Robbert A Hollemans1, Nora D L Hallensleben2, David J Mager3, Johannes C Kelder4, Marc G Besselink5, Marco J Bruno6, Robert C Verdonk7, Hjalmar C van Santvoort8. 1. Dept. of Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands; Dept. of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands. 2. Dept. of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands; Dept. of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands. 3. VU Medical Center, Amsterdam, The Netherlands. 4. Dept. of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands. 5. Dept. of Surgery, Academic Gastroenterology and Metabolism, Amsterdam, The Netherlands. 6. Dept. of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands. 7. Dept. of Gastroenterology and Hepatology, St. Antonius Hospital, Nieuwegein, The Netherlands. 8. Dept. of Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands; Dept. of Surgery, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: h.van.santvoort@antoniusziekenhuis.nl.
Abstract
OBJECTIVES: This study systematically explores the prevalence of pancreatic exocrine insufficiency (PEI) after acute pancreatitis in different subgroups of etiology (biliary/alcoholic/other), disease severity and follow-up time (<12, 12-36 and > 36 months after index admission). METHODS: PubMed and EMBASE databases were searched, 32 studies were included in this study level meta-analysis. RESULTS: In a total of 1495 patients with acute pancreatitis, tested at a mean of 36 months after index admission, the pooled prevalence of PEI was 27.1% (95%-confidence interval [CI]: 20.3%-35.1%). Patients from seven studies (n = 194) underwent direct tests with pooled prevalence of 41.7% [18.5%-69.2%]. Patients from 26 studies (n = 1305) underwent indirect tests with pooled prevalence of 24.4% [18.3%-31.8%]. In subgroup analyses on patients that underwent fecal elastase-1 tests, PEI occurred more often in alcoholic pancreatitis (22.7% [16.6%-30.1%]) than in biliary pancreatitis (10.2% [6.2%-16.4%]) or other etiology (13.4% [7.7%-22.4%]; P = 0.02). Pooled prevalence of PEI after mild and severe pancreatitis was 19.4% [8.6%-38.2%] and 33.4% [22.6%-46.3%] respectively in studies using fecal elaste-1 tests (P = 0.049). Similar results were seen in patients without (18.9% [9.3%-34.6%]) and with necrotizing pancreatitis (32.0% [18.2%-49.8%]; P = 0.053). Over time, the prevalence of PEI decreased in patients who underwent the fecal elastase-1 test and increased in patients who underwent the fecal fat analysis. CONCLUSIONS: After acute pancreatitis, a quarter of all patients develop PEI during follow-up. Alcoholic etiology and severe and necrotizing pancreatitis are associated with higher risk of PEI. The prevalence of PEI may change as time of follow-up increases.
OBJECTIVES: This study systematically explores the prevalence of pancreatic exocrine insufficiency (PEI) after acute pancreatitis in different subgroups of etiology (biliary/alcoholic/other), disease severity and follow-up time (<12, 12-36 and > 36 months after index admission). METHODS: PubMed and EMBASE databases were searched, 32 studies were included in this study level meta-analysis. RESULTS: In a total of 1495 patients with acute pancreatitis, tested at a mean of 36 months after index admission, the pooled prevalence of PEI was 27.1% (95%-confidence interval [CI]: 20.3%-35.1%). Patients from seven studies (n = 194) underwent direct tests with pooled prevalence of 41.7% [18.5%-69.2%]. Patients from 26 studies (n = 1305) underwent indirect tests with pooled prevalence of 24.4% [18.3%-31.8%]. In subgroup analyses on patients that underwent fecal elastase-1 tests, PEI occurred more often in alcoholic pancreatitis (22.7% [16.6%-30.1%]) than in biliary pancreatitis (10.2% [6.2%-16.4%]) or other etiology (13.4% [7.7%-22.4%]; P = 0.02). Pooled prevalence of PEI after mild and severe pancreatitis was 19.4% [8.6%-38.2%] and 33.4% [22.6%-46.3%] respectively in studies using fecal elaste-1 tests (P = 0.049). Similar results were seen in patients without (18.9% [9.3%-34.6%]) and with necrotizing pancreatitis (32.0% [18.2%-49.8%]; P = 0.053). Over time, the prevalence of PEI decreased in patients who underwent the fecal elastase-1 test and increased in patients who underwent the fecal fat analysis. CONCLUSIONS: After acute pancreatitis, a quarter of all patients develop PEI during follow-up. Alcoholic etiology and severe and necrotizing pancreatitis are associated with higher risk of PEI. The prevalence of PEI may change as time of follow-up increases.
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