Abstract
Apoptotic cell death, probably induced by oxidative stress, contributes to the development of pelvic organ prolapse. Because poly(ADP-ribose) polymerase-1 is an important mediator of cellular response to oxidative stress, genetic variations in the poly(ADP-ribose) polymerase-1 gene may play a role in the pathogenesis of pelvic organ prolapse. This study aimed to determine the association between advanced pelvic organ prolapse and Val762Ala polymorphism in the poly(ADP-ribose) polymerase-1 gene. A total of 340 women were enrolled in the study. The pelvic organ prolapse group consisted of 185 women with stage III or IV pelvic organ prolapse, whereas the control group consisted of 155 postmenopausal women with stage 0 or I pelvic organ prolapse who visited the hospital for treatment of benign gynecologic disease or routine gynecologic checkup. Genotyping of the poly(ADP-ribose) polymerase-1 Val762Ala polymorphism was performed by real-time polymerase chain reaction analysis using a TaqMan assay. Genotype distribution in the pelvic organ prolapse group was different from that in the control group (P = 0.024). Furthermore, C-allele frequency was lower in the pelvic organ prolapse group than in the control group (P = 0.029). Women with the CC genotype had a 0.461-fold lower risk of developing advanced pelvic organ prolapse than women with the TT genotype (95% CI, 0.245-0.870; P = 0.017), and women with the C-allele had a 0.716-fold lower risk of developing advanced pelvic organ prolapse than women with the T-allele (95% CI, 0.527-0.973; P = 0.033). These findings suggest that the poly(ADP-ribose) polymerase-1 Val762Ala polymorphism is associated with a decreased risk of advanced pelvic organ prolapse.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.