NLR and Platelet Dynamics: Simple, Cost-effective Biomarkers for Stratifying Severity in Acute Pancreatitis

Acute pancreatitis (AP) is characterized by pancreatic acinar cell injury and trypsin activation. Early identification of severe cases remains critical to reduce morbidity, mortality, and healthcare burden. This study aimed to evaluate the utility of accessible hematological indices-neutrophil-to-lymphocyte ratio (NLR), platelet counts (PLT), platelet-to-lymphocyte ratio (PLR), and platelet-to-white cell ratio (PWR)-as prognostic alternatives to current complex scoring systems.

In this retrospective prognostic study, medical records of 150 patients (aged 18-70 years) diagnosed with AP based on the Atlanta criteria (2012) at Firouzabadi Hospital (February 2015-February 2017) were reviewed. Blood tests performed at admission, 48 hours, and 72 hours after admission were used to compute the NLR, PLR, and PWR for group comparisons. The association between these indices and prognostic scores (Ranson, Acute Physiology and Chronic Health Enquiry [APACHE-II], Glasgow, Sequential Organ Failure Assessment [SOFA], and Marshall) was assessed using independent t tests or Mann-Whitney U tests, as appropriate. To examine differences related to mortality, hematological indices were compared between survivors and nonsurvivors using the Mann‑Whitney U test or independent samples t test based on normality.

NLR showed significant differences with severity criteria and mortality. At 48 hours, in severe Bedside Index of Severity in Acute Pancreatitis (BISAP) cases, NLR was significantly higher (mean, 19.7 vs. 5.26; P = 0.001). Ranson admission scores also demonstrated elevated NLR (12.8 vs. 6.5; P = 0.030). Nonsurvivors had markedly higher NLR at 48 hours (10.69 vs. 5.26; P = 0.035). PLT was significantly reduced in severe AP and was inversely related to disease severity. Patients meeting the Ranson criteria for severe disease at admission, as well as those with Marshall organ failure persisting beyond 48 hours, exhibited significantly lower PLT at 72 hours (176.5 vs. 264.8 ×10³/μL; P = 0.001 and 161.0 vs. 260.5 ×10³/μL; P = 0.006, respectively). Similarly, PWR showed a significant inverse association with severity, reflected in lower mean PWR values at 72 hours for patients with higher APACHE‑II scores at 48 hours (18.59 vs. 31.22; P = 0.009). In contrast, PLR demonstrated minimal prognostic utility, with no significant differences observed across any of the severity scores (all P > 0.05).

Significant differences between peripheral inflammatory markers across prognostic criteria suggest their potential as complementary tools for early risk stratification in AP. However, further prospective studies are warranted to confirm the prognostic utility of these indices for clinical endpoints, such as mortality and intensive care unit admission.