Asymptomatic and Persistent Elevation of Pancreatic Enzymes in an Ulcerative Colitis Patient

Azathioprine has been extensively used in the management of inflammatory bowel diseases. It might cause pancreatic damage in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis. Here we report the case of a 61-year-old patient with ulcerative colitis who had been treated with azathioprine for three years, achieving clinical remission. During treatment he presented an asymptomatic elevation of serum pancreatic enzymes, without any signs of pancreatitis at imaging. This evidence brought us to reassess the drug dosage, without achieving a normalization of biochemical analysis. Autoimmune pancreatitis was excluded. One year after the suspension of azathioprine, we still face persistent high levels of amylase/lipase. Normalization of enzymatic values in patients who develop intolerance to azathioprine, in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis, is usually achieved in about two months after stopping drug intake. Asymptomatic elevation in serum pancreatic enzymes in the absence of pancreatic disease is reported in the literature and defined as “Gullo’s syndrome,” but nobody of the subjects studied had been treated in the past with pancreatotoxic drugs. Might this case be defined as “benign pancreatic hyperenzymemia”? 1. Introduction Azathioprine (AZA) has been extensively used in the management of inflammatory bowel diseases (IBD). It plays an important role as steroid sparing agent in inducing and maintaining a stable remission of disease. This immunosuppressive medication has been associated with a number of side effects, including bone marrow suppression, liver injury, acute pancreatitis, and others. The etiopathogenesis of AZA-induced pancreatic damage, in the form of either asymptomatic elevation in serum amylase/lipase or overt acute pancreatitis, is still not clear, but some authors propose that a possible immune-mediated mechanism or a hypersensitivity to the drug could be involved. Patients treated with AZA have to check routinely biochemical tests to exclude the potential pancreatotoxicity. Hyperamylasemia and hyperlipasemia in IBD patient never treated with pancreatotoxic drug are reported in the literature. Several authors suggest a latent involvement of the pancreas as an extraintestinal manifestation of IBD, and some others lean towards an abnormal reabsorption of amylase/lipase due to the increased permeability of the inflamed mucosa. In this report, we also review the literature concerning nonspecific elevations of serum pancreatic enzymes in IBD