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. 2011 Jul;8(7):2098-105.
doi: 10.1111/j.1743-6109.2011.02292.x. Epub 2011 May 11.

Body mass index regulates hypogonadism-associated CV risk: results from a cohort of subjects with erectile dysfunction

Affiliations

Body mass index regulates hypogonadism-associated CV risk: results from a cohort of subjects with erectile dysfunction

Giovanni Corona et al. J Sex Med. 2011 Jul.

Abstract

Introduction: Obesity is an independent cardiovascular (CV) risk factor. Testosterone (T) is inversely related to body mass index (BMI) in males. There is substantial evidence suggesting that low T could play a role as a moderator of CV mortality in men.

Aim: This study is designed to assess the possible interaction between T and obesity in predicting major CV events (MACE) in a sample of subjects with erectile dysfunction.

Methods: A consecutive series of 1,687 patients were studied. Different clinical, biochemical, and instrumental parameters were evaluated. According to BMI, subjects were divided into normal weight (BMI = 18.5-24.9 kg/m(2) ), overweight (BMI = 25.0-29.9 kg/m(2) ), and obese (BMI ≥ 30.0 kg/m(2) ). Hypogonadism was defined as total T below 10.4 nmol/L. Information on MACE was obtained through the City of Florence Registry Office.

Main outcome measures: Information on MACE was obtained through the City of Florence Registry Office.

Results: Among the patients studied, 39.8% had normal weight, whereas 44.1% and 16.1% were overweight and obese, respectively. Unadjusted analysis in the whole sample showed that while hypogonadism and obesity were significantly associated with an increased risk of MACE, their interaction term was associated with a protective effect. In a Cox regression model, adjusting for confounders, hypogonadism showed a significant increased risk of MACE in normal weight subjects, whereas it was associated with a reduced risk in obese patients.

Conclusions: Hypogonadism-associated CV risk depends on the characteristics of subjects, being more evident in normal weight than in obese patients. Further studies are advisable to clarify if low T in obese patients is a (positive) consequence of a comorbid condition (i.e., to save energy) or if it represents a pathogenetic issue of the same illness. Hence, possible misuse/abuse of T treatment in obese subjects must be avoided.

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