EXOCRINE PANCREATIC INSUFFICIENCY INCIDENCE AT 12 MONTHS AFTER ACUTE PANCREATITIS: A PROSPECTIVE MULTICENTER STUDY

Background: Exocrine Pancreatic insufficiency (EPI) occurs following acute pancreatitis (AP) at variably reported rates, secondary to combination of suspected impairment in pancreatic enzyme secretion and damage to the pancreatic acinar cells. While most patients with AP experience rapid resolution of their abdominal pain, the timeline of exocrine function recovery is unknown and has not been prospectively studied. The aim of this study is to establish the incidence and predictors of EPI at 12 months after AP in a prospective cohort.

Methods: Adult participants (≥18 years) admitted to the hospital with an AP attack were enrolled at one of three centers in the Post-Acute Pancreatitis Pancreatic Exocrine Insufficiency (PAPPEI) Study at the time of attempt to resume oral or enteral diet. AP was defined according to the Revised Atlanta Classification. Patients were excluded if they had history of pre-existing or suspected pancreatic cancer, chronic pancreatitis, diagnosed EPI, or diseases of malabsorption. Blood and stool samples were collected at baseline and 12-months after enrollment. EPI was assessed by fecal elastase (FE-1) levels from stool samples (EPI defined by FE-1 <200 µg/g; severe EPI FE-1 level ≤ 100 µg/g stool; mild EPI FE-1 100-200 µg/g stool).

Results: A total of 85 subjects (44 (51.8%) male, mean age 54.7 ± 14.1 years) completed stool samples at 12 months. EPI was observed in 29 (34.1%); 19 (22.4%) had severe EPI and 10 (11.8%) had mild EPI. Factors significantly associated with EPI at 12 months in univariate analysis included male sex, recurrent (versus index) AP, pre-existing diabetes, alcohol and idiopathic etiologies, and increasing severity of AP (Table 1). In multivariable analysis, the odds of having EPI at 12 months increased 4-fold with idiopathic AP etiology, and over 3-fold with non-mild (moderately severe or severe) AP, as well as baseline diabetes mellitus. Importantly, even subjects with an index mild attack of AP (n = 39) at enrollment developed severe EPI at 12 months, with a prevalence of 12.8% (5/29 with EPI at 12 months) in the overall group with EPI having had index mild attack of AP. Evaluation of EPI natural history over the 1 year after AP showed that only approximately 25% of the 48 subjects who had EPI at baseline recovered by 12 months, and 6 of those with EPI at 12 months did not have EPI at baseline (Figure 1).

Conclusions: EPI is present in approximately one-third of prospectively assessed patients at 12-months post-AP. Factors associated with EPI included idiopathic etiology, non-mild AP, and pre-existing DM. There is a risk for development of EPI even in patients with mild EPI suggesting further investigations are needed to understand the potential mechanisms of injury and identify methods for tailored screening.