期刊文献+

Hepatocellular carcinoma in patients with metabolic dysfunctionassociated fatty liver disease: Can we stratify at-risk populations? 被引量:2

下载PDF
导出
摘要 Metabolic dysfunction-associated fatty liver disease(MAFLD)is a new nomenclature recently proposed by a panel of international experts so that the entity is defined based on positive criteria and linked to pathogenesis,replacing the traditional non-alcoholic fatty liver disease(NAFLD),a definition based on exclusion criteria.NAFLD/MAFLD is currently the most common form of chronic liver disease worldwide and is a growing risk factor for development of hepatocellular carcinoma(HCC).It is estimated than 25%of the global population have NAFLD and is projected to increase in the next years.Major Scientific Societies agree that surveillance for HCC should be indicated in patients with NAFLD/MAFLD and cirrhosis but differ in non-cirrhotic patients(including those with advanced fibrosis).Several studies have shown that the annual incidence rate of HCC in NAFLD-cirrhosis is greater than 1%,thus surveillance for HCC is costeffective.Risk factors that increase HCC incidence in these patients are male gender,older age,presence of diabetes and any degree of alcohol consumption.In non-cirrhotic patients,the incidence of HCC is much lower and variable,being a great challenge to stratify the risk of HCC in this group.Furthermore,large epidemiological studies based on the general population have shown that diabetes and obesity significantly increase risk of HCC.Some genetic variants may also play a role modifying the HCC occurrence among patients with NAFLD.The purpose of this review is to discuss the epidemiology,clinical and genetic risk factors that may influence the risk of HCC in NAFLD/MAFLD patients and propose screening strategy to translate into better patient care.
出处 《World Journal of Hepatology》 2022年第2期354-371,共18页 世界肝病学杂志(英文版)(电子版)
  • 相关文献

参考文献3

二级参考文献25

  • 1[1]Kodali VP,Gordon SC,Silverman AL,McCray DG.Cryptogenic liver disease in the United States:further evidence for non-A,non-B,and non-C hepatitis.Am J Gastroenterol 1994; 89:1836-1839
  • 2[2]Greeve M,Ferrell L,Kim M,Combs C,Roberts J,Ascher N,Wright TL.Cirrhosis of undefined pathogenesis:absence of evidence for unknown viruses or autoimmune processes.Hepatology 1993; 17:593-598
  • 3[3]Ayata G,Gordon FD,Lewis WD,Pomfret E,Pomposelli JJ,Jenkins RL,Khettry U.Cryptogenic cirrhosis:clinicopathologic findings at and after liver transplantation.Hum Pathol 2002; 33:1098-1104
  • 4[4]Uchida T,Shimojima M,Gotoh K,Shikata T,Tanaka E,Kiyosawa K."Silent" hepatitis B virus mutants are responsible for non-A,non-B,non-C,non-D,non-E hepatitis.Microbiol Immunol 1994; 38:281-285
  • 5[5]Del Gaudio A,Boschi L,Del Gaudio GA,Mastrangelo L,Munari D.Liver damage in obese patients.Obes Surg 2002; 12:802-804
  • 6[6]Ratziu V,Giral P,Charlotte F,Bruckert E,Thibault V,Theodorou I,Khalil L,Turpin G,Opolon P,Poynard T.Liver fibrosis in overweight patients.Gastroenterology 2000; 118:1117-1123
  • 7[7]Fassio E,Alvarez E,Dominguez N,Landeira G,Longo C.Natural history of nonalcoholic steatohepatitis:a longitudinal study of repeat liver biopsies.Hepatology 2004; 40:820-826
  • 8[8]Caldwell SH,Oelsner DH,Iezzoni JC,Hespenheide EE,Battle EH,Driscoll CJ.Cryptogenic cirrhosis:clinical characterization and risk factors for underlying disease.Hepatology 1999; 29:664-669
  • 9[9]Poonawala A,Nair SP,Thuluvath PJ.Prevalence of obesity and diabetes in patients with cryptogenic cirrhosis:a casecontrol study.Hepatology 2000; 32:689-692
  • 10[10]Ratziu V,Bonyhay L,Di Martino V,Charlotte F,Cavallaro L,Sayegh-Tainturier MH,Giral P,Grimaldi A,Opolon P,Poynard T.Survival,liver failure,and hepatocellular carcinoma in obesity-related cryptogenic cirrhosis.Hepatology 2002; 35:1485-1493

共引文献9

同被引文献5

引证文献2

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部