both plaque size and curvature. The study authors concluded that ESWT appears to stabilize deformity progression. However, the differences between the two treatment arms of 2°–4° do not appear clinically significant. The ICSM guidelines state, ‘There is evidence that ESWT does not improve PD-related deformity.’14
Penile traction devices
Placing tissues under tension has been used in a number of fields including orthopedics, maxillofacial and plastic surgery. Much work has gone into elucidating the mechanisms through which mechanical strain can yield a biological response in several non-penile models including bone, muscle and Dupuytren's scar. Mechanical stress modulates cell function through a process called mechanotransduction by activating multiple signal transduction pathways via the internal cytoskeleton and extracellular matrix.76 Several signaling cascades activated by cellular tension activate downstream signaling pathways such as cyclin D1-mediated cell cycle proliferation,76 paracrine signaling via fibroblast growth factor and platelet-derived growth factor,77 and activation of mechanosensitive calcium channels and the IP3/DAG pathway.78 On a histologic level, tension has been demonstrated to reorient collagen fibrils parallel to the axis of stress.79,80 On a genetic level, mechanical shear stress has been shown to cause an upregulation of ‘antifibrotic’ genes.81
In the first published pilot study on traction therapy for PD, Levine et al.82 evaluated 11 men with PD, 8 had failed non-surgical treatments. Mean duration of disease was 29 months (range 8–72 months). Penile traction therapy was then initiated with the FastSize Penile Extender (Aliso Viejo, CA, USA) for 2–8 h per day for 6 months. Curvature was noted to be reduced in all men with a mean reduction of 22° (range 10°–45°). There was an overall mean reduction of curvature of 33% from an average pre- and post-treatment curvature from 51° to 34°. The mean IIEF was found to increase from 44.6 to 55, and specifically, the IIEF-erectile function domain (IIEF-EF) increased from 18.3 to 23.6 for the treatment group. There was no change in penile sensation or new ED in this group. Also, stretched penile length improved in all subjects with an increase in length up to 2.5 cm. Gontero et al.83 also evaluated the efficacy of traction therapy in PD. Fifteen patients were evaluated for change in curvature as a primary endpoint. Patient population was composed of those with PD for greater than 12 months, curvature less than 50°, and fibrous plaque diagnosed on physical exam or ultrasound. Traction was performed using the Andropenis (Andromedical, Madrid, Spain) penile extender for 5–9 h per day for a total of 6 months. Penile curvature decreased in six patients from a mean baseline value of 31° (s.d. 1.55) to 27° (s.d. 2.79) after 6 months of treatment (P=0.059). Curvature worsened in one patient and remained unchanged in eight patients. Both studies reported length gain, which is significant in that shortening is a common occurrence in the natural history of PD. In a critical review of these two studies, Greenfield84 described factors, which may account for the different results in these two studies, including duration of disease, plaque calcification and methodology of measuring curvature.
The ICSM guidelines states, ‘Early evidence from two small non-controlled prospective trials have reported a reduction of deformity and increased penile length with traction therapy’.14 Refer to Table 3 for a summary of external energy therapies for PD.
Non-surgical treatment of PD has come a long way since the time of de la Peyronie. Yet, a reliable and effective treatment still eludes the practicing urologist. At this time, it appears that a combination of oral agents and/or intralesional injection with traction therapy may provide a synergy between the chemical effects of the drugs and the mechanical effects of traction. Ongoing trials at our institution by Abern and Levine85 are confirming this presumption. Until a reliable treatment emerges, it does appear that some of the non-surgical treatments discussed can be used to stabilize the scarring process, and may result in some reduction of deformity with improved sexual function. This seems appropriate given the low adverse event profiles and the risk of more advanced deformity when no treatment is offered.
About this article
Current Sexual Health Reports (2016)