An Unexpected Etiology of Pancreatic Panniculitis: A Case Report.

BACKGROUND: Pancreatic panniculitis is a rare cause of subcutaneous fat necrosis secondary to elevated serum levels of pancreatic enzymes. It is most often associated with pancreatic acinar cell carcinoma, but has also been seen in patients with pancreatitis. CASE REPORT: We present a case of a 64 year old Caucasian man without symptoms of pancreatitis who presents with pancreatic panniculitis manifesting in multiple subcutaneous ulcerating nodules of the bilateral lower extremities, discovered to have a previously unreported etiology for this condition. He had no evidence of pancreatitis or malignancy, but instead a pancreatic-portal fistula resulting in panniculitis. CONCLUSION: Peripancreatic vascular lesions must also be considered in the differential diagnosis of pancreatic panniculitis. The diagnosis, pathology, and treatment of pancreatic panniculitis are reviewed herein.

The many faces of pancreatic serous cystadenoma: Radiologic and pathologic correlation.

Pancreatic serous cystadenoma can be categorized into microcystic, honeycomb, oligocystic, and solid patterns based on imaging appearance. The presence of typical computed tomography (CT) features helps to differentiate serous cystadenomas from other cystic and solid pancreatic masses. Cases with atypical features present a diagnostic challenge as they can mimic malignant neoplasms. This article reviews pathophysiology, prevalence, CT features, mimickers and recommendations for management of pancreatic serous cystadenoma.

The receptor for advanced glycation end products (RAGE) enhances autophagy and neutrophil extracellular traps in pancreatic cancer.

Neutrophil extracellular traps (NETs) are formed when neutrophils expel their DNA, histones and intracellular proteins into the extracellular space or circulation. NET formation is dependent on autophagy and is mediated by citrullination of histones to allow for the unwinding and subsequent expulsion of DNA. NETs have an important role in the pathogenesis of several sterile inflammatory diseases, including malignancy, therefore we investigated the role of NETs in the setting of pancreatic ductal adenocarcinoma (PDA). Neutrophils isolated from two distinct animal models of PDA had an increased propensity to form NETs following stimulation with platelet activating factor (PAF). Serum DNA, a marker of circulating NET formation, was elevated in tumor bearing animals as well as in patients with PDA. Citrullinated histone H3 expression, a marker of NET formation, was observed in pancreatic tumors obtained from murine models and patients with PDA. Inhibition of autophagy with chloroquine or genetic ablation of receptor for advanced glycation end products (RAGE) resulted in decreased propensity for NET formation, decreased serum DNA and decreased citrullinated histone H3 expression in the pancreatic tumor microenvironment. We conclude that NETs are upregulated in pancreatic cancer through RAGE-dependent/autophagy mediated pathways.