High-grade serous ovarian carcinoma (HGSOC) frequently recurs after platinum-taxane therapy, yet recurrence-associated changes within ascites remain unclear. We performed cell-type-resolved quantitative proteomics on paired ascites samples collected at primary diagnosis and at disease recurrence from three HGSOC patients, profiling unsorted cells alongside matched CD45[-] tumor-enriched and CD45[+] immune-enriched fractions. Conventional proteomic label-free quantitative (LFQ) analysis yielded limited significant proteins due to inter-patient heterogeneity. To address this, we applied Gene Set Enrichment Analysis (GSEA) to identify coordinated pathway-level alterations associated with recurrence. Across all cellular compartments, recurrent samples exhibited consistent downregulation of interferon-α/γ-associated pathways alongside enrichment of oxidative phosphorylation and stress-adaptive metabolic programs. In the CD45[+] immune compartment, these changes were accompanied by enhanced IL-2/STAT5 signaling and reduced antigen-presentation pathways. Together, these findings suggest that recurrent ascites is characterized by a shift toward oxidative metabolism and a more immunosuppressive microenvironment.

Haemorrhagic ascites (HA) is an uncommon clinical entity commonly caused by cirrhosis, malignancy and iatrogenic intervention. In the absence of these causes, it poses a diagnostic challenge. We present a case of a female with recurrent massive HA with a negative extensive work-up of common causes of HA. Laparoscopically obtained tissue eventually confirmed the diagnosis of endometriosis. This case demonstrates important diagnostic pitfalls in HA and highlights consideration of rarer causes.

Ovarian cancer remains a leading cause of gynecologic cancer death worldwide, largely due to late diagnosis, frequent recurrence, and metastatic tendencies. Thrombosis is a common and life-threatening complication in these patients, contributing to poor prognosis and therapy resistance. Emerging evidence highlights a mechanistic link between tumor-derived extracellular vesicles and thrombotic events - particularly podoplanin-positive small extracellular vesicles (PDPN[+] sEVs). Secreted by PDPN-expressing ovarian tumor cells, these vesicles act as biologically active messengers that circulate systemically. A central mechanism involves the binding of PDPN[+] sEVs to C-type lectin-like receptor 2 (CLEC-2) on platelets, inducing platelet activation, aggregation, and the release of pro-inflammatory mediators. This interaction creates a hypercoagulable and pro-inflammatory microenvironment. Beyond coagulation, PDPN[+] sEVs promote cancer aggressiveness by enhancing cancer stem cell plasticity, driving epithelial-to-mesenchymal transition, and facilitating immune evasion - hallmarks of metastasis and chemoresistance. This dual activity establishes a thromboinflammatory tumor niche that accelerates disease progression while undermining treatment efficacy. The ability of PDPN[+] sEVs to circulate in ascitic fluid and peripheral blood positions them as promising candidates for liquid biopsy-based diagnostics. Furthermore, targeting the PDPN-CLEC‑2 axis or disrupting sEV biogenesis offers a novel therapeutic strategy to curb both thrombosis and metastatic spread. In conclusion, PDPN[+] sEVs represent a critical molecular link between coagulation and cancer progression, offering valuable diagnostic, prognostic, and therapeutic potential for improving outcomes in ovarian cancer.

Endometriosis, affecting 10-15% of women of reproductive age, is more commonly found on the left side of the pelvis. This laterality phenomenon's etiology remains obscure. We reviewed the existing literature and proposed four different theories explaining the left laterality of endometriosis. The anatomical theory is based on the structural asymmetry of the pelvis. Organs surrounding the left adnexa serve as mechanical barriers and interfere with clearance of endometrial cells migrating to the pelvis, promoting in turn endometriotic implants. The physiological theory focuses on the role of the peritoneal fluid flow, shown to be slower and weaker on the left side, allowing more time for adherence of endometrial fragments or cells. The hormonal theory rests on the right ovulatory predominance that may impose progesterone richer milieu on the right hemipelvis which in turn inhibits endometriosis on that side. The vascular theory suggests that higher hydrostatic pressure in the left venous system, secondary to differences in anatomy, may favor local stasis and implantation of endometriosis. Although each theory can explain the phenomenon independently, they are likely to be interrelated. Whether the asymmetrical distribution of endometriosis is associated with asymmetric clinical manifestation is yet to be known. Further studies are required in order to elucidate our understanding of this common disease and its features. Understanding the lateral tendency of endometriotic lesions may improve diagnostic accuracy and assist surgical decision-making in operative planning.

Meckel's diverticulum (MD) is one of the most common congenital anomalies of the gastrointestinal tract in children, although it may occasionally be detected in adults. It is typically located within 100 cm of the ileocecal valve in the distal ileum. The diverticulum varies in size and morphology; many patients remain asymptomatic throughout life. In children, the most common clinical presentation is painless gastrointestinal bleeding, followed by intestinal obstruction. Intussusception may also occur. Once complications develop, patients often present with acute abdomen. Failure to establish a timely diagnosis and initiate appropriate management may result in intestinal ischemia or even necrosis. Furthermore, acute intestinal obstruction may obscure the underlying pathology, increasing the risk of misdiagnosis or missed diagnosis on radiologic evaluation. We report a rare case of Meckel's diverticulum complicated by band adhesion resulting in internal hernia and small bowel obstruction, further associated with peritonitis and massive ascites. The diverticulum was located approximately 40 cm proximal to the ileocecal valve. A fibrous diverticular band adhered to adjacent bowel loops, forming a hernia orifice that caused obstruction of the neighboring small intestine and mesentery. The patient underwent surgical resection of the Meckel's diverticulum, partial ileal resection, and end-to-end ileo-ileal anastomosis. The procedure was uneventful, and postoperative recovery was satisfactory. Internal hernia caused by Meckel's diverticulum band adhesion with associated peritonitis and massive ascites is rare. This case broadens the differential diagnosis of pediatric intestinal obstruction without prior abdominal surgery.

Recurrent hemorrhagic pleural effusion presents as a challenge for both the clinician and the patient, with common causes being tuberculosis, malignancy, and collagen vascular diseases. Among uncommon causes of recurrent hemorrhagic effusion is catamenial hemothorax, which is a part of thoracic endometriosis syndrome (TES). Endometriosis is the extrauterine growth of endometrial glands and stroma. It is relatively common among women of reproductive age-group, with reported incidence of around 11%. Although rare, the thorax is the most common extraabdominal site for endometriosis. Here we present a rare case of recurrent hemorrhagic pleural effusion due to thoracic endometriosis in a young female with infertility. A 33-year-old female housewife presented with dyspnea on exertion modified Medical Research Council (mMRC) grade 2 and dry cough occasionally for 6 months. She had a history of tubercular cervical lymphadenopathy for which she was on treatment. Therapeutic thoracocentesis was performed thrice in 4 months. Routine microscopy showed predominantly lymphocytes, mesothelial cells, and numerous foamy histiocytes, some pigment laden. There were no malignant cells or acid-fast bacilli (AFB) detected in the fluid. Pleural fluid amylase and lipase were normal. Contrast-enhanced computed tomography (CT) thorax showed moderate right-sided pleural effusion without any evident parenchymal lesions, pleural lesions, or mediastinal lymphadenopathy. Ultrasonography (USG) abdomen and pelvis showed mild ascites which was nontappable. As we had not reached a definitive diagnosis, medical thoracoscopy was performed. It showed moderate hemorrhagic pleural fluid in the pleural cavity and a small raised erythematous glandular tissue on the parietal pleural surface from which biopsy was taken. Histopathology showed an island of endometrial stroma with a single gland. Immunohistochemistry was performed on this section, which was PAX8 and CD10 positive, confirming the diagnosis of thoracic endometriosis. Pleurodesis with talc slurry was done to prevent further refilling of the effusion. Gynecology opinion was sought, and patient was started on monthly subcutaneous injections of gonadotropin-releasing hormone (GnRH) analogue for 3 months. Chest X-ray after 3 months showed no refilling of pleural effusion. Catamenial hemothorax is the second commonest manifestation of TES, occurring in approximately 14% of cases. It affects the right side in about 80% of the cases. Diagnosis is based on high degree of suspicion and is often delayed. Video-assisted thoracic surgery (VATS) remains the gold standard for diagnosis and management of TES. Medical thoracoscopy is a viable alternative in resource-poor settings or when diagnosis is not confirmed. On histology, diagnosis is confirmed by the presence of endometriotic glands or stroma, which may also show stromal arterioles, erythrocytes, and pigmented histiocytes. In difficult-to-diagnose cases, CD10 immunohistochemical staining can help in diagnosis of endometrial tissue. There are various treatment modalities considered in the management of catamenial hemothorax, like surgical resection, medical management along with pleurodesis, combination therapy, or in some cases, simple observation. Currently, VATS with GnRH analogue therapy is considered the gold standard of management.

Iatrogenic arteriovenous (AV) fistula is a rare but treatable cause of high-output heart failure that can mimic restrictive cardiomyopathy and may lead to inappropriate listing for heart transplantation.

Posterior urethral valves (PUV) are the most common cause of congenital bladder outlet obstruction in male infants and may result in kidney damage and chronic kidney disease. In severe cases, spontaneous fetal bladder rupture with urinary ascites may occur. This study presents a rare case of fetal bladder rupture secondary to PUV requiring complex bladder reconstruction and systematically reviews similar cases.

This study retrospectively evaluates the microbiological profile, antibiotic susceptibility patterns, and the effectiveness of empirically initiated antibiotic therapies in children with perforated appendicitis, based on intraoperative peritoneal fluid culture and antibiogram results.