Intracapsular hemorrhage occurs occasionally in acute pancreatitis complicated with pseudocyst that can be managed using laparoscopic gastric cyst anastomosis and drainage. However, cyst recurrence many years later and secondary splenic artery pseudoaneurysm rupture and hemorrhage leading to bloody vomiting and syncope are uncommonly reported. A woman in her late 40s was admitted for bloody vomiting, melena, anemia, and syncope. She underwent laparoscopic gastric cyst anastomosis and drainage for severe acute pancreatitis 3 years ago. Gastroscopy identified a bleeding gastric vascular malformation. Metal clips were used for endoscopic hemostasis. Abdominal enhanced computed tomography revealed a cystic lesion in the tail of the pancreas (4.2 × 3.9 cm) connected with the stomach wall and a splenic artery pseudoaneurysm in the cyst. Splenic artery pseudoaneurysm embolization was performed. The patient remains asymptomatic 2 years after embolization. Percutaneous selective embolization of a splenic artery pseudoaneurysm may be the preferred choice for patients with a pancreatic pseudocyst complicated by rupture and hemorrhage of the splenic artery pseudoaneurysm in the pancreatic pseudocyst. Clinicians should be alert regarding the possibility of recurrence after prior drainage, highlighting the importance of long-term follow-up.

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy and continues to rank among the leading causes of cancer-related death worldwide. Imaging plays a central role in detection, staging, and treatment planning; nevertheless, PDAC remains one of the most frequently missed or misdiagnosed abdominal malignancies in clinical practice. Diagnostic challenges arise from subtle early imaging findings, anatomic blind spots within the pancreas, and a wide spectrum of inflammatory, benign, and malignant entities that closely mimic PDAC, such as focal acute pancreatitis, mass-forming chronic pancreatitis, autoimmune pancreatitis, groove pancreatitis, neuroendocrine tumors, lymphoma, metastases, solid pseudopapillary neoplasms and focal fatty infiltration. This narrative review provides a comprehensive, imaging-focused discussion of PDAC and its mimickers, with an emphasis on practical problem-solving strategies to reliably differentiate mimics from PDAC and improve diagnostic confidence, reduce unnecessary interventions, and facilitate timely and appropriate patient management.

Pancreatic cancer (PC) is a highly malignant tumor of the digestive system, characterized by the lack of effective methods for early screening, diagnosis and treatment. Despite its low incidence rate, it has an extremely high mortality rate. In recent years, the number of confirmed cases worldwide has been on a continuous rise, making PC the sixth leading cause of cancer-related deaths across the globe. At present, clinical treatment strategies including surgical resection, chemotherapy, radiotherapy, molecular targeted therapy and biological immunotherapy have not significantly improved the survival prognosis of PC patients. Therefore, exploring safe and effective therapeutic approaches and clarifying the etiological mechanisms of PC have become key priorities in clinical treatment. Its occurrence and progression involve multilayered mechanisms, including environmental exposure, genetic susceptibility, metabolic abnormalities, chronic inflammation, progression of precancerous lesions, remodeling of the tumor microenvironment, and immune escape. Based on a summary of smoking, alcohol consumption, obesity, diabetes, chronic pancreatitis, genetic mutations, and multiple signaling pathways, this article further provides a critical review from the perspectives of evidence strength, mechanistic plausibility, and clinical translational value. It aims to deepen the understanding of the initiation and progression of pancreatic cancer and to provide new directions for its early diagnosis and precision treatment.

An 87-year-old man presented with progressive steatorrhea, weight loss, and subsequent hyperglycemic crisis. Initial workup revealed combined exocrine and endocrine pancreatic insufficiency with mildly elevated immunoglobulin G4 below the diagnostic threshold and diffuse pancreatic inflammation on magnetic resonance imaging, raising suspicion for autoimmune pancreatitis. Follow-up imaging revealed an incidental renal mass, which biopsy confirmed as mucosa-associated lymphoid tissue lymphoma. Positron emission tomography-computed tomography demonstrated fluorodeoxyglucose uptake in both the renal mass and pancreatic tissue, with concordant treatment response to rituximab in both locations, suggesting lymphomatous pancreatic infiltration.

An eight-year-old boy with recurrent abdominal pain, refusal to eat, gagging, and weight loss for five months experienced a sudden clinical deterioration after a gastrointestinal endoscopy with biopsy. Initially misdiagnosed with pancreatitis, he underwent hospitalization, fasting, and parenteral nutrition (PN) for 15 days. Despite this, his symptoms persisted, and serum lactate levels progressively increased. Transferred to a university hospital, abdominal beriberi was suspected, and intravenous thiamine was promptly administered. Symptoms resolved within 24 h. A review of the PN prescribed revealed the absence of thiamine, confirming the diagnosis. Healthcare professionals often associate thiamine deficiency with alcoholic adults presenting Wernicke encephalopathy; however, abdominal beriberi should also be considered in children with acute abdomen, especially when elevated serum lactate indicates impaired cellular metabolism due to thiamine deficiency.