Prevalence of Exocrine and Endocrine Pancreatic Insufficiency After Sentinel Acute Pancreatitis (AP)

Abstract

Introduction: AP increases the risk of endocrine and exocrine insufficiency. We evaluated the prevalence and features of endocrine and exocrine insufficiency after a sentinel episode of AP in a well-defined cohort. Methods: We retrospectively studied the natural course of 127/162 (78%) patients with sentinel AP attack enrolled prospectively at University of Pittsburgh Medical Center from 2003 to 2010 who survived the index attack and had follow-up data available. Medical records were reviewed for demographics, etiology, severity of incident attack (ICU admission, organ failure [OF], pancreatic necrosis [PNec]), recurrent AP (RAP), chronic pancreatitis (CP), diabetes (American Diabetes Association criteria), and usage of oral pancreatic enzyme replacement therapy (PERT) during follow-up (median 53 months). Results: Mean age of patients was 53.4±19.1 years, 48% were male, 83% were white, 48% were transfers, and 20% (26/127) had coexisting diabetes at index admission. The most common etiology was biliary (46%). New onset diabetes was noted in 28% (28/101; 19 during index admission; 9 during follow-up). Most patients developing new-onset diabetes during index admission had moderate-severe disease and frequent readmissions (Table 1). The median time to development of new onset diabetes during follow-up (7/9) was 34.5 months. Of these, 5/9 patients had no OF or PNec. Eighty-two percent (23/28) of newly diagnosed diabetic patients required insulin with or without oral agents. Oral PERT was given for clinical symptoms (6/11) or after pancreatic surgery/extensive debridement (5/11). Due to a lower prevalence of severe AP in nontransfer patients, new-onset diabetes was seen less frequently (17%).Table 1Conclusion: While parenchymal destruction from moderate-severe AP may explain the development of new-onset diabetes after AP, other mechanisms are likely important in the remaining patients. Further studies are needed to identify these patients earlier and to define the mechanisms for development of new-onset diabetes after AP.