Clinical Significance of the Neutrophil-Lymphocyte Ratio as a Prognostic Marker for Adverse Outcomes in Patients with Acute Pancreatitis

INTRODUCTION

Acute pancreatitis is a common cause of emergency hospital admissions in India. It is an acute inflammatory process of the pancreas, beginning with local acinar cell injury and potentially involving other regional tissues or remote organ systems. While most cases are mild and self-limiting, severe acute pancreatitis (SAP) can be complicated by necrosis and organ failure in approximately 25% of patients, with mortality rates reported as high as 50%.^[1]

Multiple factors can initiate acute pancreatitis, including gallstones, alcohol, trauma, infections, and hereditary conditions. About 75% of cases are attributed to gallstones or alcohol consumption. The severity of the disease is closely linked to extrapancreatic organ failure secondary to the patient’s systemic inflammatory response. Poor prognosis in SAP is often due to uncontrolled systemic inflammatory response syndrome (SIRS) or multi-organ dysfunction syndrome.

Historically, pancreatitis has been regarded as a disorder of pancreatic self-digestion, wherein intracellular activation of digestive proteases causes tissue injury. In the early stages, macrophages, neutrophils, and endothelial cells become activated. Chemokines released from damaged pancreatic cells attract additional inflammatory cells, whose systemic effects determine disease severity.^[2]

Neutrophils drive SIRS and the inflammatory cascade in acute pancreatitis, whereas lymphocyte depletion—seen in severe sepsis—is associated with poor outcomes. An elevated neutrophil count with a concomitant reduction in lymphocyte count has been linked to severe sepsis, bacteraemia, and surgical stress. Compared to the total white blood cell (WBC) count, neutrophil and lymphocyte counts more accurately reflect the immune response.^[3]

Identifying reliable predictors of disease severity is essential for clinical decision-making. The neutrophil-lymphocyte ratio (NLR), derived from the WBC differential count, offers a simple, rapid, and inexpensive marker of inflammatory burden. In resource-limited settings like India, with a low doctor-to-patient ratio and limited diagnostic facilities in peripheral hospitals, differential WBC count is a practical option.^[4]

In clinical assessment, NLR is calculated on day 0 (admission), day 1, day 2 and is correlated with disease severity [Figures 1-3]. Severity classification is typically based on the Modified Computed Tomography Severity Index (MCTSI) for acute pancreatitis.

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Figure 1: Mean NLR at day 0. NLR: Neutrophil lymphocyte ratio.

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Figure 2: Mean NLR at day 1. NLR: Neutrophil lymphocyte ratio.

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Figure 3: Mean NLR at day 2. NLR: Neutrophil lymphocyte ratio.

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MATERIAL AND METHODS

Technique

Blood samples will be collected within two hours of hospital admission (day 0), as well as on day 1 and day 2 of hospitalisation [Figures 4 and 5]. Appropriate biochemical investigations will be performed. Imaging studies, including plain chest radiography, upright abdominal radiography, abdominal ultrasonography, and CECT of the abdomen, will be carried out as indicated. Radiological reports will be obtained from certified radiologists.

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Figure 4: Neutrophils at days 0, 1 and 2 among CT severity groups. CT: Computed tomography

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Figure 5: Lymphocytes at days 0, 1 and 2 among CT severity groups. CT: Computed tomography

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RESULTS

Figure 6 shows the mean NLR values across three days for patients categorised as having mild, moderate, and severe pancreatitis. In the mild group, the NLR shows a consistent decline from 3.43 on Day 0 to 2.62 on Day 2, suggesting a positive response or recovery trend. Similarly, the moderate group shows a decrease from 6.27 on Day 0 to 4.13 by Day 2. In contrast, the severe group exhibits a sharp rise in NLR, increasing from 10.09 on Day 0 to 15.28 on Day 2, indicating a potential escalation in disease severity or ongoing inflammatory response. This trend highlights the importance of monitoring NLR as a marker of disease progression and response to treatment in acute pancreatitis.

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Figure 6: NLR at days 0, 1 and 2 among CT severity groups. NLR: Neutrophil lymphocyte ratio, CT: Computed tomography.

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NLR reflects disease severity in pancreatitis, normalising in mild and moderate cases but remaining elevated in the severe group [Figures 7 and 8]. Severe cases show rising NLR, longer hospital stays, organ dysfunction, and more complications. The difference in NLR among mild, moderate, and severe groups was compared and noted to be statistically highly significant (P < 0.01).^[6]

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Figure 7: Organ dysfunction among CT severity groups. CT: Computed tomography, RS: Respiratory system, CVS: Cardiovascular system.

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Figure 8: Duration of stay among CT severity groups. CT: Computed tomography

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DISCUSSION

This study, involving 50 patients, found acute pancreatitis to be predominantly a male disease (96% male vs. 4% female), consistent with previous Indian studies and attributed mainly to higher alcohol consumption among men. The most affected age group was 31–40 years, with a mean age of 34.5 years. Alcohol was the leading cause (92%), followed by gallstones. Severity varied across alcohol-related cases: 11 mild, 16 moderate, and 19 severe, with no significant link between alcohol consumption and MCTSI scores.

Biochemical analysis revealed progressively higher mean serum amylase (mild: 376.67, moderate: 942.35, severe: 2516.43 U/l) and serum lipase (mild: 1036.25, moderate: 1789.29, severe: 5852.62 U/l) levels with increasing severity, both statistically significant (P < 0.01).

The NLR emerged as a strong indicator of disease severity. On day 0, NLR values were 3.43 (mild), 6.27 (moderate), and 10.79 (severe). By day 2, mild cases declined to 2.62, moderate to 4.13, but severe cases rose to 15.28, indicating persistent inflammation or worsening disease. These changes were statistically significant (P < 0.01) [Table 1].

Pathophysiologically, acute pancreatitis triggers cytokine-mediated neutrophil recruitment, leading to inflammation and tissue damage. Severe cases showed persistent neutrophilia and lymphopenia, the latter linked to ongoing inflammation, sepsis, and poorer outcomes. The elevated NLR in severe cases reflected both increased neutrophil counts and sustained lymphopenia.^[7]

Findings aligned with prior research:

• Suppiah et al. – NLR normalises in favourable outcomes but stays elevated in poor prognosis.^[1]

• Azab et al. – NLR ≥4.7 predicts ICU admission and mortality better than total WBC or individual cell counts.^[3]

A key advantage of NLR is its simplicity and cost-effectiveness. It requires only a routine total and differential WBC count, unlike complex scoring systems (e.g., Ranson’s, Glasgow) that require multiple parameters and a 48-hour delay before prognostication. In contrast, NLR can be measured on admission and monitored dynamically to detect early progression toward severe disease, enabling timely intervention.^[8]

This is especially relevant in India, where resource limitations and low doctor-patient ratios hinder complex testing. Alcohol-related pancreatitis is common among low socioeconomic groups, and frequent specialised tests may be unaffordable. NLR offers an affordable, repeatable, and rapid prognostic tool suitable for peripheral and secondary healthcare centres, helping guide referrals for intensive care in high-risk patients, potentially reducing morbidity and mortality.^[5]

CONCLUSION

In this study, the NLR has been shown to be an effective single marker for evaluating the severity of acute pancreatitis.

NLR can be easily computed and is part of standard laboratory tests conducted for all patients upon their admission. As a routine test, it imposes no extra financial burden on patients. NLR appears to have a strong correlation with the severity and outcomes of acute pancreatitis. Daily monitoring will provide a continuous overview of the body’s immune and inflammatory responses to pancreatitis, allowing for earlier prognosis predictions.

The assessment of NLR overcomes the limitations of Ranson’s scoring system, as it can be utilised upon admission and monitored within the first 48 hours. It also addresses the limitations of the APACHE II scoring system by not requiring multiple parameters for evaluation.

However, further research is necessary to accurately determine the optimal NLR and to explore whether its inclusion can enhance the precision of existing prognostic scoring systems for acute pancreatitis.