Azathioprine-Induced Acute Pancreatitis in a Patient With Inflammatory Bowel Disease.

Patients with inflammatory bowel disease (IBD) show a higher risk of developing pancreatitis, the main cause being side effects due to medication. Azathioprine (AZA) is a thiopurine immunosuppressant drug indicated for the treatment of this pathology and is one of the active ingredients most associated with acute pancreatitis in those patients.1 According to Gordon et al,2 the effect size and morbidity of thiopurine-induced pancreatitis are not known. Studies in adults report an incidence of AZA-induced pancreatitis ranging from 0% to 11%, depending on the type of study (observational vs randomized trial). Small case series report an incidence of up to 6% in pediatric IBD; however, only few prospective controlled studies with a comparison group have been published. Therefore, the absolute and relative risks of AZA-induced acute pancreatitis in children with IBD are unknown yet.3 We report a case of a pediatric patient who probably had AZA-induced pancreatitis. An 11-years-old boy, diagnosed with Crohn’s disease (CD) in June 2021, with neither known drug allergies nor other history of interest, was admitted for suffering from epigastric pain of days of evolution, accompanied by nausea and vomiting. He received treatment with exclusive enteral nutrition and oral AZA (50 mg daily), based on determination of thiopurine methyltransferase (TPMT) activity (17.6 U/mL), started 3 weeks before admission. The abdominal pain was continuous with exacerbations, predominantly at night, and no changes in bowel habits (type 4-6 according to the Bristol Stool Scale) were observed. Physical examination revealed a non-distended, but painful abdomen in the supraumbilical region, with no other findings of interest. A blood test showed normal blood and coagulation parameters, amylase value being 70 UI/L. Abdominal ultrasonography showed subcentimeter adenopathies in the flank and right iliac fossa. During admission, he was maintained on an absolute diet with intravenous fluid therapy (antiemetics—ondansetron—and gastric protection—ranitidine), without clinical improvement. Due to the persistence of the symptoms, successive analytical controls were requested. Finally, elevation of amylase to 174 UI/L and pancreatic lipase to 397 UI/L were objectifying (Figure 1). Because drug-induced pancreatitis usually develops after 2-3 weeks from starting medication,4-6 AZA was considered the possible cause of the pancreatitis. Therefore, AZA was discontinued. A decrease in serum pancreatic enzyme values was observed (Figure 1), and abdominal pain disappeared after withdrawal of AZA. After confirming the diagnosis, clinical course of the patient improved in a short time. 1126353 PMTXXX10.1177/87551225221126353Journal of Pharmacy TechnologyVázquez-Gómez and Vázquez-Gómez research-article2022