Background: Inflammatory bowel disease (IBD) is often associated with hyperamylasemia. Recently, the concurrent development of type 2 autoimmune pancreatitis (AIP) has also received considerable attention.
Methods: We retrospectively studied 1) the incidence of hyperamylasemia, 2) the clinical characteristics of patients with hyperamylasemia, 3) the relation between hyperamylasemia and concurrent medication, and 4) the clinical characteristics of patients with pancreatitis.
Objective: To clarify the clinical characteristics of IBD associated with hyperamylasemia and pancreatitis.
Subjects: Among 959 patients with IBD whose serum amylase levels were measured at least once, we studied 147 patients (91 with ulcerative colitis and 56 with Crohn's disease) whose serum amylase levels were higher than the upper limit of normal in our hospital (125 IU/L) on at least one occasion.
Results: 1) Elevated serum amylase levels were found in 147 (15.3%) of the 959 patients. The mean maximum serum amylase level was 215±186 IU/L (range, 126 to 1939). As for other enzymes, lipase levels were elevated in 10 (77%) of 13 patients, and elastase 1 levels were elevated in 7 (88%) of 8 patients. Imaging examinations such as abdominal ultrasonography and computed tomography were performed in 78 patients (53%, some overlap) and showed gallstones in 12 patients (8.7%). No patient had primary sclerosing cholangitis. 2) Drug-induced hyperamylasemia was suspected in 19 patients (13%). The causative drugs were prednisolone in 10 patients, immunomodulators in 5 patients, and 5-aminosalicylic acid preparations in 4 patients. The mean time from the initiation of treatment to the development of hyperamylasemia was 54.4±52.3 days (range, 7 to 202). Drugs that had already been continuously received for 1 year or longer at the time of elevation of the serum amylase level were excluded. 4) Acute pancreatitis was diagnosed in 9 (0.9%) of the 959 patients. Three patients had AIP, diagnosed on the basis of pancreatic duct findings on magnetic resonance cholangiopancreatography (MRCP), the concurrent presence of IBD, and the response to steroids. Three patients had immunomodulator-induced pancreatitis, and 3 patients had idiopathic pancreatitis. Among the 3 patients with severe pancreatitis, 1 patient received pancreatic regional arterial infusion. There were no deaths.
Conclusions: Hyperamylasemia can develop during follow-up in a considerable number of patients with IBD. Because drug-induced pancreatitis can occur in such patients, careful follow-up is essential after starting treatment. Our study showed that AIP can develop as a complication in Japanese patients with IBD. Therefore, AIP should be actively investigated.