Abstract

Female infertility could be attributed to various factors including; sperm isoantobody, zona pellucid antibody, ovarian antibody, Chlamydia trachomatis infection and imbalance between oxygen radical and antioxygen radical. These factors might impair infertility by different mechanisms. A retrospective case-control study was performed on 105 infertile female including 75 (71.4%) with primary infertility and 30 (28.6%) with secondary infertility. Thirty healthy women were used as a control. Antisperm antibody (ASA), antizona pelucida antibody (AZP-Ab) and antiovarian antibody (AOA) were detected in the serum and cervical secretion using Enzyme labeled and Biotin labeled antibody. PCR technique was applied to detect the presence of Chlamydia trachomatis in the cervical secretion using the following primers: KL1-F and KL2-R, whereas IgG specific antibody was examined in the serum samples. According to infertility etiology, 29 (21.5%) were classified with unexplained infertility, 32 (23.7%) with polycystic ovary, 6 (4.4%) with endometriosis, 22 (16.3%) with tubal damage, 9 (6.7%) with hormonal imbalance, while other cases showed multiple causes of infertility. ASA were detected in the serum of infertile females (13.3%) and in (30%) of fertile one. Autoantibodies to zona pelucida were detected in the serum and the cervical secretion of infertile females (9.5% and 13.3%, respectively). No detectable levels of AZP-Ab were observed in fertile females. Statistically, the prevalence of ASA was significantly correlated to the AZP-Ab detected in the serum and cervical secretion of infertile females (P˃0.05). Aautoantibodies to different ovarian antigens were detected in the cervical secretion of 47 (44.8%) of the cases, in the absence of any detectable levels among fertile females. A high percentage of ASA, AZP-Ab and AOA were detected in primary infertility-related cases. However, with respect to the etiology of infertility, it seems that tubal damage, polycystic ovary and unexplained cases showed the highest percentages of both iso and autoantibodies. Serum samples obtained from fertile and infertile females were analyzed for the presence of C. trachomatis specific IgG. Five (4.76%) of etiologically tubal damage infertile females showed the presence of Chlamydial antibody with no detectable level in the serum of fertile females. To confirm the presence of C. trachomatis, PCR was used to identify Chlamydia DNA in the cervical secretion. Only positive serum samples revealed clear, sharp bands of amplified Chlamydial DNA with 241 bp. C. trachomatis was detected in infertile female with ASA (60%), serum and cervical secretion positive for AZP-Ab (60%, 80%, respectively) and in the cervical secretion positive for AOA (60%). A significant correlation was appeared between C. trachomatis infection and the presence of ASA and AZP-Ab (p˃0.05). Infertile females with Chlamydia infection has a high probability of inducing circulating and local ASA and AZP-Ab. Diagnosis of Chlamydia infection in the endocervix is recommended to assess their possible influence on ASA, AZP-Ab formation in infertile females.

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