The Impact of Luteinizing Hormone/Chorionic Gonadotropin Hormone Receptor Gene Polymorphism rs68073206 in Men with Non-obstructive Azoospermia: A Case-control Study

Abstract

Background: The functional consequences of the luteinizing hormone/chorionic gonadotropin hormone receptor (LHCGR) gene single nucleotide polymorphism (rs68073206) on male infertility in patients with non-obstructive azoospermia (NOA) is not clear.
 Objective: To examine whether the presence of LHCGR gene; rs68073206 single nucleotide polymorphisms (SNPs) can be associated with incidence of non-obstructive azoospermia.
 Materials and methods: A case-control study comprised of a total of 70 unrelated Iraqi infertile men with non-obstructive azoospermia (zero sperm in semen) whose were on two groups: Group I that were diagnosed to have NOA but didn’t receive infertility treatment yet (33 patient with age of 31.58±1.059 year) and group II that were receiving injectable gonadotropin treatment (37 patient with age of 33.46±1.173 year). In addition to 34 age and BMI matched healthy fertile normozoospermic men (according to the parameters of WHO, 2010). The study population was genotyped by TaqMan assay for LHCGR gene single nucleotide polymorphism (rs68073206). The level of each hormone was estimated by immunoassay technique while the sperm analyses were conducted in accordance with the World Health Organization criteria.
 Results: The study revealed a statistically significant higher hormonal level of serum inhibin B in infertile group I patients with wild GG genotype (246.445±224.106 pg/ml), and the p-value is (0.0439) as compared to that hormone levels of GT and TT genotypes carriers that were (85.969±71.685 pg/ml) and (56.420±23.988 pg/ml) respectively. ). The genotyping variations of patients, whether carrying the homozygous GG, heterozygous GT or homozygous TT genotype, did not reveal a statistically significant difference in distribution as compared to control individuals.
 Conclusions: The LHCGR gene rs68073206 polymorphisms in our population having non-obstructive azoospermia can be suggested to have a modulating potential in variable gonadotropin sensitivity. The detected non-significant difference in genotypic prevalence can be attributable to the limited sample size.