• Fertility and sterility · Jun 2008

    Imbalance in the peritoneal levels of interleukin 1 and its decoy inhibitory receptor type II in endometriosis women with infertility and pelvic pain.

    • Ali Akoum, Mahéra Al-Akoum, André Lemay, Rodolphe Maheux, and Mathieu Leboeuf.
    • Unité d'endocrinologie de la Reproduction, Centre de Recherche, Pavillon Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, Faculté de Médecine, Université Laval, Québec, Canada. ali.akoum@crsfa.ulaval.ca
    • Fertil. Steril. 2008 Jun 1; 89 (6): 1618-24.

    ObjectiveTo evaluate the levels of interleukin-1beta (IL1beta) and its inhibitory soluble interleukin-1 receptor type II (IL1R2) in the peritoneal fluid (PF) of normal women and patients with endometriosis suffering from pelvic pain and infertility.DesignRetrospective study using ELISA to measure peritoneal fluid IL1beta and soluble IL1R2.SettingGynecology clinic and human reproduction research laboratory.Patient(S)Sixty-eight normal women and 154 women with endometriosis.Intervention(S)Peritoneal fluid samples were obtained at laparoscopy.Main Outcome Measure(S)IL1beta and soluble IL1R2 concentrations in the PF samples.Result(S)This study showed a marked decrease in peritoneal soluble IL1R2 levels in women with endometriosis compared to normal women and a concomitant increase in the levels of IL1beta. Both fertile and infertile women with endometriosis had lower soluble IL1R2 and higher IL1beta concentrations than fertile women having a normal gynecological status, but the difference was more significant in infertile endometriosis patients. Compared with normal controls, the decrease in soluble IL1R2 levels was less significant in women with endometriosis than without pelvic pain, whereas the increase in IL1beta concentrations was statistically significant only in women with endometriosis reporting pelvic pain.Conclusion(S)This study revealed an imbalance between IL1beta and its decoy inhibitory receptor type 2 in women with endometriosis, which was particularly obvious in those who were infertile, and suggests that a defect in the local control of IL1 may be involved in the pathophysiology of endometriosis and related infertility.

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