Association of C-reactive protein-to-lymphocyte ratio (CLR) with liver stiffness measurement (LSM): Findings from NHANES 2017 to 2018

医学 全国健康与营养检查调查 非酒精性脂肪肝 内科学 肝硬化 置信区间 脂肪肝 胃肠病学 人口 肝病 瞬态弹性成像 淋巴细胞 肝纤维化 疾病 环境卫生
作者
Junxi Liu,Qing Qiao,Min Yang,X. Wang,Boda Zhou
出处
期刊:Medicine [Wolters Kluwer]
卷期号:104 (30): e43457-e43457
标识
DOI:10.1097/md.0000000000043457
摘要

The progression of nonalcoholic fatty liver disease may lead to liver fibrosis, with liver stiffness measurement (LSM) as an important noninvasive measurement for liver stiffness, indirectly reflecting the degree of liver fibrosis. C-reactive protein-to-lymphocyte ratio (CLR) is an important inflammatory marker which has potential diagnostic value in nonalcoholic fatty liver disease. This study investigates the association between the CLR and LSM. Utilizing data from the National Health and Nutrition Examination Survey 2017 to 2018, we included participants completed the liver transient elastography exam with complete CLR value. We excluded participants lacking ultrasound data on essential covariates. Our study implemented multi-model linear regression analysis, subgroup analysis, to investigate the independent relationship between CLR and LSM. We enrolled a total of 3399 participants (51.3% male and 48.7% female). Participants were divided into 2 groups based on LSM cutoff value of 12.5 kPa, indicating severe liver fibrosis or cirrhosis. We found after adjusting every potential covariates, CLR was significantly associated with LSM (odd ratios = 0.38, 95% confidence interval: 0.28-0.48, P < .001). Subgroup analysis suggested the relationship between CLR and LSM remained consistent, a significant interaction was noted between CLR and LSM accross different race groups. The restricted cubic spline model indicated a significant nonlinear relationship between CLR and LSM. In the adult population above 20 year old of National Health and Nutrition Examination Survey in U.S., lower CLR level was associated with higher prevalence of LSM above 12.5 kPa, which may be influenced by race. These findings indicate CLR as an independent protective factor for clinically significant liver fibrosis.
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