Healing by fibrosis represents the end stage of a response to a variety of insults. Known antecedents to fibrosis in the colon include ischaemia, inflammation (e.g., Crohn's colitis), and noxious chemicals (e.g., irritant laxatives). Endogenous pancreatic enzymes may have a role in enhancing, even if not initiating, lesions which lead to fibrosis, as shown by animal experiments in which ligation of the pancreatic duct mitigated or delayed the response to ischaemia.1

It has been recognised fairly recently that a distinctive form of fibrosing colonopathy develops in young children with cystic fibrosis taking mega-doses of pancreatic enzymes, and it was suggested that the enzyme preparations themselves may be the cause.2 The most striking feature is a thick band of submucosal fibrosis, suggesting that some component of the enzyme preparation must gain access through the mucosal barrier, but evidence of healed mucosal ulceration has only been observed in a few cases. Vascular damage and a moderate eosinophilic infiltration were observed in some cases, and in several there was quite noticeable serosal fibrosis. Clinically, in addition to the signs of intestinal obstruction, several patients had chylous ascites. These features suggest that translocation of a component of the enzyme preparation—whether the enzymes themselves or the enteric coating used to protect them from gastric acid—occurs across the full thickness of the …