Objectives:
Myeloid cell-derived factors contribute to the immunopathology of endometriosis. Soluble CD14 (sCD14), CD163 (sCD163), and MIF serves as in vivo markers of myeloid function. However, these soluble molecules are largely unexplored in women with endometriosis-related infertility cases. We investigated three soluble markers, namely sCD14, sCD163, and MIF, in cases of infertility associated with endometriosis and correlated its level to the stage of endometriosis.
Design:
Eighty-seven women newly diagnosed with endometriosis or other benign gynecologic control cases linked to infertility were prospectively recruited and underwent diagnostic laparoscopy.
Participants:
Forty-four patients with endometriosis were included in this study, comprising 19 patients with early-endometriosis (stages I and II) and 25 late-endometriosis (stages III and IV) based on the revised American Society for Reproductive Medicine (rASRM) classification. The remaining 43 patients constituted a control group with infertility due to other causes.
Methods:
The levels of sCD14, sCD163, and MIF in serum and peritoneal fluid were assessed using ELISA.
Results
Endometriosis women exhibited significantly higher serum levels of sCD163 and MIF levels compared to the control group. Both sCD163 and MIF levels displayed a positive correlation with the r-ASRM adhesion score. Moreover, the MIF level in serum had a positive correlation with the r-ASRM endometriosis score. In receiver operating characteristic (ROC) analysis, serum sCD163 and MIF could significantly discriminate endometriosis and non-endometriosis in infertility cases.
Limitations
Some limitations of the current study deserve to be underlined. Firstly, the sensitive ELISA method was the sole validated tool for detecting the markers in patient samples. Secondly, healthy or fertile women were not involved as the control group.
Conclusions
The elevated systemic levels of sCD163 and MIF correlated with the severity of endometriosis. These soluble molecules have a potential diagnostic capacity as a non-invasive biomarker. Furthermore, our data warrants future studies on the underlying mechanism of sCD163 and MIF in endometriosis-related infertility.