Angiotensin-converting enzyme polymorphism and erectile dysfunction complaints in the Brazilian population.

INTRODUCTION

Angiotensin-converting enzyme (ACE) is the major regulator of circulatory homeostasis. An insertion/deletion (I/D) polymorphism in the ACE gene has been associated with marked differences in serum ACE levels and with various cardiovascular diseases. Limited and conflicting data have been published on the influence of this genetic variant on the pathophysiology of erectile dysfunction (ED).

AIM

To evaluate a potential association between ACE gene polymorphism and ED complaints in a population-based sample in São Paulo, Brazil.

MAIN OUTCOME MEASURES

The prevalence of ED complaints was estimated according to previously validated 8 item questionnaire.

METHODS

A total of 449 men were enrolled in the Epidemiologic Sleep Study and answered an 8-item questionnaire to ascertain sexual performance/ED and satisfaction. ACE gene polymorphism were genotyped using a standard polymerase chain reaction method.

RESULTS

No significant case-control difference was observed for the ACE gene I/D polymorphism either by genotype or allele-wise. Because age is a significant risk factor for ED complaints in our sample, we carried out analyses stratifying the sample by age group. The ID and II genotypes were significantly more frequent in ED complaint cases (88.9%) compared with controls (57.1%) in the men between 40 and 55 years of age. The frequency of the I allele was also significantly higher in individuals complaining of ED (66.7%) compared with men with no complaints (39.0%) (odds ratio = 3.12; 95% confidence interval = 1.48-6.59). Correction for potential confounding variables, including genetic ancestry, did not affect the strength of the association.

CONCLUSIONS

The findings of the present study suggest that the I/D polymorphism or another variant in close linkage disequilibrium with it may play a role in the development of ED in a specific age group and provides progress towards the understanding of the interaction between genetic factors and the risk of ED.