Frequency and characteristics of pancreatitis in patients with inflammatory bowel disease

Background and Aims: Clinical symptoms of inflammatory bowel disease (IBD)-associated pancreatitis are found in similar to 2% of patients, but the frequency of the disease could be much higher since IBD-associated pancreatitis could be mainly a silent disease. The aim of this study was to describe the radiological and biological features of IBD-associated pancreatitis and assess its frequency by comparing data from IBD patients with or without a history of pancreatitis. Methods: 79 patients were prospectively enrolled ( median age 36 years). Symptoms of pancreatitis had been previously recorded in 30 of them ( group P; the other 49 patients ( group C) had no history of pancreatitis. Pancreatic ductal changes were investigated by pancreato-MRI. Exocrine function was assessed by the fecal elastase test and by assaying serum amylase, lipase, C-reactive protein, PAP, IgG4 and pancreatic autoantibodies. Results: Increased levels of amylase and lipase occurred in 11% of IBD patients, that frequency being significantly higher in group P (23%) than in group C (4%) ( p = 0.01). Low fecal elastase reflecting impaired exocrine function was observed in 30% of patients and again significantly more in group P (50%) than in group C (17%) ( p = 0.04). The frequency of elevated values varied from 12% for amylase and lipase to 18% for PAP, 20% for pancreatic autoantibodies and 45% for CRP, without a difference between groups P and C. Silent exocrinopathy was observed in both groups, pancreatic autoantibodies and pancreatic duct alterations being found in 20 and 11% of patients, respectively. Conclusion: Finding pancreatic insufficiency in about 30% of the included patients and in 50% of those with a previous history of pancreatitis suggests that IBD might be associated with chronic pancreatic alteration. Episodes of mild acute pancreatitis observed in some patients are not always due to adverse effects of treatments and can be acute manifestations of the chronic disease. Copyright (C) 2006 S. Karger AG, Basel and IAP.