Introduction

Acute pancreatitis (AP) carries a sizable disease burden, with about a quarter of patients progressing to severe sepsis and requiring intensive care [1,2]. Up to a quarter of patients also experience recurrent episodes, while more than 10% may progress to chronic pancreatitis (CP), and approximately 10% to 35% experience recurrent acute exacerbations [2,3]. Acute-on-chronic pancreatitis (ACP), defined as an acute exacerbation of the inflammatory process in a patient with established CP, has gained recent interest due to its high rate of ICU admissions, prolonged hospital stays, and increased risk of local complications [4]. While clinical consensus on the distinctiveness of ACP is evolving, it is widely recognized as the most appropriate term to describe acute inflammatory changes in patients with CP [4]. ACP is distinguished from isolated AP by unique characteristics, differing biomarker profiles, and morphological findings on imaging [5,6,7]. It is also distinct from recurrent acute pancreatitis (RAP), which typically occurs before structural CP has been established [4].

Despite this consensus, prognostic prediction in ACP remains difficult, with diagnosis still relying heavily on cross-sectional imaging [8,9]. There is an urgent clinical need for a rapid, simple tool to predict the need for early ICU admissions and effectively reduce mortality [8,10]. Current prognostic tools lack the capability for timely risk stratification. The Ranson criteria are delayed by a 48-hour assessment window, while the Acute Physiology and Chronic Health Evaluation II (APACHE II) score is often too complex for emergency settings [11]. The Bedside Index for Severity in Acute Pancreatitis (BISAP) score and C-reactive protein (CRP) are frequently outperformed by biochemical markers with faster kinetics, such as procalcitonin (PCT), which can identify high-risk patients within the first 12-24 hours [12,13,14,15].

PCT, a 116-amino acid precursor of calcitonin, is a highly sensitive biomarker that reflects systemic inflammatory activation [16,17]. During pancreatic injury, PCT is secreted by multiple organs in response to tissue damage and pathogen-associated signals [1,17]. Landmark studies have established its role in predicting infected necrosis (cutoff of 11.8 ng/mL) and organ failure within 12 hours of admission [12,18]. Meta-analyses suggest that PCT levels above 0.5 ng/mL reliably identify severe pancreatitis [19]. However, specific evidence for ACP remains scarce, as most protocols are adapted from AP guidelines [4]. We therefore conducted this prospective study to evaluate serial serum PCT levels in hospitalized patients with ACP from Northeast India.