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Peyronie's Disease (Condition)

Peyronie's disease (PD) is an acquired fibrotic disorder of the tunica albuginea that produces palpable plaque, penile curvature, painful erections, erectile dysfunction, shortening, and substantial psychological morbidity. Prevalence is most often estimated at 3–9% of adult men (reports range 0.1–20.3%, highest with diabetes and ED), with mean onset about 53 years.[10][51][1] In an untreated acute-phase subset, penile deformity resolved spontaneously in 3.2% of 63 men after a mean 8.4 months; in a separate untreated cohort of 246 men assessed at a mean disease duration of 18 ± 7 months, 12% of those with curvature improved.[3][4] The single FDA-approved non-surgical treatment is intralesional collagenase clostridium histolyticum (CCH, Xiaflex); surgery is an option for stable disease with functionally significant deformity when treatment is desired.[5][6][7]

The AUA defines PD as "an acquired penile abnormality characterized by fibrosis of the tunica albuginea, which may be accompanied by pain, deformity, erectile dysfunction, and/or distress." It belongs to a broader family of superficial fibrosing disorders with Dupuytren's contracture, Ledderhose disease, and tympanosclerosis.[6][8][9]

Epidemiology​

  • Prevalence 3.2–8.9% in most population estimates (0.1–20.3% across reports; likely under-reported)[10][51]
  • Mean age at onset about 53 years in the Cochrane review; a separate 307-man series reported mean age at presentation of 52.8 years (range 23–76).[1][3]
  • Diabetic men with ED. PD was found in 42/206 (20.3%) diabetic men evaluated for ED in one study; the AUA guideline reports 20.3% as the upper end across specific populations.[6][10][64]
  • White men over-represented (adjusted OR 8.47, wide CI 1.98–36.2, in a Brazilian case-control study)[11]
  • Strong association with Dupuytren's contracture[11][12]: 26% (95% CI 17–35%) of men presenting for Dupuytren contracture reported PD-like symptoms in a survey of 85 respondents[54], and a genetic-association study found the WNT2 locus on chromosome 7, already linked to Dupuytren's disease, was also associated with PD, supporting a shared genetic basis.[55]

Pathophysiology​

PD is a penile wound-healing disorder in genetically predisposed men.[2][6][8][13]

  1. Inciting event. Microvascular trauma to the tunica from penile buckling during intercourse (often unrecalled)
  2. Inflammatory phase. Extravascular protein deposition, fibrin trapping, macrophage recruitment, cytokine overexpression (TGF-β, IL-1, IL-6, PDGF, FGF), elastase release
  3. Fibroproliferative phase. MMP/TIMP imbalance (decreased MMPs, increased TIMPs), excessive collagen deposition, shift from type I to predominantly type III collagen
  4. Plaque maturation. Progressive fibrosis, calcification in some, stable scar

TGF-β is the central profibrotic mediator; PAI-1, PTX-3, HIF, and IgG4 also contribute. Oxidative stress links PD to systemic metabolic disease.[13][14]

Risk Factors​

FactorAssociation
Penile trauma / bucklingProposed trigger for abnormal tunical wound healing in susceptible men[1][2]
Dupuytren's contractureShared fibrotic diathesis[11][12]
Diabetes mellitusIn a retrospective series of 197 men with both diabetes and PD, early-onset and poorly controlled diabetes correlated with PD complications[10]
Hypertension, hyperlipidemia, smokingCommon comorbidities; mostly tied to concurrent ED rather than PD severity[15]
NAFLD / insulin resistanceAssociated with PD in one cross-sectional pilot (49 cases, 50 controls); NAFLD was the only logistic-regression predictor in that dataset, and the pathogenic link remains hypothetical.[14]
Prior urologic instrumentationTURP, cystoscopy (case-control association)[12]
Radical prostatectomyIn a selected cohort of 1,011 men attending a sexual-medicine clinic after RP, 15.9% developed PD within 3 years (mean 13.9 ± 0.7 months); younger age and white race were associated with PD.[52]
Thiazide diureticsAdjusted OR 2.29 in a single case-control study[11]
White raceAdjusted OR 8.47[11]

In a retrospective series of 469 men with PD, comorbidity count or severity did not correlate with curvature severity, while hypertension, lipid abnormalities and diabetes were more prevalent among those with concurrent ED.[15] A separate retrospective series of 197 men with both diabetes and PD found associations of early diabetes onset and rising HbA1c with earlier PD onset or plaque formation.[10]

A pilot study of 121 men with PD found testosterone deficiency (total testosterone <300 ng/dL and/or free testosterone <1.5 ng/dL) in 74.4%; men meeting that definition had greater mean curvature than those with normal testosterone (54.3° versus 37.1°, P = .006), and free testosterone inversely correlated with curvature (r = −0.314, P = .016).[53]

Disease Phases​

PhaseDurationFeaturesImplications
Acute (active)Typically 12–18 months from onsetPainful erections, evolving deformity, plaque maturationIn a separate long-term survey, 42% reported penile pain and 64% of those with pain reported complete resolution; in an untreated recent-onset cohort, 89% of men with pain reported resolution. Non-surgical interventions favored[1][6][16][4]
Chronic (stable)After active phaseFibrosis stabilizes, pain typically gone, fixed deformityThe AUA defines stable disease as symptoms clinically quiescent or unchanged for at least 3 months (pain, if present, is less common and usually with erection); surgical series most often required 12 months of symptoms with 3–6 months of stable curvature. The EAU accepts pain resolution and curvature stability for at least 3 months as criteria of stabilization[6][51]

Trost, Mulhall and Hellstrom (2024) proposed the PTNM classification from a retrospective review of 1,098 men with penile deformity, with a mailed survey of 719 men for the relapsing-remitting subtype. It identified four Peyronie's subtypes (classical or nonclassical, calcifying, progressive and relapsing-remitting) and three non-Peyronie's curvature categories (congenital, maturational and trauma-induced), recorded as P (Peyronie's subtype), T (trauma, absent or present), N (non-Peyronie's component) and M (mode, stable or active). Stable disease was defined by subtype: at least 3 months for classical disease, and for progressive, calcifying or trauma-induced disease either 12 months or more with at least 3 months of stability or at least 6 months of stability. Penile pain did not reliably predict progression or stability.[62]

Natural History​

OutcomeRate
Curvature worsened48% in an untreated cohort; 20% self-reported among 125 eligible long-term survey responders. Penile deformity deteriorated in 30.2% of a separate 63-man acute-phase subset[3][4][16]
Curvature stable40% in an untreated cohort and 37% self-reported among 125 eligible long-term survey responders; penile deformity was unchanged in 66.7% of a separate 63-man acute-phase subset[3][4][16]
Curvature spontaneously improvedCurvature improved in 12% of men with curvature in one untreated cohort; penile deformity resolved completely in 3.2% of 63 men in a separate untreated acute-phase subset[3][4]
Pain resolutionComplete resolution in 64% of survey responders who reported penile pain and 89% of men with pain in an untreated recent-onset cohort[4][16]
Penile shortening65% self-reported among 125 eligible survey completers at a median 8.4 years since onset; mean stretched flaccid length fell from 12.2 to 11.4 cm by a mean disease duration of 18 ± 7 months in an untreated cohort[4][16]
Erectile function worsened60% of 125 eligible long-term survey completers self-reported decline (ED already present in 32–54% at presentation in two separate cohorts)[3][4][16]
Negative self-esteem impact60% of 88 survey respondents among 514 eligible conservatively managed men reported that PD negatively affected their self-esteem[17]

Among 125 eligible respondents to a survey of conservatively managed patients, the median interval from symptom onset to survey was 8.4 years; 43% reported curvature resolution, while most reported length loss and worsening sexual function and psychosocial distress.[16]

Clinical Presentation​

  • Penile curvature. Dorsal (45–72%), lateral (11–29%), ventral (about 17%)[3][4]
  • Palpable plaque
  • Painful erection. Acute phase
  • ED in 32–54% at presentation across two cohorts; probability rises with age > 60, duration > 12 mo, and ≥ 1 vascular risk factor (86.7%)[3][4]
  • Penile shortening. Reported by 65% of 125 eligible survey completers who had been conservatively managed (median 8.4 years since symptom onset)[16]
  • Hourglass deformity or hinge effect. Buckling instability that defeats penetration
  • Psychological distress. Clinical and population studies report psychosocial burden among men with PD.[1][6][18] In a single-practice cross-sectional study of 245 men with PD, 81% reported emotional problems and 54% relationship problems attributable to PD; in a separate 92-man clinical cohort, 48% exceeded the CES-D depression cutoff.[67][68]

Psychological burden​

A Swedish 3.5-million-man cohort:[18]

OutcomeHR (vs general population)
Depression1.7
Anxiety disorder1.9
Self-injurious behavior2.0

5-year cumulative depression risk 7.0% versus 4.4%; 10-year 12.5% versus 8.7%.[18][20] An online-forum thematic analysis reported depressed mood in 33% and isolation in 18% of 225 patient posters; among 52 partner posters, 21% reported sexual dissatisfaction and 7.7% dyspareunia. Across all 277 posters, relationship disruption was reported by 5.1% and termination by 3.6%.[19] The AUA calls for documenting distress during evaluation and discussing treatment options; psychological referral may be considered when distress is significant.[6][7] See the canonical Psychosexual Therapy page for the sensate-focus or CBT or MBI or couples-therapy framework.[6][7]

Diagnostic Evaluation​

All four major guidelines (AUA, EAU, CUA, ISSM) converge on the workup.[6][7][21]

StepRole
History (with genital examination)Onset, duration, deformity, pain, shortening, erectile function, prior treatment, sexual / psychological impact
Photographs of erect penis (patient-provided)Document deformity for objective comparison[22]
Physical examStretch and palpate the flaccid penis for plaque size, location and possible calcification; document stretched or erect penile length and assess curvature during erection.[51]
Intracavernosal injection (ICI) testAUA recommends before invasive intervention (with or without duplex); documents curvature, hinge effect and erectile response[6][7]
Penile duplex Doppler ultrasound (optional)Calcified vs non-calcified plaque; vascular integrity (PSV, EDV); identifies vasculogenic ED that changes the operation[6][22][23][24]
PDQ and IIEF questionnairesSymptom bother and erectile function domains
MRI (select cases)Thin-section T2-weighted MRI can characterize plaques and demonstrate subtle deformities such as corporal narrowing better than ultrasound, though it shows calcification poorly; cost and availability limit it to select-case use, not routine workup[24]

Hinge instability can be assessed by applying axial pressure to the glans during erection and observing whether the shaft buckles, with instability recorded as none, mild, moderate or severe; this grading is arbitrary and unvalidated. Each curve is measured separately, with the maximal curve's distance from the coronal sulcus recorded to help localize the site for injection, and angle measurement is best deferred until erection rigidity exceeds 80%, since curvature varies with rigidity — a center-specific threshold rather than a validated cutoff. This approach has been described by Mulhall and Jenkins.[61]

Objective measurement is preferred over patient self-report: before standardized photographs and protractor measurement during full erection, 54% of patients overestimated and 26% underestimated curvature, with only 20% accurate within 5°.[56] Ultrasound can detect sonographic variants without a palpable abnormality: in a series of 722 men evaluated for PD or ED, isolated septal scarring and punctate scarring were found in 217 (30%) and 197 (27%), respectively; physical examination was normal in 72/217 (33%) and 148/197 (75%) of those subgroups. A separate imaging review describes ultrasound detection of gross plaque calcifications, which can inform treatment planning; calcification and CCH candidacy are discussed below.[57][58]

Management​

Treatment is dictated by disease phase, deformity, erectile function, and patient goals. A 2026 Guideline of Guidelines comparison found broad consensus across AUA, EAU, CUA, and ISSM.[7][21]

Important caveat on non-surgical evidence​

The 2023 Cochrane systematic review (14 RCTs, 1,810 men) found little evidence for most non-surgical therapies. Collagenase reduced curvature by a mean 6.9° at 52 weeks versus placebo (moderate certainty) with more adverse events (RR 2.32); traction (7.4°, one trial) and verapamil or ESWT estimates were very low certainty.[1]

A. Oral therapies​

The AUA position:[6]

  • Should not offer vitamin E, tamoxifen, procarbazine, omega-3 fatty acids, or vitamin E with propionyl-L-carnitine .[6] The panel adds that oral therapy is not appropriate for stable disease
  • May offer oral NSAIDs for pain in active disease [6]
  • Evidence for pentoxifylline, potassium para-aminobenzoate (Potaba), colchicine and coenzyme Q10 is insufficient even for a conditional AUA recommendation[6]
AgentMechanismEvidenceAUA
Vitamin EAntioxidantMixed trial results for curvature; largest trial found no significant difference[25]Should not offer [6]
TamoxifenAnti-fibroticOne placebo-controlled RCT (25 men, assessed at 4 months) found no significant difference in pain, curvature, plaque size, or IIEF (low to very low certainty)[25]Should not offer [6]
PentoxifyllinePDE inhibitor / anti-inflammatoryInsufficient evidence[6]No recommendation
PotabaAnti-fibroticUncertain benefit[1][6]No recommendation
ColchicineAnti-inflammatoryInsufficient evidence[6]No recommendation

B. Intralesional injection therapies​

Collagenase clostridium histolyticum (CCH, Xiaflex) — only FDA-approved option[5][6][26][27][28]​

  • US label: Adult men with palpable plaque and curvature ≥ 30° at treatment initiation; XIAFLEX is contraindicated for a plaque involving the penile urethra or in a patient with prior hypersensitivity to XIAFLEX or therapeutic collagenase. AUA selection is narrower: stable disease, curvature >30° and <90°, and intact erectile function with or without medication, given with clinician and patient modeling , with counseling on ecchymosis, swelling, pain and corporal rupture before starting .[5][6]
  • Protocol (IMPRESS): Up to 4 cycles about 6 weeks apart (8 injections total); each cycle has two 0.58-mg injections 1–3 days apart, clinician modeling 1–3 days after the second injection, and daily home modeling for 6 weeks. Do not give subsequent cycles if curvature is <15° after an earlier cycle or further treatment is not clinically indicated.[5][26]
  • IMPRESS I & II (832 randomized; 612 in the label-defined mITT efficacy population): A post hoc pooled analysis found mean curvature improvement of 17.0° (34%) with CCH versus 9.3° (18.2%) with placebo, a net difference of about 7.7° (Cochrane estimate 6.9° at 52 weeks).[26][5][1] PDQ bother scores fell by 2.8 versus 1.8 points, and three corporal ruptures were surgically repaired.[1][5][26]
  • Real-world multi-institutional (n = 918): Mean curvature 48.2° to 32.9° (30.1% improvement); 68.7% achieved ≥ 20% improvement; completing ≥ 4 cycles predicted better outcomes[27]. In a separate single-center registry, 296 men received at least one CCH injection, but 84 had interval-to-final curvature measurements after completing 8 injections. Among those with ≤10° improvement after the first 2 cycles, 70% had further curvature improvement over the final 2 cycles, versus 31% of those with >10° initial improvement — a figure for counseling a man discouraged after 2 cycles against stopping early.[60]
  • Calcification predicts a smaller response: men with no plaque calcification had significantly greater curvature improvement with CCH than those with moderate or severe calcification (28.1° versus 10.3°, P = .04).[59]
  • Meta-analysis (n = 1,480): 35% pooled curvature improvement; 41% bother improvement[28]
  • AEs and precautions: Bruising, swelling and pain are common; corporal rupture and severe hematoma, sometimes followed by skin necrosis, are important risks. Inject only into the plaque, avoiding the corpora cavernosa, urethra, nerves and vessels. Promptly assess a post-injection pop, sudden detumescence, marked swelling or bruising, hematuria or difficulty urinating for serious penile injury.[5] The label also warns of anaphylaxis, acute post-injection back pain, and pain-associated syncope or presyncope.[5] Follow REMS and label counseling: avoid XIAFLEX in coagulation disorders or with anticoagulants other than low-dose aspirin, do not use a vacuum erection device during treatment, and avoid sexual activity between injections and for at least 4 weeks after the second injection until pain and swelling resolve.[5][27][28][29]
  • No significant penile shortening[29][30]
  • Available in the US; withdrawn from Europe[25]

Other intralesional agents​

  • Interferon-α2b. The 2015 AUA guideline states clinicians may administer it , on one placebo-controlled trial with mean curvature reduction 13.5° versus 4.5° with placebo, and asks for counseling about sinusitis, flu-like symptoms and minor penile swelling.[6] Historical curvature or pain benefit, but EAU 2026 no longer recommends it given limited evidence and withdrawal from US and European markets.[31][51]
  • Verapamil. Intralesional evidence is weak and inconsistent; AUA 2015 offers a Conditional Recommendation (Grade C) that clinicians may offer it and a Moderate Recommendation (Grade C) against electromotive delivery.[6][25][31]
  • Hyaluronic acid. EAU offers a weak acute-phase option with limited evidence; this is not an FDA-approved PD indication.[5][51]

C. Mechanical therapies​

Penile traction therapy (PTT)​

Mechano-transduction increases MMP activity and remodels collagen.[25]

  • RestoreX. The most studied modern device; only 30–90 min/day required (versus 3–8 h for older devices)[32]
    • RCT (n = 110 randomized): At 3 months, mean composite curvature changed −11.7° in 62 traction users versus +1.3° in 27 controls (p < 0.01)[32]
    • 6-month open-label, as-treated subgroup (n = 37 using RestoreX ≥15 min/day): 95% had length gains (mean 2.0–2.2 cm); 61% had curve improvements (16.8–21.4°)[33]
    • Combined with CCH (nonrandomized single-center registry; 113 of 287 men with traction-use data completed therapy with objective outcomes): RestoreX plus CCH was associated with 49% mean curvature improvement versus 31% with CCH alone; the RestoreX group was 6.9× more likely than the other groups to achieve ≥20° improvement[34]. Across heterogeneous CCH combination regimens in seven comparative studies (532 men), a 2024 meta-analysis found greater length gain than with CCH alone (mean difference 0.81 cm, 95% CI 0.17–1.45), but no significant additional curvature benefit.[65]
  • Penimaster PRO. A separate 12-week randomized trial of 93 selected men with stable PD (47 device, 46 observation) used 3–8 h/day and showed greater curvature reduction than observation; it did not compare Penimaster PRO with RestoreX.[35][66]

Other modalities​

  • Extracorporeal shockwave therapy (ESWT). May relieve acute-phase pain ; do not offer to correct curvature or plaque size . AUA also advises against radiotherapy .[6][51]
  • Vacuum erection device. Limited evidence; modest benefits in small series[31][35]

D. Surgical treatment — gold standard for stable PD with functional deformity​

Guidelines: surgery for stable disease (EAU: pain resolved and curvature stable ≥ 3 months) by experienced surgeons.[6][7]

EAU 2026 surgical recommendations. Operate only when disease is stable and intercourse is compromised by the deformity , after assessing length, curvature, erectile function including response to pharmacotherapy, and expectations . Use tunical shortening first for adequate length and rigidity, less severe curvature and no hourglass or hinge deformity ; use lengthening for normal erectile function with inadequate length, severe curvature or complex deformity ; no procedure or graft has proven superior. Do not use the sliding technique because of the risk of glans necrosis . Degloving with circumcision is the usual approach, and non-absorbable or slowly absorbed sutures such as polydioxanone are advised. In the EAU's review of non-comparable studies, shortening procedures straighten more than 85% of men, with recurrence and hypoesthesia around 10%, and shortening of 1–1.5 cm in 22–69%; lengthening procedures carry a risk of de novo ED up to 50% in men without preoperative ED, dermal grafts a veno-occlusive ED rate near 20%, and synthetic grafts (Dacron, Gore-Tex) and cadaveric dura should be avoided.[51]

Levine surgical algorithm:[2][36][37]

  • Adequate rigidity, mild–moderate curvature (< 60°), no hourglass/hinge → Tunical plication
  • Adequate rigidity, severe curvature (> 60–70°), hourglass/hinge, significant shortening → Plaque incision/partial excision and grafting
  • Refractory ED ± curvature → Inflatable penile prosthesis ± modeling, plication, or grafting

1. Tunical plication (Nesbit / 16-dot / modified Yachia)​

  • Plication was the most common PD reconstruction in the AUA 2015 evidence review, accounting for 51% of 5,818 patients who underwent surgical reconstruction other than prosthesis surgery.[6]
  • Curvature improvement: The AUA reports rates of at least 90% in most plication studies; in one prospective cohort, 14 plication patients had a mean curvature reduction of 72.0° (92.2%)[6][38]
  • Penile shortening. In one prospective comparison, the 14-man plication arm had a mean stretched penile length change of −1.0 cm[38]
  • Best candidate: rigidity adequate for coitus without treatment or with oral medication, vacuum therapy or ICI; Levine's algorithm selected plication for curvature <60° without hourglass or hinge deformity.[6][37]
  • Lower risk of de novo ED than grafting; no graft required
  • Wound complications across plication and grafting: In a 189-patient mixed surgical cohort, 12/189 (6.3%) had wound complications within 3 months; ventral and subcoronal incision rates did not differ significantly (9/94 versus 3/95; P = .081)[39]

2. Plaque incision (or partial excision) and grafting​

  • Grafting outcomes use different endpoints: The AUA reports curvature improvement in >80% of patients in most study arms; a 25-man PEG cohort had a mean 94.9% curvature reduction, while a BMG meta-analysis reported 98.6% pooled success[6][38][40]
  • Stretched penile length increased by a mean 0.9 cm in the 25-man PEG arm of one comparative cohort[38]
  • Best candidate: intact erectile function, severe curvature (> 60–70°), hourglass / hinge / significant shortening[2][37]
  • De novo ED varies substantially; counsel that risk can reach 50% in some grafting series.[40][41][51]
  • Compound curvature. In a retrospective series, 79% of 161 men treated with PEG plus supplemental TAP could engage in penetrative intercourse with or without pharmacotherapy, and 12.4% had recurrent curvature at mean 61-month follow-up[42]

Graft materials:

MaterialTypeNotes
Buccal mucosa graft (BMG)AutologousFavorable pooled outcomes in mostly single-arm series, often with lower preoperative curvature; no randomized superiority[40][41][43]
Tunica vaginalisAutologous90% technical success (residual ≤ 15°) at 24 mo, similar to BMG in a 40-patient comparison[43]
Bovine pericardiumXenograftOff-the-shelf graft used for plaque incision and grafting without prosthesis[41]
TachoSil (collagen fleece)Hemostatic patchReported operative-time advantages; no proven best graft[38][45]
DermisAutologousHistorical standard[41]
Small intestinal submucosa (SIS)XenograftVariable[38]

The 2026 BMG meta-analysis reported 98.6% surgical success, 92.1% satisfaction, 1.7% de novo ED and 1.1% shortening in selected studies.[40]

3. Inflatable penile prosthesis (IPP)​

  • Indication: For PD with ED and/or deformity preventing coitus despite pharmacotherapy or vacuum therapy, the AUA says clinicians may offer penile prosthesis and advises an inflatable device .[6][46] The Fifth ICSM recommends considering penile prosthesis for medically refractory ED with deformity or high risk of postoperative ED .[69]
  • Addresses both ED and curvature in a single operation[2][6]
  • Multicenter cohort (499 PD-IPP patients):[47]
    • Mean preop curvature 39.4°
    • 17.6% underwent IPP placement without an adjunctive correction procedure[47]
    • 82.4% received adjunctive correction. Manual modeling with or without scratch was used in 74.7% (median 26° correction), plication in 4.8% (median 40°), grafting in 2.0% (median 55°), and combined grafting and modeling in 0.8%.[47]
  • In a separate selected prosthesis series, satisfaction was assessed at 6 months[48]. In PROPPER, 1-year data were available for 177/250 men and 2-year data for 130/250; among assessed patients, >80% were satisfied or very satisfied and >88% reported device use[49]
  • Self-reported depression in optional PROPPER responses: 36/187 (19.3%) at baseline versus 6/57 (10.5%) at 1 year (p = 0.02)[49]
  • In a selected retrospective series, 29/33 (87.9%) PD patients without ED reported satisfaction 6 months after first-line prosthesis.[48][51]
  • Scratch technique and postoperative VED. Combined approach achieving residual curvature of 7.7–9.1° after 24 weeks of vacuum therapy and IIEF-5 rising from 9.8 to 24.1 at 1 yr (145 selected patients)[50]

E. Comparative outcomes​

A randomized trial enrolled 40 men; 19 per arm had three-month data, and 18 of 19 surgical patients underwent plication (one underwent incision and grafting).[63] At three months, surgery plus RestoreX and sildenafil produced a median 84% reduction in summed two-plane curvature versus 54% with CCH plus the same adjuncts; median flaccid coronal length changed −0.5 versus +1.0 cm, and 50 versus 13 persistent adverse events were recorded. The primary “very satisfied” response was 21% versus 50% (P = .08).[63]

The following table summarizes an earlier prospective nonrandomized multi-institutional comparison (n = 57) of CCH, plication and PEG:[38]

OutcomeCCHTunical plicationPEG
Mean curvature correction23.3° (34.4%)72.0° (92.2%)71.8° (94.9%)
Penile length change−0.2 cm−1.0 cm+0.9 cm
IIEF-5 change+5.7+4.9+2.2

In a retrospective series of 90 men with persistent curvature after a shortened three-injection CCH protocol, subsequent grafting with or without IPP or Nesbit surgery was feasible; 86/90 had no reported surgical complication under the authors’ tabulation, although all patients in the two graft groups reported paresthesia, and 4/90 had persistent curvature >20° at three months.[44]

Algorithm Summary​

  1. Active phase (evolving symptoms): Treat pain with NSAIDs when appropriate; discuss traction and its limitations, assess erectile function, consider a PDE5 inhibitor for concomitant ED when appropriate, and offer psychological support as needed. Defer corrective surgery until stable.[6][51]
  2. Stable phase (deformity unchanged for at least 3 months; pain usually resolved; EAU surgical timing requires 3–6 months of stability or more than 9–12 months from onset):[6][51]
    • Curvature < 60°, no hourglass/hinge, intact rigidity → Plication
    • Severe curvature (proposed >60° threshold), hourglass/hinge, or shortening with intact rigidity → Consider plaque incision/excision and grafting (BMG, bovine pericardium, TachoSil, or tunica vaginalis); for selected hourglass/hinge indentation, extra-tunical grafting has also been described in retrospective series.[51]
    • Refractory ED → IPP ± modeling, plication, or grafting
    • Patient prefers non-surgical → Discuss traction (including RestoreX) or vacuum devices to reduce deformity .[51] The US XIAFLEX label requires a palpable plaque and curvature ≥30°; the AUA says clinicians may administer CCH with modeling for stable PD with curvature >30° and <90° and intact erectile function .[5][6] CCH with RestoreX traction has been studied as a combined treatment.[34]
  3. Patients considering treatment: shared decision-making; counsel about expected outcomes (shortening with plication, de novo ED with grafting, modest CCH curvature benefit about 7.7° net versus placebo at 52 weeks); assess psychological distress and consider referral when significant distress is identified.[7][18][20][26]

Guideline Principles​

  • History and genital examination are the minimum evaluation; document erect deformity before treatment.[6]
  • Shared decision-making and thorough counseling are universally emphasized
  • Plication (shortening) and grafting (lengthening) are reserved for patients with adequate rigidity; EAU notes that the > 60° threshold for "severe" curvature has not been validated[51]
  • Penile prosthesis, with or without straightening procedures, is the recommended surgical option for PD with ED not responding to pharmacotherapy [51]
  • CCH is an established option for appropriately selected patients; current guidance differs from older recommendations for IFN-α2b
  • Vitamin E and tamoxifen should not be offered
  • Further pathophysiology and rigorous outcomes research are needed

See Also​

Podcasts​

Update Series (2026): Case Based Medical and Surgical Management of Peyronie's Disease
AUAUniversity Podcast, Ep. 376 (2026)
cme.auanet.org
Peyronie's Disease Challenges and Solutions
BackTable Urology, Ep. 72 (2022) · Jonathan Clavell, Jose Silva
backtable.com

Videos​

Peyronie's Disease Surgery: Considerations, Tips, and Pitfalls
Grand Rounds in Urology (2025)

References​

1. Rosenberg JE, Ergun O, Hwang EC, et al. "Non-surgical therapies for Peyronie's disease." Cochrane Database Syst Rev. 2023;7:CD012206. doi:10.1002/14651858.CD012206.pub2

2. Ziegelmann MJ, Bajic P, Levine LA. "Peyronie's disease: contemporary evaluation and management." Int J Urol. 2020;27(6):504–516. doi:10.1111/iju.14230

3. Kadioglu A, Tefekli A, Erol B, et al. "A retrospective review of 307 men with Peyronie's disease." J Urol. 2002;168(3):1075–1079. doi:10.1016/S0022-5347(05)64578-8

4. Mulhall JP, Schiff J, Guhring P. "An analysis of the natural history of Peyronie's disease." J Urol. 2006;175(6):2115–2118. doi:10.1016/S0022-5347(06)00270-9

5. Endo. Xiaflex (collagenase clostridium histolyticum): prescribing information, Medication Guide and safety information. Prescribing information (label revised 04/2026)

6. Nehra A, Alterowitz R, Culkin DJ, et al. "Peyronie's disease: AUA guideline." J Urol. 2015;194(3):745–753. doi:10.1016/j.juro.2015.05.098

7. Chierigo F, Fallara G, Tozzi M, et al. "Guideline of guidelines: Peyronie's disease." BJU Int. 2026;137(5):770–782. doi:10.1111/bju.70201

8. Patel DP, Christensen MB, Hotaling JM, Pastuszak AW. "A review of inflammation and fibrosis: implications for the pathogenesis of Peyronie's disease." World J Urol. 2020;38(2):253–261. doi:10.1007/s00345-019-02815-6

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