RESUMO
Introduction: This study aimed to distinguish isolated hypogonadotropic hypogonadism (IHH) from constitutional delay in growth and puberty (CDGP) by various hormonal tests in both sexes. Methods: Boys with testicular volume (TV) <4 ml (14-18 years) and girls with breast B1 stage (13-18 years) were enrolled in this study. A detailed history, clinical examination and hormonal analysis including basal luteinising hormone (LH), follicle-stimulating hormone (FSH), inhibin B, anti-Mullerian hormone (AMH), testosterone (boys), oestradiol (girls), triptorelin stimulation test and 3-day human chorionic gonadotropin (HCG) stimulation test (boys) were performed. All patients were followed for 1.5 years or till 18 years of age. Receiver operating characteristic (ROC) curve analysis was performed to determine the optimal cut-offs with sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) for various hormones to distinguish IHH from CDGP. Results: Of 34 children (male: 22 and female: 12), CDGP and IHH were diagnosed in 21 and 13 children, respectively. 4 hours post-triptorelin LH had the highest sensitivity (100%) and specificity (100%) for identifying IHH in both sexes. Basal inhibin B had good sensitivity (male: 85.7% and female: 83.8%) and specificity (male: 93.3% and female: 100%) for diagnosing IHH. 24 hours post-triptorelin testosterone (<34.5 ng/dl), day 4 post-HCG testosterone (<99.7 ng/dl) and 24 hours post-triptorelin oestradiol (<31.63 pg/ml) had reasonable sensitivity and specificity for identifying IHH. Basal LH, FSH and AMH were poor discriminators for IHH in both sexes. Conclusion: The best indicator was post-triptorelin 4-hour LH followed by inhibin B, which had a reasonable diagnostic utility to distinguish IHH from CDGP in both boys and girls.
RESUMO
Introduction: Studies investigating the alterations of serum irisin and its change with metformin therapy in patients with polycystic ovary syndrome (PCOS) are conflicting. Our aim is to study serum irisin in PCOS patients and the change of irisin levels with metformin therapy over 6 months. Methods: This is a randomized control study conducted in 187 PCOS cases and 94 age-matched controls aged 18-40 years. Detailed evaluation of anthropometric, biochemical, and hormonal parameters was performed. A subset of 99 overweight/obese patients with body mass index (BMI) ≥23 kg/m2 were stratified into a metformin group (n = 67) receiving 500 mg thrice daily and a lifestyle intervention-only group (n = 32). The effect of metformin therapy on serum irisin levels was measured at the end of 6 months. Statistical analyses were performed with SPSS version 26.0 Software. Results: Serum irisin was higher in PCOS patients than in controls [12.47 (8.1-17.7) vs 8.3 (7.0-9.6) ng/ml, P < 0.001], independent of BMI. Serum irisin showed a significant positive association with BMI (ß =0.168), waist-to-hip ratio (ß =0.166), leutinizing hormone (ß =0.225), TG (ß =0.305), FAI (ß =0.151), and testosterone (ß =0.135). Serum irisin showed a significant positive association with homeostatic model assessment of insulin resistance (HOMA-IR) (ß =0.14, P = 0.04) in overweight/obese PCOS patients only (n = 146) but not in the whole PCOS cohort (n = 187). Metformin reduced the median serum irisin levels significantly (13.9 to 12.1 ng/ml, P < 0.001), and the delta change in irisin levels was associated with HOMA-IR in the metformin group. Conclusion: Serum irisin is increased in PCOS patients independent of BMI. Metformin therapy reduced serum irisin levels in overweight/obese PCOS patients by improving insulin resistance.
