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The prevalence of Peyronie's disease in diabetic patients with erectile dysfunction


We attempted in this study to investigate the prevalence of Peyronie's disease (PD) among diabetic patients with erectile dysfunction (ED). Two-hundred and six diabetic patients were further evaluated in this study. Forty-two (20.3%) patients had PD. There were significant associations between PD and risk factors of age, obesity and smoking. All patients with PD had also ED. Penile curvature was present in 82.1% of all patients with PD. Of the patients with PD, 25.4% had pain with or without erection. Significant associations between PD and ED and ED duration were detected. This study confirmed the high prevalence of PD among diabetic patients with ED. Further work is needed probing the mechanisms through which diabetes affects the pathogenesis of ED and PD.


Peyronie's disease (PD) is a localized connective tissue disorder that affects the tunica albuginea of the penis.1 Fibrous scar tissue, which replaces normally elastic fibers, causes a characteristic penile deformity that is most evident during erection. This pathological process can manifest as increased curvature, indentation, shortening or an ‘hourglass’ irregularity of the penis.1 The diagnosis of PD is often preceded by painful erections, and can be associated with erectile dysfunction (ED) and palpable areas of induration (plaques).

Although PD was once considered to be relatively uncommon, studies now suggest that its prevalence is similar to that of diabetes or urolithiasis.2 A recent epidemiological study reported an overall prevalence of the condition of 3.2%,3 much higher than once thought, highlighting the potential physical and psychosocial impact of the disease on society. Compounding these effects on the community are the changing demographics of the population, which are predicted to increase age-related conditions. Of concern is the belief by some that even the most recent data underestimate the true prevalence of PD.4 Men might be reluctant to report a condition that they consider embarrassing, and older men might often accept their symptoms as insignificant consequences of ageing.4 Many physicians agree that the true prevalence of PD has become more apparent since the advent of oral sildenafil, which has seen a marked improvement in community awareness of ED.2

ED is a common worldwide clinical problem, with tens of thousands of new cases every year.5 Diabetes mellitus (DM) is a very common comorbidity with ED, partly because of increased life expectancy and the high incidence of these conditions in the geriatric population.6 Those expected changes in the prevalence of diabetes and ED might consequently influence the prevalence of PD.7 Unfortunately, the quality of epidemiological data on PD remains erratic, with one contributing factor being the various criteria used by researchers to define the condition.4 The most accepted objective measures include the number, size and location of plaques, as well as induration and penile curvature.4 All these factors prompted us to investigate the prevalence of PD among diabetic patients (type I and II) with ED using clinical and radiological approaches.

Patients and methods

During the period between August 2005 and February 2006, all male patients with a clinical diagnosis of diabetes (type 1 or 2) and attending the internal medicine clinic of our hospital were included in this study. Patients were screened for ED using the Sexual Health Inventory for Men.8 ED severity was classified into the following five categories based on International Index of Erectile Function-5 scores; severe (5–7), moderate (8–11), mild to moderate (12–16), mild (17–21) and no ED (22–25).

Patients were assessed for full sociodemographic and relevant medical history. Presence of other risk factors for ED such as hypertension, ischemic heart disease or dyslipidemia was investigated. Psychiatric disorders were diagnosed based on the medical history of patients on antidepressants.

All patients were also screened for PD both clinically and by penile ultrasound. Local physical examination included palpation of the penis to outline the location and extent of the plaque. The ultrasonographic examination was performed for all patients in supine position, with room temperature being 22°C lying in a comfortable setting. Examination was performed using SA 9900 Medison (Medison, CO, Seoul, Korea) with linear array transducer 5–12 MHz. The glans penis was supported gently by the patient's hand against his anterior abdominal wall, then the transducer was applied starting from base of penis until the glans transversally. The longitudinal examination was performed for every part from side to side. When a fibrotic patch was detected, it was measured in longitudinal and transverse scan with special attention to its texture and if there was any calcified foci or patch, full-scan examination of the entire penis was performed. The diagnosis of PD was based on the detection of clinically palpable penile plaques on routine examination of the penis. Confirmation of the diagnosis was through penile ultrasound or detection of acquired penile curvature; both assessed after intracorporeal injection of 10 μg prostaglandin E1. All patients underwent routine laboratory investigation, plus total testosterone and prolactin assessment.

Glycemic control was measured by glycosylated hemoglobin (HbA1c) using a high-performance liquid chromatography technique on a rinsed venous blood sample. Metabolic control was rated as good (4.7–6.2%), fair (6.3–7%) and poor (>7%).7 Metabolic control was evaluated according to the glycosylated hemoglobin values not more than 3 months before interview. Body mass index (kg/m2) was rated as normal (<25), overweight (25.1–27) and obese (>27).

The Pearson χ2 test was used to assess the relationship between of ED risk factors in diabetes and the prevalence of PD. One-way analysis of variance was used to compare the means of diabetes' characteristics in patients with or without PD.


Two-hundred and six patients fulfilled our inclusion criteria and were further evaluated in this study. Mean ages (s.d.) of all patients was 53.7±8.1 years (range 25–84). Of the patients, 83.9% were overweight or obese and 66% were current or ex-smokers. Forty-two (20.3%) patients were diagnosed as having PD. Of the patients with PD, 10% were younger than 40 years whereas 90% were older than 40 years. There were significant associations between PD and risk factors of age, obesity and smoking (P<0.05 for each, Table 1).

Table 1 Patients demographics

Of all patients, 89.2% were sexually active (at least one sexual intercourse per week); however, 85.6% (176 of 206) had various degrees of ED, namely mild in 6.3%, moderate in 19.4% and severe in 74.6%. All patients with PD had also ED. Penile curvature was present in 82.1% of those patients. Of the patients with PD, 25.4% had pain with or without erection. Significant associations between PD and ED and ED duration were detected (Table 2).

Table 2 Characteristics of Peyronie disease

Concerning plaques characteristics, the mean (s.d.) length and width (cm) were 0.82±0.06 and 0.53±0.02, respectively. The majority of these plaques (88.5%) were present at the mid-shaft of the penis whereas only 11.5% of plaques were located either proximally or distally. None of the patients with PD had more than one penile plaque. All penile plaques dimensions were detected using penile ultrasound. Clinical palpation missed very small (<0.25 cm2) penile plaques in 10 patients with PD, that were otherwise detected radiologically (Table 2). None of the patients had only subclinical plaques. Only 68% of the patients were aware of their penile fibrosis problem; however, all patients reported a long duration (>2 years) and progressive course of their complaint. None of the patients with PD received treatment for their disease.

One hundred and eighty-three (88.8%) of all diabetic patients were of type II category, whereas only 23 (11.2%) had juvenile diabetes. The mean duration of diabetes was 15.1±9.1 years (range 1–46). All patients used oral hypoglycemic agents, insulin or both but none were on diet control. There were significant associations between PD and dyslipidemia and psychological disorders (P<0.05 for each). Diabetes-related complications included neuropathy in 11.2%, cardiovasculopathy in 20.1%, retinopathy in 17.8%, nephropathy in 7% and peripheral ischemia in 9.1%. In all, 53.4% of the patients had one or more diabetes-related complications.

There was no significant association between PD and type of diabetes (Table 3). However, there were significant associations between PD and neuropathy and the presence of one or more diabetes-related complications (P<0.05 for each). Patients with more than 8 years of diabetes were 5 times more likely to have PD than men with diabetes of less than 4 years (Table 3). All patients with PD had fair metabolic control of diabetes (Table 3). None of the patients showed poor metabolic control of diabetes. There were no associations between testosterone or prolactin abnormalities and PD in diabetic patients.

Table 3 Association between diabetes and PD


Many of the theories that seek to explain the pathogenesis of PD have been derived from either animal or cell-culture research. Although trauma is considered to be the provocative stimulus, other theories include: failure of fibrin clearance; collagen alterations; genetic predisposition; autoimmune factors; free radical production and cytogenetic aberrations. In 2003, Mulhall9 described a paradigm that encompassed these different theories to explain plaque developmental pathogenesis in PD; penile trauma in genetically susceptible males, leading to;

  • endogenous and/or exogenous factors (localized autoimmune response);

  • loss of suppressor genes and activation of promoter genes;

  • cell-cycle regulator dysfunction, leading to biological transformation of constituent cells within tunica/plaque, leading to cytokine overexpression, free radical production and cytogenetic changes, leading to unregulated extracellular matrix deposition (fibrin and collagen), leading to plaque formation.

A number of studies and clinical reviews have investigated erectile function in men with DM.10 Men with DM face problems related to sexual dysfunction at an early age. Patients with PD and DM also present in the later stages of the disease. This may be related to the fact that diabetic patients with ED recognize and seek help for their penile deformities later than those without ED or risk factors. These men may also have more crucial problems related to DM, which they have to deal with urgently before addressing their sexual dysfunction. This may be another contributing factor in their presenting in the later stages of PD.10

All our patients were either using oral agents or insulin. A significant association between PD and both long duration and metabolic control of diabetes was confirmed.7 None of the patients experienced poor control of diabetes. Thus, a firm conclusion on the relationship between poor control of diabetes and PD could not be reached. Nevertheless, the trend of long duration and apparently only fair control of diabetes in these patients might suggest a detrimental effect on tunical elasticity which in turn could explain the high association of PD and diabetes.7

In the current study, we chose to examine the magnitude of prevalence of PD in diabetics with ED. For the sake of completion, we chose to include all patients with diabetes type I. Diabetes type I constitutes around 5–10% of all cases of diabetes6 and it has a higher risk of complications than type II. In our study, we found a higher incidence of diabetes type I in our observed population, which may be attributed to demographic differences. There was no significant association between the type of diabetes and occurrence of PD. It seems that the extent of diabetes-mediated vascular abnormalities that may have contributed to the development of PD may be related to the other factors as the duration and metabolic control of the diabetes rather than the type of diabetes itself.

There is no validated tool for screening PD; therefore, we relied upon history, physical and radiological examination of the penis. The diagnosis of penile plaques depends primarily on clinical palpation. Penile ultrasonography has been used as an additional tool to further confirm penile plaques diagnosis.11 However, these studies reported less sensitivity of penile ultrasound compared to local palpation in detection of penile plaques.11, 12 In a previous study, the prevalence of PD was 8.1% of the patients with DM type II.7 In the present study, the incidence of PD in DM patients was much higher. This may be due to the use of penile ultrasound to detect subclinical PD plaques that may be missed by clinical examination and also may be due to the inclusion of patients with type I DM. Nevertheless, it still remains unclear whether the detection of these subclinical plaques can affect the overall diagnosis of PD. Pain was reported in a small percentage of our patients, giving the indication that most of the patients were in the chronic phase of PD.

The specific relationship between ED and PD is difficult to confirm, and which condition predates the other is unclear. Although several studies showed that the prevalence of ED is significantly higher in men with PD3, 13 others demonstrated no significant correlation between the diagnoses.14 Organic and psychogenic factors could be the potential mechanisms responsible for ED in men with PD. Inadequate erection may occur in about 20% of patients with symptomatic PD. Vascular disease, either arterial or venoocclusive dysfunction, has been reported in as many as 70% of men who have ED.15

An interesting finding in our study group is that all patients with PD had also ED. In a recent study, El-Sakka and Tayeb7 reported a similar association of ED and PD in diabetic patients. We believe that this 100% association needs further clarification. Firstly, as all our patients were diabetic, the occurrence of vasculogenic and neurogenic abnormalities is highly probable, which could add to the complexity of association between PD and ED. Also, secondary psychological effects could also have a substantial role in patients with this devastating condition.7 We think that this 100% association of PD and ED in diabetic patients necessitates more extensive research concerning the undesirable effects of abnormal glucose metabolism on the tunica albuginea and smooth muscles of the cavernous tissue.

Our study does confirm previous reports on the significant association between PD and aging. Schwarzer and colleagues reported an increased risk of PD with increasing age, explaining that this may be due to increased risk of penile trauma, which may result from the inevitable accumulated sexual activity, or from the increased vulnerability of the tunica albuginea with aging.3 Recently, Usta et al.16 showed that, in older men abnormal vascular pathologies were significantly higher in men with PD plus ED than in patients with ED alone.16

In the current study, there was significant association between PD and smoking. Smoking has been inconsistently linked to PD in previous studies. La Pera et al.14 found smoking to be a risk factor for PD and the relative risk progressively increased with the number of cigarettes smoked. Smoking supports the oxidative and degenerative processes that have been assumed to be pathogenetic for PD.14

As all of our patients were recruited from one clinic, extrapolation of our results to the general population is difficult. On the other hand, the apparently large number of included subjects and the strict measures we used should make our findings reliable.


This study confirmed the high prevalence of PD among diabetic patients with ED. Further work is needed probing the mechanisms through which diabetes affects the pathogenesis of ED and PD.


  1. 1

    Smith BH . Peyronie's disease. Am J Clin Pathol 1966; 45: 670–678.

    CAS  Article  Google Scholar 

  2. 2

    Sommer F, Schwarzer U, Wassmer G, Bloch W, Braun M, Klotz T et al. Epidemiology of Peyronie's disease. Int J Impot Res 2002; 14: 379–383.

    CAS  Article  Google Scholar 

  3. 3

    Schwarzer U, Sommer F, Klotz T, Braun M, Reifenrath B, Engelmann U . The prevalence of Peyronie's disease: results of a large survey. BJU Int 2001; 88: 727–730.

    CAS  Article  Google Scholar 

  4. 4

    Smith CJ, McMahon C, Shabsigh R . Peyronie's disease: the epidemiology, aetiology and clinical evaluation of deformity. BJU Int 2005; 95: 729–732.

    Article  Google Scholar 

  5. 5

    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.

    CAS  Article  Google Scholar 

  6. 6

    Rendell MS, Rajfer J, Wicker PA, Smith MD . Sildenafil for treatment of erectile dysfunction in men with diabetes: a randomized controlled trial. Sildenafil Diabetes Study Group. JAMA 281; 421: 1999.

    Google Scholar 

  7. 7

    El-Sakka AI, Tayeb KA . Peyronie's disease in diabetic patients being screened for erectile dysfunction. J Urol 2005; 174: 1026–1030.

    Article  Google Scholar 

  8. 8

    Rosen RC, Cappelleri JC, Smith MD, Lipsky J, Pena BM . Development and evaluation of an abridged, 5-item version of the International Index of Erectile Function (IIEF-5) as a diagnostic tool for erectile dysfunction. Int J Impot Res 1999; 11: 319–326.

    CAS  Article  Google Scholar 

  9. 9

    Mulhall JP . Expanding the paradigm for plaque development in Peyronie's disease. Int J Impot Res 2003; 15 (Suppl 5): S93–S102.

    Article  Google Scholar 

  10. 10

    Tefekli A, Kandirali E, Erol B, Tunc M, Kadioglu A . Peyronie's disease: a silent consequence of diabetes mellitus. Asian J Androl 2006; 8: 75–79.

    CAS  Article  Google Scholar 

  11. 11

    Chew KK, Stuckey BG, Earle CM, Dhaliwal SS, Keogh EJ . Penile fibrosis in intracavernosal prostaglandin E1 injection therapy for erectile dysfunction. Int J Impot Res 1997; 9: 225–229.

    CAS  Article  Google Scholar 

  12. 12

    Lopez JA, Jarow JP . Duplex ultrasound findings in men with Peyronie's disease. Urol Radiol 1991; 12: 199–202.

    CAS  Article  Google Scholar 

  13. 13

    Rhoden EL, Teloken C, Ting HY, Lucas ML, Teodosio da Ros C, Ary Vargas Souto C . Prevalence of Peyronie's disease in men over 50-y-old from Southern Brazil. Int J Impot Res 2001; 13: 291–293.

    CAS  Article  Google Scholar 

  14. 14

    La Pera G, Pescatori ES, Calabrese M, Boffini A, Colombo F, Andriani E et al. Peyronie's disease: prevalence and association with cigarette smoking. A multicenter population-based study in men aged 50–69 years. Eur Urol 2001; 40: 525–530.

    CAS  Article  Google Scholar 

  15. 15

    Levine LA, Coogan CL . Penile vascular assessment using color duplex sonography in men with Peyronie's disease. J Urol 1996; 155: 1270–1273.

    CAS  Article  Google Scholar 

  16. 16

    Usta MF, Bivalacqua TJ, Tokatli ZR, Rivera F, Gulkesen K, Sikka S et al. Stratification of penile vascular pathologies in patients with Peyronie's disease and in men with erectile dysfunction according to age: a comparative study. J Urol 2004; 172: 259–262.

    Article  Google Scholar 

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Correspondence to R Shamloul.

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Arafa, M., Eid, H., El-Badry, A. et al. The prevalence of Peyronie's disease in diabetic patients with erectile dysfunction. Int J Impot Res 19, 213–217 (2007).

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  • Peyronie
  • erectile dysfunction
  • prevalence

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