Hysteroscopic subchorionic injection of methotrexate followed by laparoscopic excision of the gestational sac for the management of cesarean scar ectopic pregnancy: an innovative dual approach of a challenging pathology.

OBJECTIVE: To describe an effective two-step surgical approach for the management of cesarean scar ectopic pregnancies (CSEPs). CSEPs occur at an estimated frequency of 1 in 1,800 pregnancies, constituting approximately 6% of ectopic pregnancies in women with a history of prior cesarean delivery [1, 2]. Despite numerous recommended therapeutic approaches, the most effective treatment strategy remains uncertain [3]. DESIGN: We present an innovative double-step technique for the management of a patient with a CSEP involving hysteroscopic subchorionic injection of methotrexate (MTX), followed by laparoscopic resection of the residual gestational sac and simultaneous repair of the uterine defect. SETTING: Academic tertiary hospital. PATIENT: A 34-year-old G2P1001 with a history of prior cesarean section presented at 10 weeks of gestation. Ultrasound revealed a gestational sac within the niche of the previous cesarean scar, confirming the diagnosis of a CSEP. The patient included in this video gave consent for publication of the video and posting of the video online, including on social media, the journal website, scientific literature websites (such as PubMed, ScienceDirect, and Scopus, among others), and other applicable sites. INTERVENTION: The initial treatment involved hysteroscopic administration of MTX within the placental intervillous spaces, ensuring precise medication delivery. The administered dose of MTX was 1 mg/kg. Following the normalization of beta-human chorionic gonadotrophin (ß-hCG) levels, laparoscopic resection of the remaining gestational sac and reconstruction of the uterine wall defect were performed. MAIN OUTCOME MEASURES: We have implemented a management strategy focusing on ectopic pregnancy removal and addressing defect revision. The hysteroscopic approach allows for a clear assessment of the ectopic pregnancy and facilitates precise MTX administration, enhancing its effectiveness by increasing drug concentration within the placental intervillous space. Delaying surgical repair until after the ß-hCG levels have decreased reduces the risk of excessive bleeding during the procedure, as lower ß-hCG levels are associated with reduced vascularity at the ectopic site. Subsequent laparoscopic resection allows for complete removal of the remaining products of conception and repair of the defect, preserving the uterus and restoring normal anatomy. Compared to other surgical approaches, our two-step approach enables a more precise evaluation of placental implantation, making it a highly effective surgical method. RESULTS: We successfully managed a CSEP using a double-step technique. This involved hysteroscopic injection of subchorionic MTX, followed by laparoscopic resection of the residual gestational sac. Concurrently, we repaired the uterine defect. Both procedures were performed in an outpatient setting without complications detected during or after treatment. At the follow-up visit, the patient reported good health, and subsequent ultrasound confirmed an empty isthmocele. CONCLUSION: This sequential hysteroscopic and laparoscopic approach represents a definitive and effective minimally invasive surgical option for the treatment of CSEP.

Targeting galectin-1-induced angiogenesis mitigates the severity of endometriosis.

Endometriosis is characterized by the presence of endometrial tissue outside the uterus that causes severe pelvic pain and infertility in women of reproductive age. Although not completely understood, the pathophysiology of the disease involves chronic dysregulation of inflammatory and vascular signalling. In the quest for novel therapeutic targets, we investigated the involvement of galectin-1 (Gal-1), an endogenous glycan-binding protein endowed with both immunosuppressive and pro-angiogenic activities, in the pathophysiology of endometriotic lesions. Here we show that Gal-1 is selectively expressed in stromal and endothelial cells of human endometriotic lesions. Using an experimental endometriosis model induced in wild-type and Gal-1-deficient (Lgals1(-/-) ) mice, we showed that this lectin orchestrates the formation of vascular networks in endometriotic lesions in vivo, facilitating their ectopic growth independently of vascular endothelial growth factor (VEGF) and the keratinocyte-derived CXC-motif (CXC-KC) chemokine. Targeting Gal-1 using a specific neutralizing mAb reduced the size and vascularized area of endometriotic lesions within the peritoneal compartment. These results underline the essential role of Gal-1 during endometriosis and validate this lectin as a possible target for the treatment of disease.