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Background:Obesity may establish a crucial barrier for effective fertility treatment in polycystic ovary syndrome (PCOS) females.Objective: To compare results of intra-cytoplasmic sperm injection (ICSI) in females with and without polycystic ovarian syndrome and further appraise the effect of obesity in PCOS females.Materials and Methods:A cross-sectional study from June 2015 to July 2016 included non-PCOS and PCOS (recognized by Rotterdam criteria) females who underwent ICSI. The PCOS were further stratified into non-obese and Obese according to the South Asian criteria for body mass index. Results were categorized on the basis of beta-human chorionic gonadotropin (β-hCG) and transvaginal scan into non-pregnant (β-hCG <25 mIU/ml), preclinical abortion (β-hCG >25 mIU/ml with no fetal cardiac activity) and clinical pregnancy (β-hCG >25 mIU/ml with fetal cardiac activity on transvaginal scan). In addition, reproductive outcomes; implantation rate, clinical pregnancy rate and miscarriage rate among obese and non-obese PCOS and non-PCOS patients were compared.Results:Our results revealed 38.5% clinical pregnancy rate in non-PCOs females, 23.8% in non-obese PCOS females whereas 26.4% in obese PCOS. Preclinical abortions were found to be highest (31.5%) in non-obese PCOS females and were the lowest (26.2%) in non-PCOS females. In non-PCOS group and non-obese PCOS females 35.4% and 44.6%, respectively, failed to become pregnant.Conclusion: The success after ICSI in terms of number of clinical pregnancies was more in non-PCOS patients as compared to PCOS. Increase in body mass index reflected a negative impact on the reproductive outcome in PCOS patients.

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Objective The objective of this was to demonstrate the association of Inhibin α (INHα) c.‐124G>A and INHα‐c.‐16 C>T polymorphisms with altered sperm parameters in a selected male population of Karachi, Pakistan. Study Design & Settings In this pilot study, male subjects were stratified on the basis of the WHO criteria for altered sperm parameters; 83 (cases—altered sperm parameters) and 30 (controls—normal sperm parameters) subjects were included for analysis of INHα‐c.124G>A polymorphism and 88 (cases) and 38 (controls) were analysed for INHα ‐c‐16 C>T polymorphism. Genotyping of INHα‐c.‐124G>A and INHα‐c.‐16 C>T was performed by PCR‐RFLP, genotype distribution in Hardy‐Weinberg equilibrium was evaluated by binary logistic regression model. Results For the c.‐124G>A polymorphism in INHα gene, frequency of the three major genotypes in controls was: GG: 80.0%, GA: 20.0% and AA: 0% and in cases was: GG: 59.0%, GA: 30.2% and AA: 10.8%. The GG genotype was significantly associated with male infertility (P < .045, OR = 2.776, 95% CI = 1.025‐7.513) while the GA genotype was not significantly associated with infertility (P < .290 OR = 0.580, 95% CI = 0.211‐1.593). Frequency of mutant AA genotype was 10.8% in cases (altered sperm parameters) and absent (0%) in normal sperm parameter (controls). The frequencies of three major genotypes CC, CT and TT did not show any significant difference between cases and controls (P > .05). Conclusion The results from our study exhibited a significant association of c.‐124G>A polymorphism in the INHα gene promoter region with male infertility in the Pakistani population. A significant association of c.‐16 C>T polymorphism with male infertility, however, was not observed. Further large‐scale studies should be conducted to confirm this association.