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Tuberculosis is a rare but treatable infectious disease that continues to pose a significant health issue in regions with high prevalence. Its abdominopelvic localization can mimic advanced ovarian cancer, leading to diagnostic challenges. This report describes the case of a 33-year-old woman who was admitted to the gastroenterology unit with ascites, peritoneal thickening, and an ovarian mass on imaging. The diagnosis of abdominopelvic and peritoneal tuberculosis was confirmed after laparoscopy. The patient underwent antitubercular chemotherapy and showed clinical improvement.

Mesenteric panniculitis (MP), also known as sclerosing mesenteritis, is a rare idiopathic condition characterised by chronic inflammation and fibrosis in the mesentery. While small amounts of chylous ascites due to lymph drainage obstruction are not rare in patients with MP, massive ascites is a rare complication. Moreover, protein-losing enteropathy (PLE), a rare intestinal condition of uncompensated plasma protein loss, can occur in patients with MP. To the best of our knowledge, the present study is the first to report MP with massive chylous pleural effusion and PLE in a 56-year-old male presenting with dyspnoea at Osaka Medical and Pharmaceutical University Hospital (Osaka, Japan) in March 2023. Approximately 5 years prior, the patient noticed systemic oedema, transient abdominal pain and fever and weight loss, and was diagnosed with chylous ascites and PLE by abdominal paracentesis and endoscopic examination of the small intestine. Although initial prednisolone (20 mg/day) administration improved the oedema gradual and uncontrolled fluid buildup was observed. Computed tomography revealed pneumothorax, bilateral massive pleural effusion, and pneumonia. Despite extensive antibiotic therapy [voriconazole (300 mg, twice/day), Ampicillin/Sulbactam (3 g x 4/day), and Vancomycin (1,000 mg x 2/day)], the patient succumbed to respiratory failure 1 month later. Autopsy revealed massive chylous ascites, pleural effusion and the presence of thickened and calcified nodules in the mesentery. Histopathological examination showed diffuse fat necrosis with fibrosclerosis, calcification and lymphocytic infiltration within the mesentery. Therefore, a definitive diagnosis of MP was made. The present case highlighted the importance of considering MP as a differential diagnosis in cases of concurrent chylous ascites, pleural effusion and PLE in patients with abdominal pain, fever and weight loss.

Malignant ascites is commonly produced in advanced epithelial ovarian cancer (EOC) and serves as unique microenvironment for tumour cells. Acellular ascites fluid (AAF) is rich in signalling molecules and has been proposed to play a role in the induction of chemoresistance. Through in vitro testing of drug sensitivity and by assessing intracellular phosphorylation status in response to mono- and combination treatment of five EOC cell lines after incubation with AAFs derived from 20 different patients, we investigated the chemoresistance-inducing potential of ascites. We show that the addition of AAFs to the culture media of EOC cell lines has the potential to induce resistance to standard-of-care drugs (SCDs). We also show that AAFs induce time- and concentration-dependent activation of downstream signalling to signal transducer and activator of transcription 3 (STAT3), and concomitantly altered phosphorylation of mitogen-activated protein kinase kinase (MEK), phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT) and nuclear factor NF-kappa-B (NFκB). Antibodies targeting the interleukin-6 receptor (IL6R) effectively blocked phosphorylation of STAT3 and STAT1. Treatments with SCDs were effective in reducing cell viability in only a third of 30 clinically relevant conditions examined, defined as combinations of drugs, different cell lines and AAFs. Combinations of SCDs and novel therapeutics such as trametinib, fludarabine or rapamycin were superior in another third. Notably, we could nominate effective treatment combinations in almost all conditions except in 4 out of 30 conditions, in which trametinib or fludarabine showed higher efficacy alone. Taken together, our study underscores the importance of the molecular characterisation of individual patients\' AAFs and the impact on treatment resistance as providing clinically meaningful information for future precision treatment approaches in EOC.

OBJECTIVE: Aim: To evaluate the peculiarities of the course of complications and the provision of care for portal hypertension associated with the development of diureticresistant ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, and variceal bleeding.
METHODS: Materials and Methods: This research is based on a review of the literature in PubMed, CrossRef, Google Scholar sources on complicated portal hypertension. Such complications of portal hypertension as spontaneous bacterial peritonitis, ascites, hepatorenal sуndrome, variceal bleeding caused by sinistral portal hypertension are considered. The effectiveness of interventional treatment methods and laparoscopic surgical interventions has been demonstrated.
CONCLUSIONS: Conclusions: Diagnosis and treatment of patients with complicated portal hypertension requires a multidisciplinary approach, which is due to the diverse pathophysiological process of portal hypertension. The possibilities of providing emergency care to this category of patients depend on the level of medical training of the staff, the possibilities of medical and technical support in the provision of interventional care, the ineffectiveness of which necessitates surgical treatment using minimally invasive technologies.

Eosinophilic gastroenteritis poses a significant diagnostic challenge, particularly in developing countries, where the awareness of this condition may be limited. Here, the case of a patient in her early 30s, who presented with recurrent episodes of abdominal pain and diarrhea, is reported. Initial standard laboratory investigations revealed normal complete blood counts and elevated total serum immunoglobulin E levels. Upper and lower endoscopic evaluations with systemic biopsies did not reveal any significant abnormalities. However, computed tomography revealed a thickened small intestine wall, halo signs, and mild ascites. Analysis of the ascitic fluid confirmed eosinophilia. These findings prompted a diagnosis of eosinophilic gastroenteritis. The patient responded well to a targeted elimination diet, corticosteroids, and antileukotriene medication. The present case emphasizes the importance of considering eosinophilic gastroenteritis in the differential diagnosis of patients who present with abdominal pain and eosinophilic ascites.

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Eosinophilic gastroenteritis (EG) is an inflammatory bowel condition characterised by eosinophilic infiltration of the stomach and small bowel. Smoking and certain foods can trigger EG.A man in his 40s presented to the emergency department with acute abdominal pain. He had rebound tenderness and guarding on his initial abdominal examination. A subsequent CT scan showed jejunal wall thickening and ascitesHe had similar attacks of abdominal pain and was misdiagnosed with familial Mediterranean fever and Crohn\'s disease.Paracentesis revealed eosinophilic ascites. No mucosal abnormality was detected on gastroduodenoscopy and colonoscopy. A double-balloon enteroscopy revealed mucosal inflammation in the jejunum and a biopsy was taken. In this biopsy, eosinophilic jejunitis was detected. He was given corticosteroids and montelukast and his condition was resolved promptly. After discharge, he had attacks of EG until he quit smoking. After quitting smoking, he had an attack once in the last 2 years after consuming eggplant.

An immigrant woman in her 60s with a complex medical history and remote occupational exposure to patients with tuberculosis (TB) presented with abdominal pain, early satiety, bloating and weight loss. Physical exam showed abdominal distention and ascites. Diagnostic paracentesis revealed low serum ascites albumin gradient and elevated ascitic lymphocytic count. However, fluid cytology, bacterial and mycobacterial cultures were negative. An interferon-gamma release assay for TB was indeterminate. MRI of the abdomen and pelvis showed a thickened endometrial stripe. Endometrial biopsy demonstrated non-caseating granulomatous endometritis. No organisms were identified on Grocott methenamine silver or acid-fast bacilli special stains. A tissue block from the endometrial biopsy submitted for DNA sequencing was positive for mycobacterium tuberculosis (MTB) complex Urine mycobacterial cultures were obtained and the patient was started on isoniazid, rifampin, ethambutol and pyrazinamide, with significant improvement in her symptoms. Urine mycobacterial cultures were eventually positive for pansusceptible MTB.

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