实用肝脏病杂志 ›› 2025, Vol. 28 ›› Issue (1): 48-51.doi: 10.3969/j.issn.1672-5069.2025.01.013

• 非酒精性脂肪性肝病 • 上一篇    下一篇

代谢相关脂肪性肝病患者SAF评分和脂肪肝进展抑制算法应用研究*

黄嘉伟, 纪雅丽, 周玲, 陈金军   

  1. 510515 广州市 南方医科大学附属南方医院肝病中心/广东省肝脏疾病研究所
  • 收稿日期:2024-04-28 出版日期:2025-01-10 发布日期:2025-02-07
  • 通讯作者: 陈金军,E-mail:chjj@smu.edu.cn
  • 作者简介:黄嘉伟,男,27岁,八年制博士生。E-mail:1015561279@qq.com
  • 基金资助:
    *国家自然科学基金资助项目(编号:82070650/82000544);国家科技重大专项资助项目(编号:2018ZX10723203)

SAF score and fatty liver inhibition of progression algorithm in evaluation of liver fibrosis in patients with metabolic associated fatty liver disease

Huang Jiawei, Ji Yali, Zhou Ling, et al   

  1. Center for Liver Disease Study, Nanfang Hospital, Southern Medical University, Guangzhou 510515, Guangdong Province, China
  • Received:2024-04-28 Online:2025-01-10 Published:2025-02-07

摘要: 目的 探索基于脂肪变性(S)、炎症活动度(A)和纤维化程度(F)建立的SAF评分和脂肪肝进展抑制(FLIP)算法评估代谢相关脂肪性肝病(MAFLD)患者肝纤维化的价值。方法 2020年8月~2021年3月南方医科大学南方医院诊治的MAFLD患者113例,均接受肝活检,使用FibroScan行肝硬度测定(LSM)和受控衰减指数(CAP)。根据Baveno VII共识诊断代偿期进展性慢性肝病(cACLD)。结果 在113例MAFLD患者中,经肝组织病理学检查诊断纤维化F0~F2(非cACLD)患者91例和F3~F4(cACLD)患者22例;cACLD组在合并2型糖尿病、病因和酒精摄入量方面与非cACLD组存在显著性差异(P<0.05);cACLD组CAP和LSM分别为247.5(230.0~301.5) dB/m和(22.0±16.2)kPa,与非cACLD组[分别为299.0(260.2~325.2)dB/m和(9.6±4.4)kPa]比,差异显著(P<0.05);cACLD组血小板计数、血清胆红素、尿酸和LDL-C水平与非cACLD组存在显著性差异(P<0.05);cACLD组SAF评分为(8.4±1.1),显著高于非cACLD组组[(5.7±1.8),P<0.05];FLIP 算法评估发现cACLD组非酒精性脂肪性肝炎(NASH)占比为86.4%,无脂肪性肝病为13.6%,而在非cACLD组发现NASH占比为40.7%,单纯性脂肪肝为53.8%,无脂肪性肝病为5.5%。结论 MAFLD诊断不强调病因单一,SAF评分可以帮助诊断cACLD,而FLIP算法可以快速确定NASH的存在。

关键词: 代谢相关脂肪性肝病, 脂肪变性-炎症活动度-纤维化评分, 脂肪肝进展抑制算法, 代偿期进展期慢性肝病, 诊断

Abstract: Objective This study was conducted to investigate steatosis-activity-fibrosis-based SAF score and fatty liver inhibition of progression (FLIP) algorithm in evaluation of liver fibrosis in patients with metabolic associated fatty liver disease (MAFLD). Methods This study recruited 113 individuals with MAFLD in our hospital between August 2020 and March 2021, and all underwent liver biopsies. Liver stiffness measurement (LSM) and controlled attenuation parameter (CAP) were detected by FibroScan. Compensated progressive chronic liver disease (cACLD) was determined by Baveno VII consensus. Results Of 113 patients with MAFLD, liver histo-pathological examination showed F0-F2 liver fibrosis (non-cACLD) in 91 cases and F3-F4(cACLD) in 22 cases; there were significant differences as respect to percentages of concomitant type 2 diabetes, etiologies and alcohol intake between patients with and without cACLD (P<0.05); CAP and LSM in patients with cACLD were 247.5(230.0-301.5) dB/m and (22.0±16.2)kPa, much different as compared to [299.0(260.2-325.2)dB/m and (9.6±4.4)kPa] in non-cACLD (P<0.05); platelet count, total serum bilirubin, uric acid and LDL-C levels in cACLD were all significantly different compared to in non-cACLD (P<0.05); SAF score in cACLD was(8.4±1.1), much higher than [(5.7±1.8), P<0.05] in non-cACLD; FLIP algorithm found nonalcoholic steatohepatitis (NASH) accounted for 86.4% and no fatty liver disease for 13.6% in cACLD, while found NASH for 40.7%, nonalcoholic simple fatty liver for 53.8% and no fatty liver disease for 5.5% in non-cACLD. Conclusion MAFLD could include multiple etiologies, SAF score could diagnose cACLD and FLIP algorithm could help screen existence of NASH, which warrants further clinical investigation.

Key words: Metabolic associated fatty liver disease, SAF score, Fatty liver inhibition of progression, Compensated advanced chronic liver disease, Diagnosis