Acute pancreatitis remains one of the common abdominal emergencies encountered by surgeons and gastroenterologists. Its behaviour is deceptively variable: the same diagnosis may settle within a few days in one patient and progress to necrosis, sepsis, or multiorgan failure in another. Gallstones remain a major cause of acute pancreatitis, and the clinical burden is especially visible in Indian public hospitals, where patients often arrive after a period of symptom persistence and home-based treatment attempts. Early recognition of patients likely to deteriorate is therefore not just an academic exercise. It decides monitoring intensity, timing of imaging, referral for higher care, and the need for multidisciplinary support.[1] Clinically, acute pancreatitis is diagnosed through a combination of characteristic abdominal pain, elevated pancreatic enzymes, and imaging when required. Yet diagnosis alone does not guide the surgeon enough. The revised Atlanta classification brought a more practical language to severity grading by separating mild, moderately severe, and severe disease using local complications and organ failure as the defining anchors.[2] This classification has become a common framework for both reporting outcomes and deciding how aggressively a patient should be observed in the early phase.[3] Guidelines consistently emphasize that early severity assessment matters because the first 48 to 72 hours often define the subsequent course. Fluid resuscitation, analgesia, nutrition, antibiotics only when appropriate, and the timing of biliary intervention depend on careful triage rather than on enzyme elevation alone.[4] In gallstone pancreatitis, this is particularly relevant because definitive management of the biliary source must be planned while avoiding unnecessary intervention during a systemic inflammatory phase.[5] Traditional prognostic scores have value, but they can be cumbersome in busy emergency settings. Biomarkers are attractive because they are objective and relatively easy to repeat. CRP is an acute-phase reactant that usually becomes more informative after 48 hours. Procalcitonin, originally used as a marker of bacterial infection and systemic inflammation, has been investigated for severe pancreatitis and infected necrosis.[6] Systematic evidence suggests that procalcitonin may help identify clinically significant severity, while CRP remains one of the simplest and most widely available inflammatory markers.[7,8] Against this background, the present study assessed the relationship of CRP at 48 hours and procalcitonin with the severity and short-term outcome of acute gallstone-induced pancreatitis in a tertiary-care public hospital setting.

Study design and setting A prospective observational study was conducted in the Department of General Surgery, Government Medical College and Hospital, Kallakurichi, Tamil Nadu, India. Study period The study was carried out from May to October 2025. Study population The study included 66 patients diagnosed with acute gallstone-induced pancreatitis and assessed during the study period. Patients were evaluated clinically and biochemically, and severity was assigned using the Atlanta classification. Study variables The recorded variables were age, gender, body mass index, serum amylase, alanine transaminase, alkaline phosphatase, Atlanta severity class, CRP at 48 hours, serum procalcitonin, duration of hospital stay, pancreatic necrosis, and final short-term outcome. Outcome measures The primary outcome was severity of acute pancreatitis classified as mild, moderately severe, or severe. Secondary outcomes included pancreatic necrosis, duration of hospital stay, and in-hospital mortality. Ethical considerations The ethics approval was obtained prior to this study. Patient confidentiality was maintained throughout the study. Statistical analysis Continuous variables were summarized as mean ± standard deviation. Categorical variables were expressed as frequencies and percentages. Kruskal-Wallis test was used to compare continuous variables across severity groups, while chi-square test was used for categorical associations. Spearman rank correlation was used to assess the relationship of biomarkers with severity and hospital stay. Exploratory diagnostic performance was calculated for clinically meaningful CRP and procalcitonin cutoffs. A p-value <0.05 was considered statistically significant

The study included 66 patients with acute gallstone-induced pancreatitis. The mean age was 49.55 ± 16.44 years, with an age range of 22 to 77 years. Females accounted for 42 (63.64), while males accounted for 24 (36.36). The overall baseline profile is shown in Table 1, and the gender distribution is illustrated in Figure 2. Table 1. Baseline clinical and biochemical profile of the study population (n=66) Variable Overall result Age (years) 49.55 ± 16.44 (22-77) Female gender 42 (63.64) Male gender 24 (36.36) BMI (kg/m²) 28.96 ± 3.90 (21.0-37.0) Serum amylase (U/L) 2145.17 ± 887.02 (600-3461) ALT (U/L) 330.89 ± 129.47 (128-595) Alkaline phosphatase (U/L) 314.48 ± 96.34 (169-490) CRP at 48 h (mg/L) 131.64 ± 97.05 (10.3-446.6) Procalcitonin (ng/mL) 0.94 ± 1.80 (0.06-9.28) Hospital stay (days) 7.89 ± 5.46 (4-29) Pancreatic necrosis 6 (9.09) Death 6 (9.09) Values are presented as mean ± SD (range) or n (%). Atlanta severity grading showed mild pancreatitis in 45 (68.18), moderately severe pancreatitis in 15 (22.73), and severe pancreatitis in 6 (9.09). This distribution is shown in Figure 1. Pie chart displays the proportion of female and male patients. Biomarkers and clinical outcomes across severity groups Both inflammatory markers showed a stepwise increase with clinical severity. Mean CRP at 48 hours was lowest in mild disease and highest in severe disease. Procalcitonin followed the same pattern. Hospital stay also increased sharply across severity groups. These trends are summarized in Table 2 and shown graphically in Figures 3, 4, and 6. Table 2. Biomarker levels and outcomes according to Atlanta severity class Severity class n (%) CRP at 48 h (mg/L) Procalcitonin (ng/mL) Hospital stay (days) Pancreatic necrosis n (%) Death n (%) Mild 45 (68.18) 78.52 ± 44.11 0.23 ± 0.13 4.98 ± 0.84 0 (0.00) 0 (0.00) Moderately Severe 15 (22.73) 206.16 ± 34.19 1.08 ± 0.41 11.07 ± 2.31 0 (0.00) 0 (0.00) Severe 6 (9.09) 343.67 ± 77.73 5.94 ± 2.67 21.83 ± 5.12 6 (100.00) 6 (100.00) p-value - <0.001 <0.001 <0.001 <0.001 <0.001 Continuous variables were compared using Kruskal-Wallis test. Categorical outcomes were compared using chi-square test. Necrosis and mortality Pancreatic necrosis was documented in 6 patients (9.09%), and all these patients belonged to the severe category. Similarly, all 6 deaths occurred in the severe group. No death or pancreatic necrosis was observed in the mild or moderately severe groups. The outcome distribution by severity is shown in Figure 5. Correlation analysis CRP and procalcitonin both showed significant positive correlations with hospital stay and Atlanta severity class. The correlation with hospital stay was slightly stronger for procalcitonin (r=0.662) than CRP (r=0.634), while both biomarkers had almost identical correlations with severity grading. The detailed correlation results are presented in Table 3. Table 3. Spearman correlation of biochemical markers with hospital stay and severity Marker r with hospital stay p-value r with severity class p-value CRP at 48 h (mg/L) 0.634 <0.001 0.819 <0.001 Procalcitonin (ng/mL) 0.662 <0.001 0.819 <0.001 Serum amylase (U/L) -0.096 0.441 -0.018 0.889 ALT (U/L) -0.181 0.147 -0.223 0.072 Alkaline phosphatase (U/L) -0.067 0.595 0.090 0.471 Severity class was analysed as an ordinal variable: mild=1, moderately severe=2, severe=3. Exploratory diagnostic performance of selected biomarker cutoffs For identifying moderately severe or severe disease, both CRP ≥150 mg/L and procalcitonin ≥0.5 ng/mL separated the mild group from clinically significant disease in this cohort. For identifying severe disease, CRP ≥250 mg/L and procalcitonin ≥2.0 ng/mL identified all severe cases without false positives. These estimates are shown in Table 4 and should be interpreted as cohort-specific exploratory findings rather than externally validated thresholds. Table 4. Exploratory diagnostic performance of selected biomarker cutoffs Cutoff Target outcome TP FP TN FN Sensitivity (%) Specificity (%) PPV (%) NPV (%) Accuracy (%) CRP ≥150 mg/L Moderately severe/severe disease 21 0 45 0 100.00 100.00 100.00 100.00 100.00 Procalcitonin ≥0.5 ng/mL Moderately severe/severe disease 21 0 45 0 100.00 100.00 100.00 100.00 100.00 CRP ≥250 mg/L Severe disease 6 0 60 0 100.00 100.00 100.00 100.00 100.00 Procalcitonin ≥2.0 ng/mL Severe disease 6 0 60 0 100.00 100.00 100.00 100.00 100.00 TP: true positive; FP: false positive; TN: true negative; FN: false negative; PPV: positive predictive value; NPV: negative predictive value.

relationship between inflammatory biomarkers and clinical severity in acute gallstone-induced pancreatitis. CRP at 48 hours and procalcitonin increased from mild to moderately severe and severe disease. More importantly, these laboratory changes moved in the same direction as outcomes that matter at the bedside: longer hospital stay, pancreatic necrosis, and mortality. The pattern was not subtle. The severe group had a mean hospital stay more than four times that of the mild group, and all deaths occurred in patients classified as severe. These observations are consistent with the biological behaviour of acute pancreatitis. CRP rises as part of the hepatic acute-phase response and becomes more informative after the inflammatory cascade has matured. Procalcitonin reflects a different but related axis: systemic inflammatory activation and, in complicated disease, the possibility of infected necrosis or sepsis physiology. Rau et al. found that procalcitonin helped in the early assessment of pancreatic infection and overall prognosis in severe acute pancreatitis.[9] A later meta-analysis by Chen and Jiang also supported the diagnostic usefulness of procalcitonin for severe acute pancreatitis, although heterogeneity across cutoffs and timing remains an important issue.[10] The findings also sit well with Indian clinical experience. Dias et al. reported that a rapid procalcitonin strip test had independent prognostic value in acute pancreatitis.[11] In public hospitals, especially where emergency workload is heavy, a practical biomarker that can support triage has clear value. At the same time, procalcitonin is costlier than CRP and may not be ordered routinely in smaller centres. This is why the paired interpretation of CRP and procalcitonin is useful: CRP provides a low-cost severity signal at 48 hours, while procalcitonin may add confidence when systemic deterioration or necrotic complications are suspected. The stepwise rise in CRP observed here agrees with the broader literature. Tian et al. reported diagnostic value for CRP, procalcitonin, interleukin-6, and lactate dehydrogenase in severe acute pancreatitis, suggesting that a single marker may not fully capture the inflammatory burden.[12] Khanna et al., in an Indian study comparing multiple scoring systems and biomarkers, showed that CRP and procalcitonin were relevant to severity, organ failure, pancreatic necrosis, and mortality.[13] The present findings echo that direction, although the current study focused specifically on gallstone-induced pancreatitis. Hospital stay correlated significantly with both biomarkers. This matters clinically because prolonged stay is not merely a numerical outcome. It reflects persistent pain, need for monitoring, delayed oral intake, complications, imaging burden, and family-level economic strain. Choudhuri et al. reported that serial change in procalcitonin, along with APACHE II score, was useful for mortality prediction in acute pancreatitis.[14] The current study did not evaluate dynamic procalcitonin change, but the single procalcitonin value still showed meaningful association with severity and duration of admission. The perfect separation produced by selected exploratory cutoffs in this cohort should be read cautiously. Such performance is possible in small, well-defined cohorts, especially when severe disease is clustered with necrosis and mortality. It does not mean that these thresholds will behave identically in another hospital or in a mixed aetiology pancreatitis population. Current guideline-based management still requires clinical examination, organ failure assessment, imaging when indicated, and judgement about biliary intervention rather than reliance on one laboratory value.[15] From a service-hospital perspective, the practical message is simple. Patients with rising CRP at 48 hours and elevated procalcitonin deserve closer observation, early reassessment, and lower threshold for escalation. Alberti et al. also showed that procalcitonin had prognostic relevance for infections in acute pancreatitis and acute cholangitis, which is especially relevant to biliary disease.[16] In a gallstone pancreatitis pathway, biomarkers may help decide who can safely remain on routine ward care and who requires more intensive monitoring. Several limitations should be acknowledged. The study was conducted at a single centre with a sample size of 66, and the severe group was small. The analysis focused on short-term hospital outcomes. Long-term recurrence, timing of cholecystectomy, readmission, and serial biomarker trends were not evaluated. The cutoff analysis was exploratory and should be validated prospectively in larger cohorts before being used as a protocol-level decision tool.

In patients with acute gallstone-induced pancreatitis, CRP at 48 hours and procalcitonin showed a clear and statistically significant increase across Atlanta severity classes. Both biomarkers correlated with duration of hospital stay, and higher values were associated with pancreatic necrosis and mortality. Within this cohort, selected CRP and procalcitonin thresholds showed excellent exploratory discrimination for clinically significant and severe disease. These findings support the use of CRP and procalcitonin as practical adjuncts for early risk stratification, while clinical assessment and guideline-based management remain central to decision-making.

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