肝脏 ›› 2024, Vol. 29 ›› Issue (3): 303-307.

• 代谢相关脂肪性肝病 • 上一篇    下一篇

肥胖和高尿酸血症对代谢相关脂肪性肝病脂肪变性和纤维化的影响

刘云霄, 王转国, 徐强, 窦婧, 王晓波, 郭燕, 郭峰, 王晓忠   

  1. 830000 乌鲁木齐 新疆医科大学第四临床医学院(刘云霄);新疆医科大学附属中医医院(王转国,窦婧,徐强,王晓波,郭燕,郭峰,王晓忠)
  • 收稿日期:2023-07-20 出版日期:2024-03-31 发布日期:2024-05-16
  • 通讯作者: 王晓忠, Email:wzx125@sina.com
  • 基金资助:
    2023年新疆医科大学研究生创新创业项目;乐德行全国名中医工作室;新疆维吾尔自治区自然科学基金(2022D01C173);国家自然科学基金(81760832)

The effect of obesity and hyperuricemia on liver steatosis and fibrosis in metabolic dysfunction-associated fatty liver disease

LIU Yun-xiao1, WANG Zhuan-guo2, XU Qiang2, DOU Jing2, WANG Xiao-bo2, GUO Yan2, GUO Feng2, WANG Xiao-zhong2   

  1. 1. Fourth Clinical Medical College of Xinjiang Medical University, Urumqi 830000, China;
    2. Traditional Chinese Medical Hospital Affiliated to Xinjiang Medical University, Urumqi 830000, China
  • Received:2023-07-20 Online:2024-03-31 Published:2024-05-16
  • Contact: WANG Xiao-zhong, Email:wzx125@sina.com

摘要: 目的 探索肥胖和高尿酸血症对代谢相关脂肪性肝病(MAFLD)脂肪变性和纤维化的影响。方法 纳入2020年1月至2022年12月在新疆医科大学附属中医医院诊断为MAFLD的患者402例,其中非肥胖无高尿酸血症组186例,非肥胖高尿酸血症组34例,肥胖无高尿酸血症组151例,肥胖高尿酸血症组31例,比较4组患者临床数据。基于瞬时弹性成像Fibrotouch结果,分析4组脂肪变性和肝纤维化程度的差异。利用二元logistic回归分析肥胖和高尿酸血症的交互作用对肝脂肪变性和纤维化的影响因素。结果 4组患者的年龄、性别、BMI、ALT、GGT、TG、Cr、UA、Alb、ALT/AST、D-D、FIB-4、BARD、LSM、CAP、饮酒史、吸烟史,差异有统计学意义(P<0.05)。分别根据脂肪衰减参数和肝脏硬度值进行各组脂肪变性分期和肝纤维化分期,差异有统计学意义(P<0.05)。肥胖无高尿酸血症组和肥胖高尿酸血症组发生中重度脂肪变性分别为81.5%(123/151)、83.9%(26/31),进展性肝纤维化分别为76.8%(116/151)、87.1%(27/31)明显高于其余两组。二元logistic回归发现,肥胖是引起所有MAFLD患者发生中重度脂肪变性、进展性肝纤维化的危险因素,且肥胖和高尿酸血症对中重度肝脂肪变性和进展性纤维化的患病率存在相乘相互作用(肥胖*高尿酸血症交互项OR>1)。结论 肥胖和高尿酸血症对MAFLD脂肪变性和纤维化的协同作用。

关键词: 肥胖, 高尿酸血症, 代谢相关脂肪性肝病, 脂肪变性, 肝纤维化

Abstract: Objective To investigate the influence of obesity and hyperuricemia on steatosis and fibrosis in metabolic dysfunction-associated fatty liver disease (MAFLD). Methods A total of MAFLD 510 patients treated at the Department of Hepatology of the Traditional Chinese Medical Hospital Affiliated to Xinjiang Medical University between January 2020 and December 2022 were included in this study. After application of strict the inclusion and exclusion criteria, 402 patients were ultimately selected for analysis. Patients were divided into four groups based on their body mass index (BMI) and hyperuricemia status: non-obese without hyperuricemia group, non-obese hyperuricemia group, obese without hyperuricemia group and obese hyperuricemia group. Clinical parameters were compared across these groups, and liver steatosis and fibrosis were assessed using transient elastography Fibrotouch. Binary Logistic regression was utilized to evaluate the potential interaction between obesity and hyperuricemia in relation to hepatic steatosis and fibrosis. Results Of the 402 patients included in the study, distribution was as follows; 186 patients in the non-obese without hyperuricemia group, 34 patients in the non-obese with hyperuricemia group, 151 patients in the obese without hyperuricemia group, and 31 patients in the obese with hyperuricemia group. Statistically differences were observed in various demographic and clinical parameters among the groups, including age, sex, BMI, ALT, GGT, TG, Cr, UA, Alb, ALT/AST, D-D, FIB-4, BARD, LSM, CAP, drinking and smoking history (P<0.05). Evalution of liver steatosis and liver fibrosis stage based on the fat attenuation parameters and liver stiffness values revealed statistically significant differences among the groups (P<0.05). The proportion of moderate and severe steatosis (81.5%,83.9%, respectively) and progressive hepatic fibrosis (76.8%,87.1%, respectively) was significantly higher in the obese group compared to the non-obese groups. Binary Logistic regression analysis indicated that obesity was a risk factor for moderate-severe steatosis and progressive fibrosis in MAFLD patients. Moreover, the interaction between obesity and hyperuricemia demonstrated a multiplicative effect on the the likelihood of moderate-severe steatosis and progressive fibrosis (Obesity * hyperuricemia interaction term OR>1). Conclusion The findings of this study suggest a synergistic relationship between obesity and hyperuricemia in driving liver steatosis and fibrosis progression in MAFLD patients.

Key words: Obesity, Hyperuricemia, Metabolic dysfunction-associated fatty liver disease, Steatosis, Fibrosis