ABSTRACT

Introduction

The clinical identification of metabolic syndrome is based on measures of abdominal obesity, atherogenic dyslipidemia, elevated blood pressure, and glucose intolerance. However, the impact of hypogonadism associated with obesity on penile hemodynamics is not well investigated.

Aim

In this retrospective study, we sought to evaluate the effect of obesity on serum total testosterone (TT) level and penile duplex parameters in men with erectile dysfunction (ED).

Methods

Our participants (N=158) were evaluated for erectile function using an abridged, five-item version of the International Index of Erectile Function-5. Determination of body mass index (BMI) was performed. Measurements of TT, fasting lipid profile, and blood sugar were conducted. Penile hemodynamics was assessed using intracavernosal injection and penile duplex study.

Main Outcome Measures

Bivariate associations among BMI and serum testosterone, blood pressure, and lipid profile, as well as penile duplex parameters. We compared all clinical, laboratory, and penile duplex parameters between lean men (BMI<25) and overweight and obese men (BMI ≥ 25).

Results

The participants' age ranged between 20 and 56 years. A significant negative correlation between BMI and TT was detected (r =−0.431, P =0.0001). Hypogonadism was identified in 54/158 (34.2%) of men with ED. The incidence of hypogonadism varied from as low as 1/18 (5.6%) in lean men to as high as 18/36 (50%) to 21/35 (60%) in morbid and severe obesity, respectively. Vasculogenic ED was detected in 32/54 (59.3%) men with BMI ≥ 25, compared with 5/18 (27.8%) in lean men (P =0.029). In order to study the effect of obesity on erectile function, cases with other risk factors were excluded. Of 67 men suffering from ED with no other risk factor(s) apart from obesity, vasculogenic ED was detected in 32/54 (59.3%) men with BMI ≥ 25, compared with 3/13 (23.1%) in lean men (P =0.029).

Conclusion

Obesity is associated with lower TT and disturbances of penile hemodynamics. It is an independent clinical factor for vasculogenic ED.

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