15 In fact, the observed pancreatic alterations of patients with UC are more frequent than initially expected. Although UC patients present an increase incidence of gallbladder lithiasis and are administered drugs that can potentially be pancreato-toxic, these factors alone are probably not enough to explain the great incidence of pancreatic alterations among UC patients.16 Some studies demonstrate insufficient levels of pancreatic exocrine

in 21–80% of IBD patients and autopsy studies register pancreatic alterations, macroscopic or microscopic, in 14–53% of UC patients. Pancreatic duct changes, such as irregularities or short-segment stenosis of the main pancreatic duct, were observed in 8.4–10.8% of IBD patients independently

of prior history of pancreatitis or exocrine insufficiency.4 and 17 It seems that predominantly asymptomatic pancreatic alterations of indolent development might exist in these patients, albeit the fact that the Dolutegravir mouse exact aetiology and pathogenesis are still poorly understood. We believe that a large spectrum of pancreatic changes can be documented in IBD patients, from symptom-free cases (likely the majority) to clinically exuberant forms such as the case of our patient. The aetiopathogenesis could be related to an abnormal immunological response leading to pancreatic inflammation such as Ectors et al. previously suggested.18 The association between AIP and UC presents a clinical challenge concerning the treatment strategy. UC patients need immunosuppressive treatment in up to 30% of cases.19 Thiopurins www.selleckchem.com/products/azd5363.html (azathioprine and 6-mercaptopurine)

continue to be the most widely used. However, potential pancreatic adverse effects are well established, raising concerns of its use in patients with AIP. In this setting other therapies PtdIns(3,4)P2 (e.g. methotrexate or biological therapy) could step-in as first line options.20 There are some authors who advise against the use of thiopurins in AIP, although its use has been described as presenting good results in cases of relapse of AIP with a low level of adverse effects.21, 22 and 23 Albeit more studies are needed, its use can be justified to avoid long-term treatment with corticosteroids, under close monitoring for pancreatic toxicity. In respect to corticotherapy, a good clinical response is considered by some groups as a diagnostic criterion for AIP.7 In our case, a clinical and analytical improvement was seen, with no cholestasis relapse after biliary stent removal. Pancreatic morphology improvement on EUS was not observed after corticotherapy, supporting the idea of an irreversible extensive fibrotic process.11 A word of caution is in order, concerning the uneventful evolution of the presented case. A long-term follow-up strategy is mandatory, namely to maintain a low threshold for future associated autoimmune illnesses. The authors have no conflicts of interest to declare.