Oral Presentation
Context: Endometriosis is a complex gynecological disorder where protective effects of progesterone are reduced due to lower expression of the nuclear progesterone receptors or accelerated progesterone metabolism. As ectopic endometrial tissue causes inflammation, endometriosis is also considered a chronic inflammatory disease. Aldo-keto reductase 1C3 (AKR1C3) has roles in progesterone metabolism as well as in biosynthesis of prostaglandins PGF2α and 9α,11β-PGF2α. These prostaglandins have inflammatory effects, but also influence angiogenesis, adhesion and enhance proliferation of endometriotic cells. Our previous studies showed higher expression of AKR1C3 in ovarian endometriosis compared to normal endometrium (1, 2). Similarly, up-regulation of AKR1C3 was reported in peritoneal endometriosis (3), while expression in deep infiltrating endometriosis has not yet been examined. Objective: To examine the levels of AKR1C3 in different types of endometriosis and control endometrial samples and to evaluate potential correlations with clinical parameters. Methods: Immunohistochemical staining with a specific, validated monoclonal antibody against AKR1C3. Patients: Patients with ovarian, peritoneal and deep infiltrating endometriosis and control patients from University Medical Centre Ljubljana, Slovenia. Interventions: Collection of archived paraffin samples and clinical data from women undergoing laparoscopy. Results: Immunohistochemical staining of ovarian, peritoneal and deep infiltrating endometriosis samples showed intensive epithelial and weak stromal staining (4). However, there were no statistically significant differences between ovarian endometriosis and control endometrial samples. Immunohistochemical analysis on a larger number of samples is currently in progress; as also analysis of various clinical parameters such as stage of disease, progestin treatment and usage of oral contraception which may affect AKR1C3 levels. Conclusion: We expect our study to elucidate the involvement of AKR1C3 in pathopysiology of endometriosis and thus to assess its potential as a target for treatment. (1) N. Hevir et al. Chemico-biological interactions 191, 217-226 (2011). (2) T. Smuc et al. Molecular and cellular endocrinology 301, 59-64 (2009). (3) H. Rakhila et al. Fertility and sterility 100, 1650-1659 e1651-1652 (2013). (4) M. Sinreih et al. Chemico-biological interactions 234, 320-331 (2015).