Chronic pancreatitis (CP), a disease that develops as a result of repeated episodes of pancreatic inflammation and associated fibrosis, restricting functional exocrine and endocrine pancreatic function and causing severe upper abdominal pain. Treatment strategies include conservative therapy, consisting of a step-up approach with pharmacological and lifestyle modifications. For more advanced cases, endoscopic or surgical interventions are proposed. However, the exact role and qualification criteria for surgical management have not been established yet. In this cohort study, we analysed the results of surgical interventions in 388 patients with CP performed in the years 2004-2024 in our centre, including drainage procedures and resections. We assessed the overall results of the intervention, the possible complications (assessed by Clavien-Dindo classification), and the risk of occurrence. Also, the surgery results and the complication risk between the groups of patients who underwent respective procedures were compared. The findings indicate that surgery remains an important tool in CP management, and organ-preserving procedures may be successful in pain control and overall quality of life improvement. It is emphasised that personalised surgical strategies should be the basis of CP management, and the therapy choice must be established by an experienced multidisciplinary team consisting of gastroenterologists, endoscopists, radiologists, and surgeons.

Autoimmune pancreatitis (AIP) is an uncommon fibroinflammatory pancreatic disorder that may closely mimic pancreatic malignancy, particularly when presenting with focal or multifocal mass-like lesions. Prompt recognition is essential to prevent unnecessary invasive procedures, inappropriate oncological management, and to allow timely initiation of glucocorticoid therapy. We report the case of a 32-year-old call center employee with a history of asthma who presented with a three-week history of progressive epigastric pain radiating to the back. Notably, he had no clinical or biochemical evidence of obstructive jaundice, with a total bilirubin level of 0.24 mg/dL at presentation. Initial abdominal CT demonstrated multifocal poorly defined hypovascular pancreatic lesions associated with pancreatic enlargement, raising concern for a pancreatic neoplasm. Laboratory evaluation revealed preserved hepatic function, normal serum calcium and triglyceride concentrations, mild inflammatory response, elevated total immunoglobulin G (IgG) (1673 mg/dL), mildly elevated IgG4 (153.5 mg/dL), and positive antinuclear antibodies. Tumour markers were negative. Subsequent MRI showed multifocal enlargement involving the pancreatic head, body, and tail, with delayed homogeneous enhancement, preservation of the main pancreatic duct calibre, and peripheral capsule-like features. These findings strongly suggested autoimmune pancreatitis. Histological confirmation was not initially obtained because corticosteroid therapy had already been initiated following multidisciplinary evaluation. The patient demonstrated rapid clinical improvement and remained asymptomatic during corticosteroid tapering. Endoscopic ultrasound-guided tissue acquisition and urgent imaging reassessment were planned to consolidate diagnostic certainty and exclude alternative diagnoses. This case highlights the diagnostic complexity of autoimmune pancreatitis presenting as multifocal pancreatic masses and illustrates the challenges associated with initiating corticosteroid therapy before histological confirmation. Recognition of characteristic radiological patterns and integration of clinical and serological findings remain crucial to avoid unnecessary invasive or surgical interventions.

Epstein-Barr virus (EBV) is a common viral agent causing infectious mononucleosis and can present with fever, fatigue, pharyngitis and cervical lymphadenopathy. Isolated gallbladder wall thickening without leukocytosis or splenomegaly is an atypical presentation of EBV infection. We present a case of a young woman with 2-3 days of epigastric pain, nausea and vomiting with gallbladder wall thickening on imaging. Despite an initial diagnosis of acalculous cholecystitis, a hepatobiliary iminodiacetic acid scan did not reveal acute cholecystitis. Positive EBV serology suggested a viral cause. This case emphasizes the need for clinicians to broaden their differential when considering isolated gallbladder wall thickening. Early identification of a viral cause can reduce unnecessary invasive interventions such as cholecystectomy.

Acute pancreatitis (AP), among the most common causes of acute abdomen, is characterized by persistent left upper abdominal pain and vomiting, without pain relief after vomiting. Its pathological features include abnormal activation of pancreatic enzymes and induction of pancreatic autodigestion by various etiologies. Emerging evidence indicates a strong association between the gut microbiota and AP progression, primarily mediated by intestinal barrier disruption, bacterial translocation, and immune dysregulation. Alterations in the gut microbiota, including overgrowth of pathogenic bacteria (eg, Enterobacteriaceae) and a reduction in beneficial commensals (eg, Lactobacillaceae and Bifidobacteriaceae), are consistently observed among patients with AP. The gut microenvironment, including factors such as bile acids, oxygen levels, and pH, shapes the microbial community and its interactions with the host. These changes can promote local and systemic inflammation, thereby exacerbating pancreatic necrosis and contributing to multiple organ dysfunction. Consequently, the bidirectional interaction between the gut microbiome and AP has received increasing attention. This review provides a comprehensive summary of the current understanding of how gut microbiota dysbiosis contributes to AP pathogenesis. We focus on mechanisms linking microbial and microenvironmental alterations to disease severity, including the roles of the gut-pancreas axis, short-chain fatty acids, and pattern recognition receptors. Finally, we discuss the potential of novel therapeutic strategies targeting these pathways for the management of AP.

Cerebral venous sinus thrombosis (CVST) is an uncommon yet potentially serious cerebrovascular condition characterized by thrombosis of the intracranial venous sinuses. Its presentation is often nonspecific and clinically variable, which may delay diagnosis. Hepatic dysfunction, including hepatocellular injury in the setting of viral hepatitis seropositivity, may be associated with complex hemostatic changes; however, the relationship between hepatic inflammation and venous thrombosis remains difficult to establish in individual cases. We describe the case of a 35-year-old man who presented with acute left-sided pulsatile headache associated with epigastric pain, vomiting, and mild conjunctival discoloration. Laboratory evaluation revealed elevated hepatic transaminases, mild coagulation abnormality, and positive hepatitis B surface antigen and anti-hepatitis C virus antibody serology, suggestive of hepatocellular injury in the setting of viral hepatitis seropositivity. Neuroimaging demonstrated thrombosis involving the left transverse and sigmoid sinuses with associated hemorrhagic infarction affecting the left temporal lobe and cerebellar hemisphere. The patient was managed conservatively with close neurological and hepatic surveillance and experienced progressive symptomatic improvement. This case highlights the importance of considering CVST in patients with persistent or atypical headache, even when neurological examination is initially nonfocal. Although hepatic inflammation and viral hepatitis seropositivity may represent possible contributing factors, the association remains hypothesis-generating, particularly in the absence of confirmatory viral load testing, cryoglobulin testing, and complete thrombophilia evaluation.

Pseudomyxoma peritonei (PMP) is a rare clinical entity characterized by the accumulation of mucinous fluid within the peritoneal cavity. While often indolent, it can lead to severe mechanical complications. This case describes an elderly patient with advanced PMP presenting with acute obstructive uropathy, highlighting the complexity of managing frail oncologic patients. An 83-year-old female with a history of ovarian cancer and PMP (previously treated with cytoreductive surgery and HIPEC (hyperthermic intraperitoneal chemotherapy)) presented with a two-day history of right-sided flank pain, abdominal distention, and severe constipation. Laboratory results showed leukocytosis (13,790/µL) and elevated C-reactive protein (169 mg/L). A CT scan revealed progression of calcified peritoneal implants and a large epigastric mass causing extrinsic compression of the right ureter, leading to severe ureterohydronephrosis (7 cm). Despite the obstruction, renal function was preserved (creatinine 0.73 mg/dL). Due to her frailty and personal preferences, the patient declined invasive urinary diversion. She was managed conservatively, remained clinically stable, and was discharged with outpatient follow-up. PMP symptoms often mimic benign gastrointestinal issues, such as constipation. In elderly patients, the decision between aggressive intervention and conservative care is challenging. This case highlights the value of shared decision-making in advanced oncology; when renal function is stable, this model allows for a non-invasive approach that, beyond being a viable clinical alternative, stands as the best path to honor patient autonomy and optimize quality of life. Clinical vigilance is crucial in PMP, as nonspecific symptoms may mask serious obstructive complications. Individualized, patient-centered care is essential when balancing the risks of surgical intervention against conservative management in advanced oncology.

Background Gallbladder carcinoma (GBC) is an aggressive malignancy characterized by rapid local invasion, delayed clinical presentation, and poor survival outcomes. Despite the high disease burden in North-East India, region-specific data on the demographic and diagnostic characteristics of GBC remain limited. Aim This study aims to describe the demographic characteristics, clinical presentation, laboratory abnormalities, radiological findings, cytopathological features, and diagnostic stages among patients with GBC in Tripura. Materials and methods This hospital-based cross-sectional study included 192 consecutive patients with cytologically confirmed GBC who were managed at a tertiary-care center in Tripura between October 2024 and September 2025. Demographic characteristics, clinical features, laboratory parameters, imaging findings, cytopathological diagnoses, and clinical stage at presentation were analyzed using descriptive statistics. Results A total of 192 patients were included, with a mean age of 61.3 ± 6.1 years. Females constituted 93.8% of the study population, and 56.3% of patients were older than 60 years. Three-fourths of patients belonged to lower-middle, upper-lower, or lower socioeconomic classes and resided in rural areas (75.0%). A non-vegetarian diet was reported by 81.3% of patients, and betel-nut chewing by 71.9%. Abdominal pain and loss of appetite were present in all patients, and significant weight loss was observed in 90.6% of patients. Jaundice and palpable gallbladder were noted in 62.5% and 81.3% of patients, respectively. Anemia was present in 96.9% of patients, and hyperbilirubinemia in 59.4%. Ultrasonography identified a gallbladder mass in 56.3% of patients, and contrast-enhanced computed tomography frequently demonstrated locally advanced disease. Cytopathological evaluation revealed adenocarcinoma in 168 (87.5%) patients. Cytopathological evaluation revealed adenocarcinoma in 168 (87.5%) patients. Clinical staging demonstrated that 75.0% of patients presented with stage III-IV disease, indicating substantial diagnostic delay. Conclusions GBC in Tripura predominantly affects elderly women and is commonly diagnosed at an advanced stage. Most patients in this cohort originated from rural and lower socioeconomic backgrounds. The high proportion of advanced-stage disease at presentation highlights the need for improved awareness, earlier diagnostic evaluation of symptomatic patients, and strengthened referral pathways in high-burden regions of North-East India.

Acute pancreatitis is a recognized toxicity of L-asparaginase therapy during the treatment of pediatric acute lymphoblastic leukemia (ALL). Its management requires a delicate balance between avoiding leukemic relapse and preventing pancreatic recurrence. We report the case of a five-year-and-eight-month-old girl with Philadelphia chromosome-positive B-cell ALL, initially treated with imatinib combined with the high-risk MARALL 2006 protocol, and subsequently with the COOPRALL 97 protocol following an isolated central nervous system relapse. Seventy-two hours after the 18th cumulative administration of L-asparaginase, she developed epigastric pain and vomiting. Serum lipase was greater than three times the upper limit of normal, confirming the diagnosis of acute pancreatitis. The episode was classified as grade 2 according to the Ponte di Legno group classification. After clinical and biological resolution of pancreatitis, L-asparaginase was reintroduced because of the patient's high-risk relapsed leukemia. After 10 weeks of follow-up after reintroduction, no recurrence was observed. This case supports the feasibility of L-asparaginase rechallenge in selected high-risk pediatric patients following a multidisciplinary risk-benefit assessment.

Acute cholangitis is a potentially life-threatening infection of the biliary tract that usually results from biliary obstruction, most commonly secondary to choledocholithiasis. Although prompt diagnosis and treatment often lead to favorable outcomes, uncommon complications such as pylephlebitis (septic thrombosis of the portal vein) may significantly increase morbidity and mortality. We report the case of a 47-year-old woman with no significant past medical history who presented with right upper quadrant abdominal pain, fever (38.2°C), asthenia, and nausea. Physical examination revealed diffuse abdominal tenderness and mild jaundice. Abdominal point-of-care ultrasound (POCUS) made by the emergency physician on call showed multiple gallbladder calculi with sludge but without visible biliary dilatation. Laboratory evaluation demonstrated an inflammatory syndrome with C-reactive protein of 72 mg/L, normal leukocyte count, total bilirubin of 87 IU/L, and direct bilirubin of 56 IU/L, and cholestatic liver enzyme abnormalities, including alkaline phosphatase (ALP) of 190 IU/L and gamma-glutamyl transferase (GGT) of 108 IU/L. The diagnosis of acute angiocholitis was thus suspected. Abdominal imaging (computed tomography (CT) with contrast) showed intrahepatic and extrahepatic biliary dilatation caused by a distal common bile duct stone, multiple gallbladder calculi, and segment II left portal vein thrombosis consistent with pylephlebitis. A diagnosis of acute cholangitis secondary to choledocholithiasis complicated by pylephlebitis was established. The patient was treated with intravenous (IV) antibiotics, fluid resuscitation, and supportive care, with planned biliary decompression and definitive surgical management. This case highlights a rare but serious vascular complication of biliary stone disease. Clinicians should maintain a high index of suspicion for portal venous involvement in patients with cholangitis and persistent systemic symptoms. Early imaging, timely antimicrobial therapy, and coordinated multidisciplinary management are essential to reduce the risk of severe complications and improve outcomes.