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Endocrine Abstracts (2018) 56 S9.3 | DOI: 10.1530/endoabs.56.S9.3


Italy.


Introduction: Obesity is a cause of erectile dysfunction (ED) whereas its relationship with male infertility is more conflicting. The term metabolically healthy obesity (HO) has been used to describe an obese phenotype that does not have the burden of any metabolic disorder. The aim of the present study is to analyse the contribution of HO in the pathogenesis of ED and male infertility and to verify the value of HO in predicting major adverse cardiovascular events (MACE).

Methods

An unselected series of 4382 (51.4±13.1 years) men with sexual dysfunction (SD) and 222 (37.3±8.6 years) males of infertile couples were studied. A subset of men with SD (n=1687) was enrolled in a longitudinal study. Several clinical, biochemical and ultrasound parameters were evaluated. HO was defined as the presence of body mass index > 30 kg/m2, HDL > 40 mg/dl and absence of diabetes or hypertension.

Results

Among the patients with SD, 723 (16.5%) were obese and among them 163 (3.7%) were HO and 560 (12.8%) had a complicated obesity (CO). Similarly, among men of infertile couple 55 (24.8%) were obese and among them 18 (8.1%) had HO and 37 (16.7%) CO. After adjustment for confounders, when compared to healthy normal weight individuals, in both samples, either subjects with HO or CO had lower total T levels. Conversely, no difference between HO and CO were observed. In addition, in both samples men with CO but not those with HO reported worse erectile function when compared to healthy normal weight individuals. When PCDU parameters were considered, peak systolic velocity evaluated in flaccid conditions was lower in both HO and CO when compared to normal weight subjects in subjects with sexual dysfunction as well as in those of infertile couples. In addition, men of infertile couples with CO but not those with HO showed higher risk of ultrasound and biochemical (semen IL-8) features of prostatic inflammation when compared to normal weight subjects. Conversely, no differences in seminal parameters among groups were observed. Finally, the longitudinal study, after adjusting for confounders, both HO and CO were independently associated with a higher incidence of MACE (HR=4.800 [1.265;18.214]; HR=3.041 [1.078;8.573] 2.469 [1.019;5.981], respectively; both P<0.05), when compared to the rest of the sample.

Conclusions

Our data suggest that healthy obesity induces subclinical ED and prostatic inflammation independent of T levels and it is associated with an increased CV risk.

Volume 56

20th European Congress of Endocrinology

Barcelona, Spain
19 May 2018 - 22 May 2018

European Society of Endocrinology 

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