Over One Third Develop EPI After Acute Pancreatitis

TOPLINE:

Over one third of patients with acute pancreatitis develop exocrine pancreatic insufficiency (EPI) at 12 months, with the key predictors being idiopathic etiology, moderately severe or severe disease, and preexisting diabetes.

METHODOLOGY:

• EPI has traditionally been associated with chronic pancreatitis, but its prevalence and natural history following acute pancreatitis are less well defined.
• Researchers conducted a prospective cohort study including 85 hospital inpatients (mean age, 54.7 years; 48.2% women) diagnosed with acute pancreatitis from three tertiary institutions in the United States.
• Severity of acute pancreatitis was classified according to the Revised Atlanta Criteria.
• EPI was assessed by measuring fecal elastase 1 (FE-1) levels from stool samples at baseline and at 3 and 12 months after enrollment. EPI was defined by FE-1 levels ≤ 200 μg/g stool, with mild and severe EPI categorized by FE-1 levels of 101-200 μg/g stool and ≤ 100 μg/g stool, respectively.
• The prevalence of EPI was assessed at 3 and 12 months after acute pancreatitis. The study also identified the predictors of EPI, including the role of etiology and severity of acute pancreatitis and preexisting diabetes.

TAKEAWAY:

• EPI was present in 34.1% participants at 12 months after an acute pancreatitis attack, with 22.4% having severe EPI.
• Even 12.8% of those with an index mild attack of acute pancreatitis had severe EPI at 12 months.
• The odds of developing EPI at 12 months increased fourfold with idiopathic etiology of acute pancreatitis (P = .0094).
• The odds of developing EPI increased over threefold with moderately severe or severe acute pancreatitis (P = .025) and preexisting diabetes (P = .031).
• The prevalence of severe EPI after acute pancreatitis decreased from 29% at baseline to 26% at 3 months and 22% at 12 months.

IN PRACTICE:

“While specific subpopulations may have identified clinical risk factors, it will remain important to have a low threshold for testing and treatment as there remains much to learn about mechanisms leading to EPI after [acute pancreatitis],” the authors wrote.

SOURCE:

This study, led by Anna Evans Phillips, MD, MS, University of Pittsburgh School of Medicine, Pittsburgh, was published online in eClinicalMedicine.

LIMITATIONS:

Participants were often transferred from other hospitals with differing management techniques, which may have introduced selection bias. The use of FE-1 levels may have had diagnostic limitations. The study did not assess the impact of pancreatic enzyme replacement therapy on recovery from EPI. Some patients with early chronic pancreatitis may have been included owing to the lack of diagnostic clarity.

DISCLOSURES:

The study was supported by an investigator-initiated research grant from AbbVie. Some authors received funding for research from AbbVie. One of the authors declared serving as a consultant and scientific advisory board member and being an equity holder in biotechnology, biopharmaceutical, and diagnostics companies. Another author declared support from the Cystic Fibrosis Foundation and the American Society for Parenteral and Enteral Nutrition.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.