Noninvasive investigations for non alcoholic fatty liver disease and liver fibrosis

被引:55
作者
Fierbinteanu-Braticevici, Carmen [1 ]
Dina, Ion [2 ]
Petrisor, Ana [1 ]
Tribus, Laura [1 ]
Negreanu, Lucian [1 ]
Cirstoiu, Catalin [1 ]
机构
[1] Univ Hosp Bucharest, Med Clin 2, Bucharest 7001, Romania
[2] St Johns Hosp, Dept Gastroenterol, Bucharest 7001, Romania
关键词
Non-alcoholic fatty liver disease; Biomarkers; Necroinflammation; Liver fibrosis; POLYPEPTIDE SPECIFIC ANTIGEN; BODY-MASS INDEX; NONALCOHOLIC STEATOHEPATITIS; HEPATIC STEATOSIS; SERUM CONCENTRATIONS; INSULIN-RESISTANCE; NATURAL-HISTORY; DIAGNOSIS; SEVERITY; PENTOXIFYLLINE;
D O I
10.3748/wjg.v16.i38.4784
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Non-alcoholic fatty liver disease (NAFLD) includes a spectrum of diseases that have insulin resistance in common and are associated with metabolic conditions such as obesity, type 2 diabetes mellitus, and dyslipidemia. NAFLD ranges from simple liver steatosis, which follows a benign course, to nonalcoholic steatohepatitis (NASH), a more severe entity, with necroinflammation and fibrosis, which can progress to cryptogenic cirrhosis and end-stage liver disease. Liver biopsy remains the gold standard for evaluating the degree of hepatic necroinflammation and fibrosis; however, several noninvasive investigations, such as serum biomarkers, have been developed to establish the diagnosis and also to evaluate treatment response. These markers are currently neither available in all centers nor validated in extensive studies. Examples include high-sensitivity C reactive protein and plasma pentraxin 3, which are associated with extensive liver fibrosis in NASH. Interleukin-6 correlates with inflammation, and cytokeratin-18 represents a marker of hepatocyte apoptosis (prominent in NASH and absent in simple steatosis). Tissue polypeptide specific antigen seems to have a clinical utility in the follow-up of obese patients with NASH. (C) 2010 Baishideng. All rights reserved.
引用
收藏
页码:4784 / 4791
页数:8
相关论文
共 73 条
[1]   A pilot trial of pentoxifylline in nonalcoholic steatohepatitis [J].
Adams, LA ;
Zein, CO ;
Angulo, P ;
Lindor, KD .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2004, 99 (12) :2365-2368
[2]  
Adams Leon A, 2007, Clin Liver Dis, V11, P25, DOI 10.1016/j.cld.2007.02.004
[3]   Independent predictors of liver fibrosis in patients with nonalcoholic steatohepatitis [J].
Angulo, P ;
Keach, JC ;
Batts, KP ;
Lindor, KD .
HEPATOLOGY, 1999, 30 (06) :1356-1362
[4]   NONALCOHOLIC STEATOHEPATITIS - AN EXPANDED CLINICAL ENTITY [J].
BACON, BR ;
FARAHVASH, MJ ;
JANNEY, CG ;
NEUSCHWANDERTETRI, BA .
GASTROENTEROLOGY, 1994, 107 (04) :1103-1109
[5]  
BARANOVA A, 2006, ADIPOSE TISSUE ADIPO, P291
[6]  
Braun M, 2005, HEPATOLOGY, V42, p752A
[7]   Prevalence of hepatic steatosis in an urban population in the United States: Impact of ethnicity [J].
Browning, JD ;
Szczepaniak, LS ;
Dobbins, R ;
Nuremberg, P ;
Horton, JD ;
Cohen, JC ;
Grundy, SM ;
Hobbs, HH .
HEPATOLOGY, 2004, 40 (06) :1387-1395
[8]   The spectrum expanded: cryptogenic cirrhosis and the natural history of non-alcoholic fatty liver disease [J].
Caldwell, SH ;
Crespo, DM .
JOURNAL OF HEPATOLOGY, 2004, 40 (04) :578-584
[9]  
Caldwell SH, 2001, AM J GASTROENTEROL, V96, P519
[10]   Cytokines in the pathogenesis of fatty liver and disease progression to steatohepatitis: Implications for treatment [J].
Carter-Kent, Christine ;
Zein, Nizar N. ;
Feldstein, Ariel E. .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2008, 103 (04) :1036-1042