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Lymphoplasmacytic Sclerosing Pancreatitis (Autoimmune Pancreatitis): Evaluation with Multidetector CT¹

¹ From the Russell H. Morgan Department of Radiology and Radiological Science (S.K., S.S.S., E.K.F.) and Department of Pathology, Sol Goldman Pancreatic Cancer Research Center (R.H.H.), Johns Hopkins Medical Institutions, JHOC 3235A, 601 N Caroline St, Baltimore, MD 21287. Recipient of a Certificate of Merit award for an education exhibit at the 2005 RSNA Annual Meeting. Received November 7, 2006; revision requested April 18, 2007, and received June 21; accepted June 28. All authors have no financial relationships to disclose. Address correspondence to S.K. (e-mail: skawamo1{at}jhmi.edu).

Lymphoplasmacytic sclerosing pancreatitis is a form of chronic pancreatitis characterized by a mixed inflammatory infiltrate that centers on the pancreatic ducts. It is a cause of benign pancreatic disease that can clinically mimic pancreatic cancer. Preoperative detection of lymphoplasmacytic sclerosing pancreatitis is important because patients usually respond to steroid therapy. Patients with lymphoplasmacytic sclerosing pancreatitis are often referred for computed tomography (CT) when they are suspected of having a pancreatic or biliary neoplasm; therefore, it is important to search for potential findings suggestive of lymphoplasmacytic sclerosing pancreatitis when typical findings of a pancreatic or biliary neoplasm are not found. Typical CT findings include diffuse or focal enlargement of the pancreas without dilatation of the main pancreatic duct. Focal enlargement is most commonly seen in the head of the pancreas, and the involved pancreas on contrast material–enhanced CT images may be isoattenuating relative to the rest of the pancreas, or hypoattenuating, especially during the early postcontrast phase. Thickening and contrast enhancement of the wall of the common bile duct and gallbladder may reflect inflammatory infiltrate and fibrosis associated with lymphoplasmacytic sclerosing pancreatitis. There are several features seen at CT that may help to differentiate lymphoplasmacytic sclerosing pancreatitis from pancreatic cancer, such as diffuse enlargement of the pancreas with minimal peripancreatic stranding in patients with obstructive jaundice, an absence of significant pancreatic atrophy, and an absence of significant main pancreatic duct dilatation. When these findings are encountered, clinical, other imaging, and serologic data should be evaluated.

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