Adult-onset Hypogonadism Research Articles

Impaired aortic elastic properties in patients with adult-onset hypogonadism

Background. Recent studies have shown a strong relationship between testosterone levels and vasomotor actions. The aim of this study is to compare the elastic properties of the aorta in male patients with hypogonadism and eugonadal healthy control subjects. Method. A total of 22 male with hypogonadism (mean age: 35.2 ± 9.5 years, mean disease duration: 5.3 ± 1.8 years) and 25 age-, sex- and weight-matched eugonadal healthy subjects (mean age: 34.5 ± 8.2 years) were enrolled in the study. Aortic stiffness (β) index, aortic strain (AoS) and aortic distensibility (AoD) were calculated from the aortic diameters measured by transthoracic echocardiography and blood pressure obtained by sphygmomanometer. Results. The routinely performed echocardiographic parameters were similar between patient and control groups. There were significant differences between the control and patient groups in β index (1.75 ± 0.44 vs 2.68 ± 1.72, p < 0.001), AoS (18.52 ± 6.44 vs 12.35 ± 3.88%, p < 0.001) and AoD (7.56 ± 2.86 vs 3.96 ± 1.24, 10−6 cm2/dyn, p < 0.001). There were statistically significant positive correlations between the serum total testosterone level and AoD (r = 0.539, p < 0.001) and AoS (r = 0.372, p = 0.036); moreover, there was a negative correlation between the serum total testosterone level and β index (r = − 0.462, p = 0.001). In multivariate analysis, serum total testosterone level was significantly related with AoD, AoS and β index (respectively, RR = 2.88, p = 0.004; RR = 3.45, p = 0.001; RR = 2.64, p = 0.01). Conclusion. The study results showed that aortic elasticity was impaired in patients with hypogonadism. We also have demonstrated a statistically significant correlation between aortic elastic properties and the serum total testosterone level.

Men, bone and estrogen: unresolved issues.

Gonadal function has long been known to be important for skeletal health in men. Prepubertal hypogonadism is clearly associated with impairment in peak bone mass development and adult-onset hypogonadism with accelerated bone loss. Gonadal failure results in deficits in both androgen and estrogen action, but traditionally androgens were assumed to have the most important skeletal effect in men. Recently that model has been reconsidered as a variety of kinds of evidence have appeared to document a critical role for estrogen in bone physiology. As a result of this fresh perspective a host of interesting new dilemmas and hypotheses are being examined, including those related to the mechanisms of sex steroid action in bone, the origins of gender differences in skeletal morphology and physiology, and the role of estrogen in diagnostic and therapeutic strategies in men with metabolic bone disorders.