Introduction Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS) are characterized by insulin resistance and often associated with male hypogonadism. Aim To discriminate the specific contribution of T2DM and MetS to male hypogonadism. Methods A consecutive series of 1,134 (mean age 52.1 ± 13 years) male patients with sexual dysfunction was studied. Main Outcome Measures Several hormonal and biochemical parameters were studied along with ANDROTEST, a 12-item validated structured interview, specifically designed for the screening of hypogonadism (total testosterone [TT] <10.4 nmol/L or free testosterone [FT] <37 pmol/L) in a male population with sexual dysfunction. Results Irrespective of the criteria used to define hypogonadism, MetS was associated with a significantly higher prevalence of the condition, both in subjects with and without T2DM (41% and 29% vs. 13.2% and 77.1% and 58% vs. 40.6%, respectively, for TT and FT in patients with MetS and with or without T2DM, when compared with subjects without MetS and T2DM; both P < 0.0001). Conversely, T2DM was associated with a higher prevalence of hypogonadism in subjects with MetS but not in those without MetS. Patients with MetS, with or without T2DM, also showed a higher ANDROTEST score when compared with patients without MetS. Logistic multivariate regression analysis, incorporating the five components of MetS, identified a significant association of elevated waist circumference and hypertriglyceridemia with hypogonadism both in patients, with or without T2DM. Conclusions Our study demonstrated that MetS, and in particular visceral adiposity (as assessed by increased waistline and hypertriglyceridemia), is specifically associated with hypogonadism in subjects consulting for sexual dysfunction.
While the association of Klinefelter's Syndrome (KS) with infertility is well-known, very few investigations have evaluated the prevalence of sexual dysfunction in KS. The aim of the present study was to systematically analyse the prevalence of KS in a consecutive series of adult male patients consulting for sexual problems and to investigate its specific correlates. Among a consecutive series of 1386 men (mean age 48.9 +/- 12.7 years old), 23 (1.7%) subjects with KS were found. Patients with KS were younger and more often hypogonadal when compared with the rest of the sample. Among patients with KS, five (22.7%) subjects reported severe erectile dysfunction, 14 (60.9%) hypoactive sexual desire (HSD), two (9.5%) premature and two (9.5%) delayed ejaculation. Only the association between KS and HSD was confirmed after adjustment for age [HR = 3.2 (1.37-7.5)], however, when patients with KS were compared with age, smoking habit, and testosterone matched controls, even the association between KS with HSD disappeared. In comparison to matched hypogonadal controls, subjects with KS had lower levels of education, a higher frequency of cryptorchidism and poorer pubertal progression. In conclusion, our results indicate that sexual dysfunction present in KS is not specifically associated with the syndrome but is caused by the underlying hypogonadal state. Further studies are needed to evaluate the efficacy of testosterone substitution in ameliorating the hypoactive sexual desire often reported in subjects with KS.
We had previously demonstrated that Coenzyme Q10 [(CoQ10) also commonly called ubiquinone] is present in well-measurable levels in human seminal fluid, where it probably exerts important metabolic and antioxidant functions; seminal CoQ10 concentrations show a direct correlation with seminal parameters (count and motility). Alterations of CoQ10 content were also shown in conditions associated with male infertility, such as asthenozoospermia and varicocele (VAR). The physiological role of this molecule was further clarified by inquiring into its variations in concentrations induced by different medical or surgical procedures used in male infertility treatment. We therefore evaluated CoQ10 concentration and distribution between seminal plasma and spermatozoa in VAR, before and after surgical treatment, and in infertile patients after recombinant human FSH therapy. The effect of CoQ10 on sperm motility and function had been addressed only through some in vitro experiments. In two distinct studies conducted by our group, 22 and 60 patients affected by idiopathic asthenozoospermia were enrolled, respectively. CoQ10 and its reduced form, ubiquinol, increased significantly both in seminal plasma and sperm cells after treatment, as well as spermatozoa motility. A weak linear dependence among the relative variations, at baseline and after treatment, of seminal plasma or intracellular CoQ10, ubiquinol levels and kinetic parameters was found in the treated group. Patients with lower baseline value of motility and CoQ10 levels had a statistically significant higher probability to be responders to the treatment. In conclusion, the exogenous administration of CoQ10 increases both ubiquinone and ubiquinol levels in semen and can be effective in improving sperm kinetic features in patients affected by idiopathic asthenozoospermia.
Although preliminary, our findings are consistent with previous studies and suggest an increased prevalence of MDD and other axis-I disorders among women with newly diagnosed endocrine disorders, providing further evidence suggesting that women with endocrine abnormalities may be at increased risk of depression and/or anxiety disorders.
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