LAUSR

Exocrine pancreatic insufficiency (EPI) is caused by inadequate delivery of pancreatic digestive enzymes to the intestinal lumen, leading to maldigestion. While longstanding chronic pancreatitis (CP) is the most well-known cause, EPI is also very common in patients with pancreatic malignancy, and in those who have undergone pancreatic resection for benign or malignant disease. Less commonly known are a number of additional conditions, which may also have EPI as a consequence (Table 1). One such condition is acute pancreatitis. While clinicians might recognize that EPI could develop after an episode of severe acute pancreatitis (AP) associated with significant pancreatic necrosis, it is becoming more apparent that EPI may occur even in those with less severe episodes of AP. The systematic review and meta-analysis published in this issue of Digestive Diseases and Sciences [1] provide an estimate of the prevalence and predictors of EPI after AP. Estimating the true prevalence of EPI following acute pancreatitis is difficult due to significant heterogeneity among relevant studies. Moreover, methods used to detect and measure EPI are extremely varied among studies, making it difficult to draw conclusions on the true prevalence of EPI. In this current systematic review and meta-analysis, Huang et al. [1] were able to determine the pooled prevalence of EPI during the index hospitalization for AP and during follow-up, in contrast to the only other large-scale meta-analysis that was focused on EPI after AP, reported by Holleman et al. [2], that measured the prevalence of EPI following AP only during up to 36 months of follow-up. Huang et al. found that the cumulative prevalence of EPI in all studies with AP was a rather shocking 62%, when including those with EPI at any point during the index hospitalization, much greater than the 27% prevalence reported in previous meta-analysis [2]. Nevertheless, when comparing the prevalence of EPI in AP patients only after long-term follow-up, both analyses had very similar EPI prevalence rates (33% and 27%, respectively), suggesting approximately a third of patients with acute pancreatitis will develop persistent EPI after discharge, still a startlingly high prevalence. Importantly, Huang demonstrated that the prevalence of EPI during the index attack of AP was approximately 2/3, implying a significant majority of patients with acute pancreatitis will have at least some degree of maldigestion during their initial hospitalization for acute pancreatitis. Interestingly, the pooled analysis demonstrated roughly half of the patients who developed EPI during the index AP attack will recover at least some exocrine function, implying either recovery of function of injured acinar cells or their regeneration [3]. The analysis from Huang et al. and the second meta-analysis suggest a paradigm shift toward understanding AP as a clinical condition that can have long-lasting consequences even without the development of obvious radiologic evidence of chronic pancreatitis such as pancreatic calcifications. The study also heightens the value of identifying EPI earlier in the course of an AP attack in order to ensure that adequate long-term monitoring of maldigestion can be established. This then begs the question: is it possible to identify those patients most at risk for EPI after an attack of AP? The literature has already reached consensus on the pancreatic diseases most at risk for EPI: chronic pancreatitis [4], pancreatic cancer [5], and pancreatic resection. Cystic fibrosis, autoimmune pancreatitis, and diabetes can also result in EPI through several mechanisms (Table 1). Less is known regarding which patients need to be screened for EPI after an episode of AP. Both Huang and Holleman’s studies, however, were able to conclude that alcohol-induced acute pancreatitis, severe pancreatitis (based on Atlanta Classification), and necrotizing pancreatitis were the highest predictors of EPI during long-term follow-up [2], which * Chris E. Forsmark [email protected]