Objective The aim of this study is to investigate the correlation between neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) with nonalcoholic fatty liver disease (NAFLD). Methods All subjects underwent medical check-ups, which included the measurement of basic clinical, biochemical tests and imaging tests. Univariate and multivariate logistic regression models and piece-wise linear regression were used to assess the relationship between NLR and PLR with NAFLD. Results All participants were divided into two groups: the Non-NAFLD group and the NAFLD group. Univariate analysis model indicated PLR was negatively correlated with NAFLD (P < 0.001) and NLR was not significantly associated with NAFLD (P > 0.05). Multiple logistic regression showed that no correlation between NLR and PLR with NAFLD after adjusting all covariates (P > 0.05). Interestingly, a nonlinear association was detected between NLR and PLR with NAFLD by piece-wise linear regression adjusting for all confounding factors. The inflection points of NLR and PLR were 1.23 and 42.29, respectively. On the left side of the inflection point (NLR < 1.23), a positive correlation was detected between NLR and NAFLD (β = 2.35, 95% CI: 1.20~4.61, P = 0.013). And PLR was found to be negatively associated with NAFLD on the right side of the inflection point (β = 0.99, 95% CI: 0.98~0.99, P < 0.001). Conclusion This study demonstrated that the relationship between NLR and PLR with NAFLD was nonlinear after adjusting for potential confounding factors. The result suggested that PLR ≥ 42.29 might be a protective factor of NAFLD, while NLR < 1.23 might be a risk factor of NAFLD.

BACKGROUND Nonalcoholic fatty liver disease (NAFLD) is characterized by hypertriglyceridemia, increased low-density lipoprotein cholesterol levels, and reduced high-density lipoprotein cholesterol (HDL-C) particles. Previous studies have shown that the total cholesterol to high-density lipoprotein cholesterol ratio (TC/HDL-C) was superior to other lipid metabolism biomarkers for predicting NAFLD risk and could be a new indicator of NAFLD. However, the association between TC/HDL-C and NAFLD in patients with hepatitis B virus (HBV) has not yet been determined. AIM To investigate the association between TC/HDL-C and NAFLD in a population with chronic hepatitis B (CHB). METHODS In this study, 183 HBV-infected patients were enrolled. All participants underwent blood chemistry examinations and abdominal ultrasound. Univariate and multivariate logistic regression models, curve fitting analysis, and threshold calculation were used to assess the relationship between TC/HDL-C and NAFLD. RESULTS The overall prevalence of NAFLD was 17.49% ( n = 32) in the 183 CHB participants. The TC/HDL-C of non-NAFLD and NAFLD patients were 3.83 ± 0.75 and 4.44 ± 0.77, respectively ( P < 0.01). Logistic regression analysis showed that TC/HDL-C was not associated with NAFLD after adjusting for other pertinent clinical variables. However, at an optimal cutoff point of 4.9, a non-linear correlation between TC/HDL-C and NAFLD was detected. The effect size of the left and right sides of the inflection point were 5.4 (95% confidence interval: 2.3-12.6, P < 0.01) and 0.5 (95% confidence interval: 0.1-2.2, P = 0.39), respectively. On the left side of the inflection point, TC/HDL-C was positively associated with NAFLD. However, no significant association was observed on the right side of the inflection point. CONCLUSION This study demonstrated a non-linear correlation between TC/HDL-C and NAFLD in a population with CHB. TC/HDL-C was positively associated with NAFLD when TC/HDL-C was less than 4.9 but not when TC/HDL-C was more than 4.9.

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