This study evaluates serum amylase, lipase, IL-10, and procalcitonin in healthy controls, mild acute pancreatitis, and severe acute pancreatitis. Results indicate significant biomarker variations across groups, highlighting diagnostic and prognostic roles, particularly for procalcitonin and IL-10 in predicting severity.
Acute pancreatitis (AP) is a potentially life-threatening inflammatory disorder of the pancreas characterized by autodigestion of pancreatic tissue and variable systemic complications [1,2]. The disease exhibits a broad clinical spectrum ranging from mild, self-limiting illness to severe necrotizing pancreatitis with multiorgan failure and high mortality [3]. The global incidence of AP ranges between 13 and 73 per 100,000, and the prevalence in India is approximately 7.9 per 100,000 [4,5]. Alcohol and gallstones constitute the leading etiological factors, while genetic, metabolic, and idiopathic cases account for the remainder [6,7]. The pathophysiology involves premature activation of digestive zymogens, acinar cell injury, and release of inflammatory mediators, resulting in systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction [8,9]. Biochemical markers play an essential role in the early diagnosis and prognosis of AP. Serum amylase and lipase are classical diagnostic markers, though they do not always correlate with disease severity [10]. Cytokines such as interleukin-10 (IL-10), with its potent anti-inflammatory properties, and procalcitonin (PCT), a marker of systemic inflammation, are recognized as promising severity predictors [11,12]. This study was conducted to compare serum amylase, lipase, IL-10, and PCT levels in healthy controls, mild AP, and severe AP, and to explore their prognostic significance.
This observational case-control study was conducted at J.L.N. Medical College & Associated Group of Hospitals, Ajmer. A total of 330 participants were included: 110 healthy controls, 110 patients with mild acute pancreatitis, and 110 with severe acute pancreatitis, classified using the Revised Atlanta Classification. Acute pancreatitis diagnosis was based on clinical features, elevated amylase or lipase (>3 times the upper limit of normal), and radiological findings. Exclusion criteria included chronic pancreatitis, pancreatic malignancy, major comorbidities, and recent infections. Blood samples were collected within 48 hours of admission. Serum amylase and lipase were estimated using enzymatic methods. IL-10 levels were measured by enzyme-linked immunosorbent assay (ELISA), and procalcitonin was determined by chemiluminescent assay. Statistical analysis was performed using ANOVA, independent t-test, Pearson correlation and post-hoc tests, with p <0.001 considered significant. The study acquired consent from all participants has taken also with ethical permission.
Serum amylase and lipase levels were significantly elevated in mild and severe AP compared to controls (p<0.001), with higher mean values in severe AP (Table 1, Figure 1). IL-10 levels showed a significantly decrease in severe AP in comparison with mild AP & healthy controls (Table 1, Figure 2). Procalcitonin levels were minimal in controls, moderately elevated in mild AP, and markedly elevated in severe AP (p<0.001), as shown in (Table 1 and Figure 3). These findings highlight the diagnostic value of amylase and lipase and the prognostic utility of IL-10 and procalcitonin.
Table 1: Comparison of serum biomarkers among study groups.
Parameter |
Control (n=110) |
Mild AP (n=110) |
Severe AP (n=110) |
p-value |
Amylase (U/L) |
42.88 ±7.15 |
530.32 ±117.66 |
1482.44 ±437.04 |
<0.001* |
Lipase (U/L) |
35.73 ±5.73 |
256.07± 55.32 |
879.65 2±52.92 |
<0.001* |
IL-10 (pg/mL) |
6.06 ±0.31 |
5.08 ±0.30 |
3.91 ±0.31 |
<0.001* |
Procalcitonin (ng/mL) |
0.33 ± 0.06 |
1.05 ± 0.27 |
2.90 ± 0.92 |
<0.001* |
Figure 1: Serum amylase and lipase levels across groups.
Figure 2: Serum IL-10 levels across groups.
Figure 3: Serum procalcitonin levels across groups.
The present study demonstrates that while serum amylase and lipase are useful for diagnosing AP, they lack specificity in predicting severity. Our findings corroborate previous studies indicating that procalcitonin is a highly sensitive and specific marker for identifying severe cases [13,14]. Our study is consistent with the study conducted by Fisic E et al (2006) [15] , Berney T et al (1999) [16], Rongione AJ et al (1997) and various studies which reported a significant decrease in the level of IL-10 in patients with mild AP& severe AP subjects in comparison with health controls. Berney T et al (1999) study showed IL‑10 on day 0 to be an extremely good marker for predicting the progression to severity AP. IL‑10 is an anti‑inflammatory cytokine which inhibits the release of pro‑inflammatory cytokines (i.e., IL‑1 β, IL‑6, and tumor necrosis factor‑α) from monocytes/macrophages thus preventing subsequent tissue damage. Studies have correlated lower levels of IL‑10 with a higher severity of pancreatitis.[16] Procalcitonin, by contrast, rises proportionally with severity and correlates well with clinical scoring systems such as Ranson and APACHE II [17,18]. Thus, combining classical enzymatic markers with cytokine and inflammatory biomarkers may improve early risk stratification.
The sample size was modest, and the study was conducted at a single center, which may limit generalizability. Serial measurements of biomarkers were not performed, which could provide better insights into dynamic changes. Advanced imaging correlations with biomarkers were limited.
Serum amylase and lipase remain diagnostic cornerstones of acute pancreatitis, but their prognostic utility is limited. IL-10 and procalcitonin provide additional insights into disease severity, with procalcitonin emerging as a reliable biomarker for early identification of severe acute pancreatitis. IL-10 can be also used therapeutically in patients of AP.