Female Reproductive Hormones and Biomarkers of Oxidative Stress in Genital Chlamydia Infection in Tubal Factor Infertility

Background: Genital Chlamydia infection (GCI) and the associated pathologies have been implicated in tubal infertility. Though the actual pathologic mecha-nisms are still uncertain, oxidative stress and other factors have been implicat-ed. The purpose of the study was to determine the possible contribution of fe-male reproductive hormones and biomarkers of oxidative stress in genital Chlamydial infection to tubal occlusion. Methods: This prospective case control study was carried out by recruiting 150 age matched women grouped into infertile Chlamydia positive women (n=50), fertile Chlamydia positive women (n=50) and fertile Chlamydia negative wom-en as controls (n=50). High vaginal swabs and endocervical swabs were collect-ed for screening Neisseria gonorrhoeae, Chlamydia trachomatis, Trichomonas vaginalis, Trepo-nema pallidum, Staphylococcus aureus, and Candida albicans. Sera were collected for estimation of Chlamydia trachomatis anti-body, female reproductive hormones [Follicle Stimulating Hormone (FSH), Lu-teinizing Hormone (LH), Oestradiol (E2), Progesterone (P4), Prolactin (PRL)] and biomarkers of oxidative stress [Total Antioxidant Capacity (TAC) and 8-hydroxyl-2-deoxyguanosine (8-OHdG)] by enzyme immunoassay (EIA). Data were analyzed using chi square, analysis of variance and LSD Post hoc to de-termine mean differences at p=0.05. Results: Among women with GCI, higher levels of LH and 8-OHdG were ob-served in infertile Chlamydia positive women compared to fertile Chlamydia positive women (p<0.05). Higher levels of LH and 8-OHdG and lower TAC levels were observed in infertile Chlamydia positive women compared to fertile Chlamydia negative controls (p<0.05). Conclusion: Mechanisms including oxidative DNA damage and reduced antiox-idant capacity may be involved in the pathology of Chlamydia induced tubal damage.