Abstract

Introduction: A 63-year-old woman with a 5-year history of ulcerative colitis controlled with Lialda® for 2 years, psoriasis, and atrial fibrillation presented with acute pancreatitis. For the past several months, the patient experienced intermittent severe epigastric pain that radiated to her right upper quadrant and shoulder associated with nausea and vomiting. Her symptoms persisted despite a cholecystectomy for cholelithiasis in January 2014. In March, she had severe pancreatitis with a lipase level of 3000 U/L and a CT abdomen/pelvis showing inflammation surrounding the pancreas. She did not drink alcohol and a subsequent MRCP did not observe any evidence of common bile duct dilation or filling defect and showed resolving pancreatitis without obvious complications. The patient was kept NPO and her Lialda was stopped. However, the patient could not tolerate a diet and started to have watery, bloody, non-mucoid, explosive diarrhea 5 times per day associated with crampy, abdominal pain similar to her ulcerative colitis flares. She was started on mesalamine rectal enemas and Asacol®. Her diet was advanced and she was initially doing well, until she had abdominal pain after taking mesalamine. Due to concern over recurrent mild pancreatitis, the mesalamines were stopped and budesonide was started. The patient tolerated the medication well and was discharged with resolution of gastrointestinal symptoms. While azathioprine and mercaptopurine have been widely associated with acute pancreatitis (between 1-6% of exposed individuals develop acute pancreatitis), mesalamine-induced pancreatitis is rare. A population-based case-control study by Munk et al did not discern a significant association between the use of 5-ASA agents and increased risk of acute pancreatitis. In fact, Munk et al observed that patients with ulcerative colitis had a 1.5-fold greater risk of developing pancreatitis than patients without ulcerative colitis. Lialda-induced pancreatitis was only observed in 2 cases in clinical trials, both of which were attributed to hypersensitivity reactions. In this case, the patient likely first developed a Lialda-induced pancreatitis and then an ulcerative colitis flare once the Lialda was held. She was tried on an alternative 5-ASA agent but again developed abdominal pain possibly secondary to a mild pancreatitis. These episodes of drug-induced pancreatitis may have been due to the pH-dependent coating Lialda and Asacol share or to a general class effect of 5-ASA agents. This case describes a rare side effect of a common ulcerative colitis medication. In the future, physicians should consider pancreatitis on their differential for chronic abdominal pain in patients taking Lialda or other 5-ASA agents.

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