Lala Lajpat Rai Memorial Medical College

Endometrial carcinoma (EC) is one of the most prevalent gynecological malignancies, with an increasing incidence globally. This review explores the role of molecular markers in revolutionizing the diagnosis, prognosis, and management of EC. This article provides an overview of endometrial carcinoma, emphasizing its subtypes and the molecular mechanisms driving disease progression. Current biomarkers, while clinically significant, often present limitations in sensitivity, specificity, and predictive value, necessitating the discovery of novel markers. Recent advances in genetic and epigenetic profiling have identified key mutations, such as PTEN, TP53, and POLE, along with DNA methylation patterns and microRNAs, as crucial contributors to EC pathophysiology. Furthermore, transcriptomic and proteomic studies reveal the potential of RNA-based markers (e.g., lncRNAs, mRNAs) and proteomic signatures in improving early diagnosis and prognostic predictions. Immunohistochemical markers and insights into tumor microenvironment dynamics pave the way for targeted therapeutic strategies. In the context of endometrial carcinoma (EC), clinical trials play a pivotal role in validating targeted therapies based on molecular subtypes and biomarkers, such as HER2 amplification, POLE mutations, and mismatch repair deficiency (MMRd). This review underscores the integration of biomarkers into precision oncology, enabling personalized treatment regimens. However, challenges such as barriers to clinical translation and the need for advanced technologies highlight the importance of continued research in marker discovery for EC.

Postpartum hemorrhage (PPH) is a leading cause of maternal morbidity and mortality worldwide, particularly in developing countries. Effective uterotonic agents are crucial for minimizing blood loss and maintaining hemodynamic stability during deliveries. Carbetocin has emerged as a promising alternative to oxytocin for preventing PPH, especially in high-risk pregnancies.

This study aimed to compare the efficacy of carbetocin and oxytocin in controlling intraoperative blood loss, maintaining uterine tone, and reducing the need for additional uterotonics in women undergoing cesarean section (CS) with a high risk of PPH.

This prospective case-control study was conducted on 200 pregnant women at high risk for PPH undergoing CS after obtaining written informed consent. Participants were randomly assigned to two groups. Group I (n = 100) received injection carbetocin (100 µg IV), while Group II (n = 100) received injection oxytocin (10 IU IV in 500 mL normal saline). The hemodynamic parameters of the participants, uterine tone, blood loss, and the need for additional uterotonics were recorded and analyzed.

Carbetocin significantly reduced intraoperative blood loss, with 81 participants (81%) in the carbetocin group experiencing blood loss less than 500 mL compared to 54 participants (54%) in the oxytocin group. The need for additional uterotonics was significantly lower in the carbetocin group (13% vs. 43%; n = 100). Uterine tone was better in the carbetocin group both intraoperatively and two hours postoperatively (p < 0.0004), and the postoperative fall in hemoglobin was also less compared to the oxytocin group. Hemodynamic stability was maintained better in the carbetocin group, with fewer fluctuations in blood pressure.

Carbetocin was found to be more effective than oxytocin in managing high-risk cesarean deliveries, offering better control over intraoperative blood loss, maintaining uterine tone, and reducing the need for additional uterotonics. Its prolonged uterotonic effect and stable hemodynamic profile make it a superior choice for PPH prevention in CSs.

Glandular odontogenic cysts(GOC) are among the rarest odontogenic cysts defined by the presence of glandular epithelium in the epithelial lining posing some diagnostic difficulties. GOC associated with ameloblastoma is extremely rare with only 5 cases reported. This report deals with this rare occurrence of GOC along with unicystic ameloblastoma.