Section of Gastroenterology, Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts.
Clin Gastroenterol Hepatol. 2019 May;17(6):1157-1164.e4. doi: 10.1016/j.cgh.2018.11.037. Epub 2018 Nov 23.
BACKGROUND & AIMS: Nonalcoholic fatty liver disease is an inflammatory condition that results in progressive liver disease. It is unknown if individuals with hepatic steatosis, but not known to have liver disease, have higher serum concentrations of markers of systemic inflammation and oxidative stress.
We collected data from 2482 participants from the Framingham Heart Study (mean age, 51 ± 11 y; 51% women) who underwent computed tomography and measurement of 14 serum markers of systemic inflammation. Heavy alcohol users were excluded. The liver:phantom ratio (a continuous parameter of liver attenuation relative to a calibration phantom) was used to identify individuals with radiographic evidence of liver fat. Primary covariates included age, sex, smoking, alcohol, aspirin use, hypertension, dyslipidemia, diabetes, and cardiovascular disease. Body mass index and visceral fat were secondary covariates. We used multivariable linear regression models to assess the association between liver fat and systemic inflammatory markers.
In multivariable-adjusted models, liver fat was associated with the following inflammatory markers: high-sensitivity C-reactive protein (P < .001), urinary isoprostanes (P < .001), interleukin 6 (P < .001), intercellular adhesion molecule 1 (P < .001), and P-selectin (P = .002). Additional adjustment for body mass index or visceral fat attenuated the results slightly, although all associations remained statistically significant (P for all ≤ .01).
In a community-based cohort, individuals with hepatic steatosis without known liver disease had higher mean serum concentrations of systemic markers of inflammation. Studies are needed to determine whether treatment of hepatic steatosis reduces systemic inflammation.
非酒精性脂肪性肝病是一种炎症性疾病，可导致进行性肝病。目前尚不清楚是否存在肝脂肪变性但无已知肝病的个体，其血清系统炎症和氧化应激标志物浓度是否更高。
我们从接受计算机断层扫描和 14 种血清系统炎症标志物测量的弗雷明汉心脏研究（平均年龄 51 ± 11 岁，51%为女性）的 2482 名参与者中收集数据。排除大量饮酒者。肝脏：幻影比（肝脏衰减相对于校准幻影的连续参数）用于识别具有放射学证据的肝脂肪的个体。主要协变量包括年龄、性别、吸烟、饮酒、阿司匹林使用、高血压、血脂异常、糖尿病和心血管疾病。体重指数和内脏脂肪为次要协变量。我们使用多变量线性回归模型来评估肝脂肪与全身炎症标志物之间的关系。
在多变量调整模型中，肝脂肪与以下炎症标志物相关：高敏 C 反应蛋白（P <.001）、尿异前列烷（P <.001）、白细胞介素 6（P <.001）、细胞间黏附分子 1（P <.001）和 P-选择素（P =.002）。进一步调整体重指数或内脏脂肪可略微减弱结果，但所有关联仍具有统计学意义（所有 P 值均≤.01）。
在基于社区的队列中，无已知肝病的肝脂肪变性个体的血清全身炎症标志物平均浓度较高。需要研究是否治疗肝脂肪变性可以降低全身炎症。
