Endocrine Abstracts

Background: Low testosterone levels in men appear to be an independent cardiovascular risk factor closely associated with the metabolic syndrome. Reciprocally, the metabolic syndrome leads to a decrease in testosterone levels, suggesting a bidirectional relationship. It has been hypothesized that increased inflammation is causative for the development of obesity-associated hypogonadism. However, clinical evidence supporting this hypothesis is lacking. The aim of the present study was to determine whether anti-inflammatory treatment may restore endogenous testosterone production in obesity-associated hypogonadism.

Methods: This is a randomized, placebo-controlled, double-blind, trial including 70 hypogonadal men with the metabolic syndrome. Patients were randomly assigned to either receive 100 mg of a recombinant human interleukin-1–receptor antagonist subcutaneously twice daily for 4 weeks or to receive placebo. The primary endpoint was the change in total testosterone levels between baseline and 4 weeks. Predefined secondary end points included a change by week 4 in insulin resistance, body composition, muscle strength, hypogonadal symptoms and hemodynamic parameters.

Results: From April 2016 to January 2017, 66 patients have been enrolled at two tertiary care centers in Switzerland. Median age was 51 years (IQR 41–65) and patients had a median BMI of 37 kg/m² (34–39 kg/m²). Patients had hypogonadotropic hypogonadism with median baseline testosterone levels of 8.8 nmol/l (231 ng/dl) (7.6–10.1), median LH levels of 3.7 IU/l (3–5.2 IU/l), and median C-reactive protein levels of 2.9 mg/l (1.4–4.0 mg/l) mirroring a low-grade inflammatory state. Final results will be available in March 2017 and will be presented first at the ECE 2017.

Significance: This study will show whether there exists causality between obesity-associated inflammation and hypogonadism.