Association between Neutrophil to Lymphocyte Ratio and Steatosis and Fibrosis in Patients with Non-Alcoholic Fatty Liver Disease

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum from steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma, and is closely associated with metabolic comorbidities. Global prevalence is approximately 25.24%, with higher rates in patients with type 2 diabetes mellitus. Neutrophil to lymphocyte ratio (NLR), a readily available marker of subclinical systemic inflammation, may predict advanced NAFLD. However, prior studies report inconsistent NLR-NAFLD associations. This study aimed to evaluate NLR's association with steatosis and fibrosis in NAFLD using transient elastography (TE) with controlled attenuation parameter (CAP).

Methods: A cross-sectional observational study enrolled 100 NAFLD patients aged 18–65 years at T. S. Misra Medical College & Hospital, Lucknow, over 18 months. Inclusion criteria required ultrasonographic fatty liver in non-alcoholic patients with written consent. Patients with viral hepatitis, alcohol use, acute liver conditions, active infections, chronic illnesses, or pregnancy were excluded. Clinical evaluation included detailed history, anthropometric measurements, and physical examination. Fasting blood tests assessed liver enzymes, lipid profile, blood glucose, and complete blood count; NLR was calculated from the differential leucocyte count. Ultrasonography graded steatosis. TE-CAP measured liver stiffness (kPa) and steatosis (dB/m). Data were analyzed with SPSS v29.0; correlations assessed via Pearson's coefficient; p<0.05 was considered statistically significant.

Results: Mean age was 55.2 ± 14.2 years; 66% of patients were female. Predominant symptoms included malaise (78%) and abdominal discomfort (58%). Hepatomegaly was the most common sign (58%). Mean NLR was 2.7 ± 1.0; mean AST 83.7 ± 36.1 IU/L; mean ALT 89.5 ± 24.1 IU/L. Steatosis distribution: mild (Grade 1) 38%, moderate (Grade 2) 50%, severe (Grade 3) 12%; mean CAP 283.6 ± 38.4 dB/m. Fibrosis distribution: none (Score 0) 32%, mild (Score 1) 38%, moderate (Score 2) 22%, severe (Score 3) 8%; mean liver stiffness 7.4 ± 4.8 kPa. NLR increased significantly with steatosis grade (Grade 1: 2.3 ± 0.7; Grade 2: 3.6 ± 1.5; Grade 3: 3.9 ± 1.9; p<0.001) and fibrosis score (Score 0: 1.4 ± 0.4; Score 1: 2.7 ± 0.5; Score 2: 3.2 ± 0.6; Score 3: 3.7 ± 1.1; p<0.001). Significant positive correlations were found: TE-CAP (R=0.680), CAP-NLR (R=0.794), TE-NLR (R=0.723); all p<0.001. At an NLR cut-off of 2.45: sensitivity 98.4% and specificity 92.0% for steatosis; sensitivity 85.3% and specificity 81.2% for fibrosis.

Conclusion: NLR positively and significantly associates with both steatosis and fibrosis severity in NAFLD, serving as a reliable, non-invasive, and cost-effective biomarker alongside TE-CAP for disease risk stratification.