PDF下载 ( 1685 KB)
代谢相关脂肪性肝病对颈动脉狭窄程度的影响
DOI: 10.3969/j.issn.1001-5256.2023.08.016
伦理学声明：本研究方案于2022年4月8日经由昆明医科大学第二附属医院伦理委员会审批，批号：审-PJ-科-2022-108，患者均签署知情同意书。
利益冲突声明：本文不存在任何利益冲突。
作者贡献声明：姜梓萌负责文章的构思设计，论文撰写与修订；陈宇航、张志娇负责数据的获取及分析处理过程；郑梦瑶、李未华负责研究思路的设计；黄华、赵公芳参与修改文章的关键内容。
Influence of metabolic associated fatty liver disease on the degree of carotid stenosis
-
摘要:
目的 探讨分析代谢相关脂肪性肝病(MAFLD)对颈动脉狭窄的影响。 方法 随机纳入2014年1月1日—2020年6月30日在昆明医科大学第二附属医院消化内科住院期间同时行腹部超声、颈部血管超声的834例患者，收集基线资料、临床诊断，根据病史、临床检验及影像学指标分为MAFLD组(n=469)和非MAFLD组(n=365)。颈动脉按照狭窄程度分为：正常血管、狭窄＜50%，狭窄≥50%。符合正态分布的计量资料两组间比较采用成组t检验，不符合正态分布的计量资料两组间比较采用Mann-Whitney U秩和检验；计数资料两组间比较采用χ2检验。采用单因素和多因素Logistic回归分析颈动脉狭窄的影响因素。 结果 MAFLD组患者颈动脉狭窄≥50%的比例高于非MAFLD患者，差异有统计学意义(10.66% vs 5.21%，χ2=8.050，P=0.005)。单因素Logistic回归分析结果显示，男性患者、吸烟、MAFLD、BMI、TC、HDL、服用降脂药、收缩压、高血压或服药、2型糖尿病、胰岛素抵抗，AST在两组间差异有统计学意义(P值均＜0.05)。校正了性别、吸烟、HDL、BMI、高血压病史或服药、2型糖尿病、AST后，多因素Logistic回归分析结果显示MAFLD是颈动脉狭窄≥50%的危险因素(OR=1.979，95%CI：1.055~3.713，P=0.033)。 结论 MAFLD是颈动脉狭窄≥50%形成的独立危险因素。 Abstract:Objective To investigate the influence of metabolic associated fatty liver disease (MAFLD) on carotid stenosis. Methods This study was conducted among the patients who underwent abdominal ultrasound and cervical vascular ultrasound at the same time during hospitalization in Department of Gastroenterology, The Second Affiliated Hospital of Kunming Medical University, from January 1, 2014 to June 30, 2020, and baseline data and clinical diagnosis were collected. According to medical history, clinical tests, and imaging indicators, they were divided into MAFLD group with 469 patients and non-MAFLD group with 365 patients. Carotid artery were assessed as normal carotid artery, carotid stenosis < 50%, and carotid stenosis ≥50% according to the degree of stenosis. The independent-samples t test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U rank sum test was used for comparison of non-normally distributed quantitative data between two groups; the chi-square test was used for comparison of qualitative data between two groups. The univariate and multivariate logistic regression analyses were used to investigate the influencing factors carotid stenosis. Results Compared with the non-MAFLD group, the MAFLD group had a significantly higher proportion of patients with carotid stenosis ≥50% (10.66% vs 5.21%, χ2=8.050, P=0.005). The univariate logistic regression analysis showed that there were significant differences between the two groups in the proportion of male patients, smoking, MAFLD, body mass index (BMI), total cholesterol, high-density lipoprotein (HDL), administration of lipid-lowering drugs, systolic pressure, hypertension or medication, type 2 diabetes, insulin resistance, and aspartate aminotransferase (AST). After adjustment for sex, smoking, HDL, BMI, history of hypertension or medication, type 2 diabetes, and AST, the multivariate logistic regression analysis showed that MAFLD was a risk factor for carotid stenosis (≥50%) (odds ratio=1.979, 95% confidence interval: 1.055-3.713, P=0.033). Conclusion MAFLD is an independent risk factor for carotid stenosis (≥50%). -
Key words:
- Metabolic Fatty Liver Disease /
- Atherosclerosis /
- Carotid Stenosis /
- Risk Factors
-
表 1 非MAFLD组与MAFLD组一般资料比较
Table 1. Comparison of general data between non-MAFLD group and MAFLD group
指标 非MAFLD组
(n=365)MAFLD组
(n=469)统计值 P值 年龄(岁) 67.76±10.21 63.08±10.95 t=6.304 ＜0.001 男性[例(%)] 231(63.29) 214(45.63) χ2=25.718 ＜0.001 吸烟[例(%)] χ2=4.102 0.043 是 161(44.11) 240(51.17) 否 204(55.89) 229(48.83) 服用降脂药[例(%)] χ2=6.439 ＜0.001 是 257(70.41) 386(82.30) 否 108(29.59) 83(17.70) 高血压病史或服药史[例(%)] χ2=11.275 0.001 是 277(75.89) 399(85.07) 否 88(24.11) 70(14.93) 2型糖尿病[例(%)] χ2=66.387 ＜0.001 是 151(41.37) 326(69.51) 否 214(58.63) 143(30.49) 糖尿病前期[例(%)] χ2=6.045 0.014 是 30(8.22) 64(13.65) 否 335(91.78) 405(86.35) 胰岛素抵抗[例(%)] χ2=99.086 ＜0.001 是 59(16.16) 231(49.25) 否 306(83.84) 238(50.75) 身高(m) 1.63 ±0.08 1.64 ±0.08 t=-0.565 0.572 体质量(kg) 61.54±10.54 68.60±10.94 t=-9.398 ＜0.001 BMI(kg/m2) 22.98 ±2.97 25.55 ±3.19 t=-11.909 ＜0.001 收缩压(mmHg) 134.57±21.53 138.18±21.17 t=-2.423 0.016 舒张压(mmHg) 77.38±13.31 81.08±12.70 t=-4.007 ＜0.001 TC(mmol/L) 1.29(0.96~1.78) 1.89(1.43~2.72) Z=-10.730 ＜0.001 HDL(mmol/L) 1.07(0.86~1.27) 1.00(0.86~1.19) Z=-2.369 0.018 ALT(U/L) 18.00(13.00~26.00) 22.00(17.00~34.00) Z=-6.204 ＜0.001 AST(U/L) 23.00(18.00~28.00) 25.00 (19.00~32.00) Z=-3.255 0.001 
下载: 导出CSV
表 2 非MAFLD组与MAFLD组颈动脉狭窄程度的比较
Table 2. Comparison of carotid stenosis between non-MAFLD group and MAFLD group
项目 非MAFLD组
(n=365)MAFLD组
(n=469)χ2值 P值 正常血管[例(%)] 34(9.32) 30(6.40) 2.468 0.116 颈动脉狭窄＜50%[例(%)] 312(85.48) 389(82.94) 0.986 0.321 颈动脉狭窄≥50% [例(%)] 19(5.21) 50(10.66) 8.050 0.005
下载: 导出CSV
表 3 单因素Logistic回归分析
Table 3. Univariate Logistic regression analysis
指标 OR(95%CI) P值 男性(否=0，是=1) 1.568(1.151~2.137) 0.004 吸烟(否=0，是=1) 3.646(2.071~6.420) ＜0.001 MAFLD(否=0，是=1) 2.173 (1.257~3.755) 0.005 BMI 1.590(1.143~2.211) 0.006 TC 1.652(1.178~2.318) 0.004 HDL 1.560(1.119~2.175) 0.009 服用降脂药(否=0，是=1) 1.590(1.130~2.238) 0.008 收缩压 1.014(1.003~1.025) 0.013 舒张压 1.010(0.992~1.029) 0.274 高血压史或服药史(否=0，是=1) 2.604(1.106~6.128) 0.028 2型糖尿病(否=0，是=1) 1.619(1.159~2.260) 0.005 糖尿病前期(否=0，是=1) 1.035(0.479~2.233) 0.929 胰岛素抵抗(否=0，是=1) 1.931(1.177~3.169) 0.009 ALT 1.001(0.990~1.013) 0.858 AST 1.639 (1.149~2.338) 0.006
下载: 导出CSV
表 4 多因素Logistic回归分析
Table 4. Multifactorial Logistic regression analysis
项目 OR(95%CI) P值 Model 1 2.120(1.197~3.753) 0.010 Model 2 2.101(1.185~3.722) 0.011 Model 3 2.182(1.187~4.009) 0.012 Model 4 2.014(1.134~3.577) 0.017 Model 5 2.037(1.130~3.672) 0.018 Model 6 2.117(1.195~3.752) 0.010 Model 7 1.979(1.055~3.713) 0.033 注：Model 1，根据性别、吸烟进行调整后；Model 2，根据性别、吸烟、HDL进行调整后；Model 3，根据性别、吸烟、BMI进行调整后；Model 4，根据性别、吸烟、高血压或服药进行调整后；Model 5，根据性别、吸烟、2型糖尿病进行调整后；Model 6，根据性别、吸烟、AST进行调整后；Model 7，根据MAFLD、性别、吸烟、HDL、BMI、高血压或服药、2型糖尿病、AST进行调整后。
下载: 导出CSV
-
[1] ESLAM M, GEORGE J. Reply to: Correspondence on "A new definition for metabolic associated fatty liver disease: an international expert consensus statement": MAFLD: Moving from a concept to practice[J]. J Hepatol, 2020, 73(5): 1268-1269. DOI: 10.1016/j.jhep.2020.06.036. [2] LEI F, QIN JJ, SONG X, et al. The prevalence of MAFLD and its association with atrial fibrillation in a nationwide health check-up population in China[J]. Front Endocrinol (Lausanne), 2022, 13: 1007171. DOI: 10.3389/fendo.2022.1007171. [3] OZTURK K, UYGUN A, GULER AK, et al. Nonalcoholic fatty liver disease is an independent risk factor for atherosclerosis in young adult men[J]. Atherosclerosis, 2015, 240(2): 380-386. DOI: 10.1016/j.atherosclerosis.2015.04.009. [4] BENJAMIN EJ, VIRANI SS, CALLAWAY CW, et al. Heart disease and stroke statistics-2018 update: a report from the American Heart Association[J]. Circulation, 2018, 137(12): e67-e492. DOI: 10.1161/CIR.0000000000000558. [5] LOZANO R, NAGHAVI M, FOREMAN K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010[J]. Lancet, 2012, 380(9859): 2095-2128. DOI: 10.1016/S0140-6736(12)61728-0. [6] KOZAKOVA M, PALOMBO C, ENG MP, et al. Fatty liver index, gamma-glutamyltransferase, and early carotid plaques[J]. Hepatology, 2012, 55(5): 1406-1415. DOI: 10.1002/hep.25555. [7] JOHRI AM, NAMBI V, NAQVI TZ, et al. Recommendations for the assessment of carotid arterial plaque by ultrasound for the characterization of atherosclerosis and evaluation of cardiovascular risk: from the American Society of Echocardiography[J]. J Am Soc Echocardiogr, 2020, 33(8): 917-933. DOI: 10.1016/j.echo.2020.04.021. [8] YU C, WANG M, ZHENG S, et al. Comparing the diagnostic criteria of MAFLD and NAFLD in the Chinese population: a population-based prospective cohort study[J]. J Clin Transl Hepatol, 2022, 10(1): 6-16. DOI: 10.14218/JCTH.2021.00089. [9] SAKURAI Y, KUBOTA N, YAMAUCHI T, et al. Role of insulin resistance in MAFLD[J]. Int J Mol Sci, 2021, 22(8): 4156. DOI: 10.3390/ijms22084156. [10] DUAN Y, PAN X, LUO J, et al. Association of inflammatory cytokines with non-alcoholic fatty liver disease[J]. Front Immunol, 2022, 13: 880298. DOI: 10.3389/fimmu.2022.880298. [11] HUANG X, YAO Y, HOU X, et al. Macrophage SCAP contributes to metaflammation and lean NAFLD by activating STING-NF-κB signaling pathway[J]. Cell Mol Gastroenterol Hepatol, 2022, 14(1): 1-26. DOI: 10.1016/j.jcmgh.2022.03.006. [12] WU T, YE J, SHAO C, et al. Varied relationship of lipid and lipoprotein profiles to liver fat content in phenotypes of metabolic associated fatty liver disease[J]. Front Endocrinol (Lausanne), 2021, 12: 691556. DOI: 10.3389/fendo.2021.691556. [13] ARROYAVE-OSPINA JC, WU Z, GENG Y, et al. Role of oxidative stress in the pathogenesis of non-alcoholic fatty liver disease: implications for prevention and therapy[J]. Antioxidants (Basel), 2021, 10(2): 174. DOI: 10.3390/antiox10020174. [14] HERNANDEZ GV, SMITH VA, MELNYK M, et al. Dysregulated FXR-FGF19 signaling and choline metabolism are associated with gut dysbiosis and hyperplasia in a novel pig model of pediatric NASH[J]. Am J Physiol Gastrointest Liver Physiol, 2020, 318(3): G582-G609. DOI: 10.1152/ajpgi.00344.2019. [15] YANG B, LUO W, WANG M, et al. Macrophage-specific MyD88 deletion and pharmacological inhibition prevents liver damage in non-alcoholic fatty liver disease via reducing inflammatory response[J]. Biochim Biophys Acta Mol Basis Dis, 2022, 1868(10): 166480. DOI: 10.1016/j.bbadis.2022.166480. [16] HE Y, HWANG S, CAI Y, et al. MicroRNA-223 ameliorates nonalcoholic steatohepatitis and cancer by targeting multiple inflammatory and oncogenic genes in hepatocytes[J]. Hepatology, 2019, 70(4): 1150-1167. DOI: 10.1002/hep.30645. [17] YOU D, QIAO Q, ONO K, et al. miR-223-3p inhibits the progression of atherosclerosis via down-regulating the activation of MEK1/ERK1/2 in macrophages[J]. Aging (Albany NY), 2022, 14(4): 1865-1878. DOI: 10.18632/aging.203908. [18] ANSTEE QM, MANTOVANI A, TILG H, et al. Risk of cardiomyopathy and cardiac arrhythmias in patients with nonalcoholic fatty liver disease[J]. Nat Rev Gastroenterol Hepatol, 2018, 15(7): 425-439. DOI: 10.1038/s41575-018-0010-0. [19] GUO YC, ZHOU Y, GAO X, et al. Association between nonalcoholic fatty liver disease and carotid artery disease in a community-based Chinese population: a cross-sectional study[J]. Chin Med J (Engl), 2018, 131(19): 2269-2276. DOI: 10.4103/0366-6999.241797. [20] SINN DH, GWAK GY, CHO J, et al. Modest alcohol consumption and carotid plaques or carotid artery stenosis in men with non-alcoholic fatty liver disease[J]. Atherosclerosis, 2014, 234(2): 270-275. DOI: 10.1016/j.atherosclerosis.2014.03.001. [21] CHEN Z, YANG YG. Guidelines for the diagnosis and treatment of carotid stenosis[J/CD]. Chin J Vasc Surg(Electronic Version), 2017, 9(3): 169-175. DOI: 10.3760.cma.j.issn.2096-1863.2017.02.003 .陈忠, 杨耀国. 颈动脉狭窄诊治指南[J/CD]. 中国血管外科杂志(电子版), 2017, 9(3): 169-175. DOI:10.3760.cma.j.issn.2096-1863.2017.02.003 .[22] SINN DH, CHO SJ, GU S, et al. Persistent nonalcoholic fatty liver disease increases risk for carotid atherosclerosis[J]. Gastroenterology, 2016, 151(3): 481-488. e1. DOI: 10.1053/j.gastro.2016.06.001. [23] HAACKE C, ALTHAUS A, SPOTTKE A, et al. Long-term outcome after stroke: evaluating health-related quality of life using utility measurements[J]. Stroke, 2006, 37(1): 193-198. DOI: 10.1161/01.STR.0000196990.69412.fb. [24] PISTO P, SANTANIEMI M, BLOIGU R, et al. Fatty liver predicts the risk for cardiovascular events in middle-aged population: a population-based cohort study[J]. BMJ Open, 2014, 4(3): e004973. DOI: 10.1136/bmjopen-2014-004973. [25] Writing Group Members, LLOYD-JONES D, ADAMS RJ, et al. Heart disease and stroke statistics—2010 update: a report from the American Heart Association[J]. Circulation, 2010, 121(7): e46-e215. DOI: 10.1161/CIRCULATIONAHA.109.192667. [26] LAL BK, DUX MC, SIKDAR S, et al. Asymptomatic carotid stenosis is associated with cognitive impairment[J]. J Vasc Surg, 2017, 66(4): 1083-1092. DOI: 10.1016/j.jvs.2017.04.038. [27] AMBROSETTI M, PEDRETTI RF. Does metabolic syndrome predict silent carotid stenosis in coronary patients?[J]. Intern Emerg Med, 2008, 3(1): 81-82. DOI: 10.1007/s11739-008-0103-9. [28] REN Z, SIMONS P, WESSELIUS A, et al. Relationship between NAFLD and coronary artery disease: A Mendelian randomization study[J]. Hepatology, 2023, 77(1): 230-238. DOI: 10.1002/hep.32534. -
本文二维码
表(4)
计量
- 文章访问数: 210
- HTML全文浏览量: 55
- PDF下载量: 28
- 被引次数: 0
