Is endometrial receptivity affected in women with endometriosis? Results from a matched pair case-control study of assisted reproductive technology treatments.

RESEARCH QUESTION: Is endometriosis detrimental to embryo implantation? DESIGN: A retrospective matched case-control study of women with a surgical or ultrasound diagnosis of endometriosis at Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico di Milano between 2015 and 2021. Women with endometriosis who underwent a 'freeze-all' cycle during an IVF treatment were eligible to be included. They were matched to patients without the disease, who also underwent cryopreserved blastocyst transfer cycles, in a 1:1 ratio by age (±1 year), and number (=) and quality (±1 top versus low) of cryopreserved blastocysts. All women underwent single frozen embryo transfer, and assisted reproductive technology outcomes suggested by the Core Outcome Measure for Infertility Trials initiative were evaluated. The main outcome was the cumulative live birth rate per cycle. RESULTS: One hundred and one women with endometriosis and 101 matched unaffected women were included. Cumulative live birth rate per cycle did not vary between women with and without endometriosis (50% versus 58%, respectively; P = 0.32). On the basis of the Kaplan-Meier analysis, the predicted success rates over four embryos transferred were also similar (74% versus 82%, respectively; P = 0.67). CONCLUSION: In women with moderate or severe endometriosis, these retrospective results seem to indicate no or a limited effect of the disease on endometrial receptivity.

Dual trigger with gonadotropin-releasing hormone agonist and human chorionic gonadotropin significantly improves oocyte yield in normal responders on GnRH-antagonist cycles.

OBJECTIVE: During in vitro fertilization (IVF) cycles, final oocyte maturation is usually triggered by human Chorionic Gonadotropin (hCG) for its known effect in mimicking Luteinizing Hormone (LH) surge; however, with the widespread use of the 'antagonist protocol', Gonadotropin Releasing Hormone agonist (GnRHa) is being more commonly employed as a trigger in order to minimize or eliminate the risk of ovarian hyper-stimulation syndrome (OHSS). Many studies proved its efficacy in inducing oocyte maturation and its safety in preventing OHSS in high-risk groups. Moreover, some studies showed that GnRHa trigger may improve oocyte yield. This study aimed to further explore any beneficial effect of adding GnRHa to hCG (dual trigger) on oocyte yield and fertilization rate in normal responder women. METHODS: We retrospectively reviewed and analyzed the data from 127 patients on antagonist protocol (67 dual trigger and 60 HCG trigger). RESULTS: The number of total oocytes, the number of MII oocytes and the number of fertilized oocytes were all significantly higher with the dual trigger protocol compared to hCG-only trigger. However, there is no significant difference in clinical pregnancy rate. CONCLUSIONS: Using the dual trigger improved the number and quality of oocytes, and the fertilization rate in normal responders.

Diagnostic value of serum activin A and follistatin levels in women with peritoneal, ovarian and deep infiltrating endometriosis.

BACKGROUND: Activin A is a growth factor, produced by the endometrium, whose actions are modulated by the binding protein follistatin. Both proteins are detectable in the peripheral serum and their concentrations may be increased in women with endometriosis. The present study was designed to evaluate whether serum levels of activin A and follistatin are altered, and therefore have a potential diagnostic value, in women with peritoneal, ovarian and deep infiltrating endometriosis. METHODS: We performed a multicenter controlled study evaluating simultaneously serum activin A and follistatin concentrations in women with and without endometriosis. Women with endometriosis (n = 139) were subdivided into three groups: peritoneal endometriosis (n = 28); ovarian endometrioma (n = 61) and deep infiltrating endometriosis (n = 50). The control group (n = 75) consisted of healthy women with regular menstrual cycles. Blood samples were collected from a peripheral vein and assayed for activin A and follistatin using commercially available enzyme immunoassay kits. RESULTS: The ovarian endometrioma group had serum activin A levels significantly higher than healthy controls (0.22 ± 0.01 ng/ml versus 0.17 ± 0.01 ng/ml, P < 0.01). None of the endometriosis groups had serum follistatin levels which were significantly altered compared with healthy controls; however, levels found in the endometrioma group (2.34 ± 0.32 ng/ml) were higher than that in the deep endometriosis group (1.50 ± 0.17 ng/ml, P < 0.05). The area under the receiver operating characteristic curve of activin A was 0.700 (95% confidence interval: 0.605-0.794), while that of follistatin was 0.620 (95% confidence interval: 0.510-0.730) for the diagnosis of ovarian endometrioma. The combination of both markers into a duo marker index did not improve significantly their diagnostic accuracy. CONCLUSIONS: The present study demonstrated that serum activin A and follistatin are not significantly altered in peritoneal or deep infiltrating endometriosis and have limited diagnostic accuracy in the diagnosis of ovarian endometrioma.