Search

A growing body of evidence suggests that endometrial immune disorders may be responsible for endometrial dysfunctions that can lead to gynecological and obstetrical pathology. The aim of this study was to explore the potential relationship between different killer cell immunoglobulin-like receptor (KIR) genotypes and reproductive outcomes. We conducted a prospective cohort study that included 104 infertile patients undergoing an in vitro fertilization procedure. All participants underwent clinical and ultrasound examination, genetic evaluation (KIR genotyping), endometrial washing fluid sampling for cytokine determination, endometrial tissue sampling for histologic assessment and hysteroscopic evaluation. Our analysis showed statistically significant lower levels of uterine cytokines TNF-α (p = 0.001) and IL-1beta (p = 0.000) in the KIR AA genotype group as compared to KIR AB and BB among study participants with chronic endometritis. The study results suggest that the KIR AA genotype population subgroups may be more susceptible to developing endometrial disorders such as chronic endometritis. The changes in the behavior of NK cells seem to be subtle and expressed as an altered regulatory pattern.

“Poor responders” (PR) are an important category of infertile women who experience a modest response to controlled ovarian stimulation. In this study, we evaluated response to growth hormone (GH) administration among PR patient subtypes stratified by follicle stimulation hormone receptor (FSHR) polymorphism (c.2039A > G p.Asn680Ser). We conducted a cohort study of 125 women with poor ovarian response, 58 of whom received GH in addition to the standard treatment, and 67 of whom received the standard treatment only. The Ala307Thr polymorphism genotypes were analyzed using a polymerase chain reaction-restriction fragment length polymorphism method, and the FSHR gene polymorphism was analyzed using a predesigned TaqMan SNP Genotyping Assay (rs6166). A comparative analysis detected statistically significant differences in mean mature follicles (p = 0.0002), metaphase-II oocytes (p = 0.0005), progesterone levels (p = 0.0036), and IGF levels (follicle IGF1, p = 0.0004) between GH-treated and non-GH-treated participants with the FSHR (Ser/Ser) polymorphism. However, the differences were modest among participants with the other two FSHR polymorphisms (Ser/Asn and Asn/Asn). The subcategory of patients with the FSHR Asn680Ser (Ser/Ser) polymorphism showed a stronger response when GH was added to the IVF protocol.

Objectives: Interleukin 4 plays a critical role in T helper 2 responses to HPV infection and angiogenesis. The present study aim to study the association between the IL4 promoter polymorphism – 590 C>T, respectively VNTR intron 2 polymorphism and cervical intraepithelial neoplasia. Material and method: We have realized a prospective case controls study that included 128 cases of intraepithelial neoplasia positive for HPV HR testing and 111 controls negative for intraepithelial lesion and also negative for HPV HR. Clinical examination was performed on each patient; blood and cervical sample were obtained. Cervical probes were analyzed regarding cytology and HPV HR testing. From peripheral blood DNA sample was obtain followed by genotype analysis for IL4 -590 C>T using PCR RFLP, respectively IL4 70 bp VNTR determined by PCR. Results: The absolute frequency of genotypes for IL4 -590 C>T was T/T-5, C/T-42, C/C-81 in the cases group respectively T/T-2, C/T-32, C/C-77 in the control group. The chi-square test had a value of 0.983 (p=0.321) while considering the presence of a minimum one single variant allele as a risk factor for cervical cancer, respectively 0.926 (p=0.336) for homozygous variant genotype. Odds ratio was 0.761 (95%CI [0.443-1.306]) while considering C/T+T/T respectively 2R/3R, 2R/2R as a risk factor, and 0.451 (95%CI 95% [0.086-2.374]) - TT respectively 2R/2R as a risk factor. Conclusion: No linear statistical significant association has been found between IL4 polymorphism and cervical neoplasia (p = 0.322).