Elevated Lipase in Newly Diagnosed IBD: Reluctance or Impetus for Treatment?

Abstract

There are 3 unique pathways through which inflammatory bowel disease (IBD) and elevated pancreatic enzymes are associated with each other. Acute interstitial pancreatitis (AIP) can occur with IBD likely via a similar immunologic mechanism. Second, inflamed bowel tissue can trigger pancreatic enzyme release and mimic pancreatitis clinically. Finally, pharmacological treatment of IBD, normally with immunomodulators, can be complicated by AIP. We report a case of a 20-year-old male who presented with abdominal pain and bloody diarrhea. He described 3 weeks of deep cramping pain, associated with bloody diarrhea, urgency, bloating and anorexia. He had no risk factors for pancreatitis. Exam revealed a soft but tender abdomen without distention. His WBC was 10.5, hemoglobin 14.2, albumin 4.5, total bilirubin 0.5, lipase 3430, ESR 23, CRP 4.87 with normal transaminases. Stool studies showed abundant fecal leukocytes but were negative for enteric pathogens including C. diff, as well as ova and parasites. Fecal calprotectin was 364. IgG4 was normal. Imaging showed colonic wall thickening with mucosal enhancement in the left colon and a normal appearing pancreas and biliary tree. He underwent colonoscopy revealing continuous and circumferential pancolitis consistent with ulcerative colitis, confirmed by histology with chronic and active colitis with acute cryptitis and crypt abscesses. He was started on steroids and mesalamine and had significant improvement over the next week. His lipase improved to 240, CRP to 0.98 and fecal calprotectin to 118 after 1 week of therapy, and all normalized at 30 days. Elevated pancreatic enzymes are an uncommon but likely underreported diagnosis in patients presenting with IBD. Our case illustrates that we should not undervalue elevated pancreatic enzymes in patients with IBD. The coincidence of these 3 unique associations between IBD and pancreatic enzyme elevation requires diligent history taking, examination, and clinical evaluation to delineate proper management. Based on the etiology of elevated pancreatic enzymes, these levels can improve by directly treating the IBD, as was seen with our patient. Literature suggests a correlation between disease activity and the level of pancreatic enzyme elevation. Formal evaluation for pancreatitis will prevent delaying therapy initiation over concern of AIP and possible immunomodulator side effects, in patients with actual elevated pancreatic enzymes from inflamed bowel.