ABSTRACT
Objective To assess the variation of sexual hormone and mechanisms of low testosterone in young male obesity with acanthosis nigricans. Methods Retrospective analysis was performed in 125 male obesity patients [ body mass index( BMI)≥28 kg/m2 ] . According to their clinical characteristics, they were divided into two groups including obesity without acanthosis nigricans(OB group, n=62) and obesity with acanthosis nigricans(AN group, n=63). 60 normal weight men were also recruited as a control group. Body fat and body weight were measured. Blood insulin, lipid profile, sex hormones levels, and inflammation factors were measured. Parameters of each group were compared and the correlations between total testosterone level and other index were analyzed. Results All the male obesities have the significant lower total testosterone levels than those of control group(P>0. 05), and those in AN group were lower than those in OB group(P>0. 05). The BMI and body fat in OB group and AN group were both significantly higher than those in control group(P>0. 05). The fasting insulin levels in all obese men were significantly higher than those in control group(P>0. 05), highest in AN group. Triglycerides(TG) in both OB and AN group were higher than those in controls, and not significant between later 2 groups. But high-density lipoprotein-cholesterol ( HDL-C) in the two groups were significantly lower than control, which in AN group were significantly lower than OB group. Total testosterone levels in AN group were negatively correlated with weight, waist circumference, hip circumference, fasting insulin, and homeostasis model assessment for insulin resistance ( HOMA-IR ) , and also negatively correlated with inflammation factors including C-reactive protein ( CRP ) , erythrocyte sedimentation rate ( ESR) , tumor necrosis factor-α( TNF-α) , and uric acid. However, total testosterone levels in AN group were not correlated with lipid metabolism index. Conclusion Young male obesity with acanthosis are associated with secondary hypogonadism. Hyperinsulinemia, insulin resistance, and inflammatory factors are risk factors for the occurrence of this secondary male hypogonadism.
ABSTRACT
<p><b>Objective</b>To analyze the clinical characteristics of secondary male hypogonadism induced by sellar space-occupying lesion, explore its pathogenesis, and improve its diagnosis and treatment.</p><p><b>METHODS</b>We retrospectively analyzed the clinical data about 22 cases of secondary male hypogonadism induced by sellar space-occupying lesion, reviewed related literature, and investigated the clinical manifestation, etiological factors, and treatment methods of the disease. Hypogonadism developed in 10 of the patients before surgery and radiotherapy (group A) and in the other 12 after it (group B). The patients received endocrine therapy with Andriol (n=7) or hCG (n=15).</p><p><b>RESULTS</b>The average diameter of the sellar space-occupying lesions was significantly longer in group A than in B (［2.35±0.71］ vs ［1.83±0.36］ cm, P<0.05) and the incidence rate of prolactinomas was markedly higher in the former than in the latter group (60% vs 0, P<0.01). The levels of lutein hormone (LH), follicle stimulating hormone (FSH) and testosterone (T) were remarkably decreased in group B after surgery and radiotherapy (P<0.01). Compared with the parameters obtained before endocrine therapy, all the patients showed significant increases after intervention with Andriol or hCG in the T level (［0.78±0.40］ vs ［2.71±0.70］ ng/ml with Andriol; ［0.93±0.44］ vs ［3.07±0.67］ ng/ml with hCG) and IIEF-5 score (5.00±2.61 vs 14.50±3.62 with Andriol; 5.36±1.82 vs 15.07±3.27 with hCG) (all P<0.01). The testis volume increased and pubic hair began to grow in those with hypoevolutism. The patients treated with hCG showed a significantly increased testis volume (P<0.01) and sperm was detected in 7 of them, whose baseline testis volume was markedly larger than those that failed to produce sperm (［11.5±2.3］ vs ［7.5±2.3］ ml, P<0.01). Those treated with Andriol exhibited no significant difference in the testis volume before and after intervention and produced no sperm, either.</p><p><b>CONCLUSIONS</b>Hypothyroidism might be attributed to surgery- or radiotherapy-induced damage to the pituitary tissue, space-occupying effect of sellar lesion, and hyperprolactinemia. Both Andriol and hCG can improve the T level and erectile function, but the former does not help spermatogenesis.</p>