Non-Hodgkin’s lymphoma often involves extranodal sites, but pancreatic infiltration remains exceptionally uncommon. Primary pancreatic lymphoma accounts for less than 0.5% of all pancreatic tumours. Secondary pancreatic involvement, usually by direct extension from gastric or retroperitoneal lymphomas. We present a case of gastric diffuse large B-cell lymphoma (DLBCL) with contiguous pancreatic extension manifesting as gastric outlet obstruction and acute pancreatitis.

A 48-year-old man with no significant past medical history presented with a 2-month history of epigastric colicky pain radiating to the back worsening over the past 72 hours, associated with nausea, vomiting and unintended 17-kg weight loss. He reported intermittent low-grade fever. Two weeks earlier, an upper endoscopy had been suspended because of large amounts of retained food. Laboratory tests revealed elevated serum amylase and lipase (3x ULN) and eosinophilia. He was initially managed as mild acute pancreatitis. Abdominal ultrasound demonstrated a well-defined 33×34 mm rounded hypoechoic pancreatic lesion.

Repeated upper endoscopy identified a large ulcerated, exophytic lesion involving the incisura and antrum, extending along the greater curvature and into the descending part of the duodenum, causing partial gastric outlet obstruction. Biopsies showed diffuse large B-cell lymphoma, germinal-center phenotype. Staging computed tomography (CT) and endoscopic ultrasound (EUS) revealed a 35–40 mm transmural hypoechoic gastric mass infiltrating all wall layers with direct extension into the pancreatic neck, along with several small perigastric and peripancreatic lymph nodes. Fine-needle aspiration of the pancreatic lesion confirmed a clonal B-cell population. Bone marrow biopsy and flow cytometry showed no infiltration. Final diagnosis was gastric DLBCL, germinal-center type, stage IV. The patient received a pre-phase with cyclophosphamide and dexamethasone, followed by R-EDOCH (rituximab, etoposide, doxorubicin, vincristine, cyclophosphamide, prednisone) immunochemotherapy. Treatment was well tolerated. Interim PET-CT demonstrated marked radiologic improvement with complete metabolic response, consistent with clinical remission. Follow-up endoscopies showed progressive ulcer healing and a persistent fibrotic duodenal stenosis. He is currently without active oncologic treatment and undergoing clinical and endoscopic follow-up.

This case illustrates a rare presentation of gastric DLBCL with contiguous pancreatic invasion mimicking acute pancreatitis. Pancreatic involvement by lymphoma may resemble both pancreatitis and pancreatic carcinoma. Diagnosis relies on imaging, endoscopy, EUS-guided sampling, and histopathology. Immunochemotherapy is the standard treatment and typically induces rapid tumor regression. DLBCL should be considered in the differential diagnosis of pancreatic masses or acute pancreatitis-like presentations, especially when gastric lesions or obstructive symptoms are present. Early histologic confirmation and prompt initiation of immunochemotherapy are essential to avoid delays and unnecessary surgery.