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      Systematic review: the diagnosis and staging of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis

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          Abstract

          Background

          Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent cause of liver disease in Western countries. The development of non-alcoholic steatohepatitis (NASH) and fibrosis identifies an at-risk group with increased risk of cardiovascular and liver-related deaths. The identification and management of this at-risk group remains a clinical challenge.

          Aim

          To perform a systematic review of the established and emerging strategies for the diagnosis and staging of NAFLD.

          Methods

          Relevant research and review articles were identified by searching PubMed, MEDLINE and EMBASE.

          Results

          There has been a substantial development of non-invasive risk scores, biomarker panels and radiological modalities to identify at-risk patients with NAFLD without recourse to liver biopsy on a routine basis. These modalities and algorithms have improved significantly in their diagnosis and staging of fibrosis and NASH in patients with NAFLD, and will likely impact on the number of patients undergoing liver biopsy.

          Conclusions

          Staging for NAFLD can now be performed by a combination of radiological and laboratory techniques, greatly reducing the requirement for invasive liver biopsy.

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          Most cited references113

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          Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease

          Stefano Romeo, Julia Kozlitina, Chao Xing … (2008)
          Nonalcoholic fatty liver disease (NAFLD) is a burgeoning health problem of unknown etiology that varies in prevalence among ethnic groups. To identify genetic variants contributing to differences in hepatic fat content, we performed a genome-wide association scan of nonsynonymous sequence variations (n=9,229) in a multiethnic population. An allele in PNPLA3 (rs738409; I148M) was strongly associated with increased hepatic fat levels (P=5.9×10−10) and with hepatic inflammation (P=3.7×10−4). The allele was most common in Hispanics, the group most susceptible to NAFLD; hepatic fat content was > 2-fold higher in PNPLA3-148M homozygotes than in noncarriers. Resequencing revealed another allele associated with lower hepatic fat content in African-Americans, the group at lowest risk of NAFLD. Thus, variation in PNPLA3 contributes to ethnic and inter-individual differences in hepatic fat content and susceptibility to NAFLD.
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            Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease.

            J. Ludwig, T Viggiano, D McGill … (1980)
            Nonalcoholic steatohepatitis is a poorly understood and hitherto unnamed liver disease that histologically mimics alcoholic hepatitis and that also may progress to cirrhosis. Described here are findings in 20 patients with nonalcoholic steatohepatitis of unknown cause. The biopsy specimens were characterized by the presence of striking fatty changes with evidence of lobular hepatitis, focal necroses with mixed inflammatory infiltrates, and, in most instances, Mallory bodies; Evidence of fibrosis was found in most specimens, and cirrhosis was diagnosed in biopsy tissue from three patients. The disease was more common in women. Most patients were moderately obese, and many had obesity-associated diseases, such as diabetes mellitus and cholelithiasis. Presence of hepatomegaly and mild abnormalities of liver function were common clinical findings. Currently, we know of no effective therapy.
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              Independent predictors of liver fibrosis in patients with nonalcoholic steatohepatitis.

              P Angulo, J Keach, K P Batts … (1999)
              Nonalcoholic steatohepatitis (NASH) may present with increased hepatic fibrosis progressing to end-stage liver disease. No factors that determine increasing fibrosis and histologically advanced disease have been recognized, thus, liver biopsy is recommended in all patients for diagnosis and prognosis. Our aim was to identify independent predictors of severe hepatic fibrosis in patients with NASH. One hundred and forty-four patients were studied. All patients underwent liver biopsy. Clinical and biochemical variables were examined with univariate and multivariate analysis. Thirty-seven (26%) patients had no abnormal fibrosis, 53 (37%) had mild fibrosis, 15 (10%) had moderate fibrosis, 14 (10%) had bridging fibrosis, and 25 (17%) had cirrhosis. In multivariate analysis, older age (P =. 001), obesity (P =.002), diabetes mellitus (P =.009), and aspartate transaminase/alanine transaminase (AST/ALT) ratio greater than 1 (P =.03) were significant predictors of severe liver fibrosis (bridging/cirrhosis). Body mass index (P =.003) was the only independent predictor of the degree of fat infiltration. Increased transferrin saturation correlated positively with the severity of fibrosis (P =.02) in univariate analysis, and there was a trend for more female patients among those with more advanced fibrosis (P =. 09). However, iron studies or gender were not significant when controlled for age, obesity, diabetes, and AST/ALT ratio. In conclusion, older age, obesity, and presence of diabetes mellitus help identify those NASH patients who might have severe liver fibrosis. This is the subgroup of patients with NASH who would be expected to derive the most benefit from having a liver biopsy and considering investigational therapies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Aliment Pharmacol Ther
                Journal ID (publisher-id): apt
                Title: Alimentary Pharmacology & Therapeutics
                Publisher: Blackwell Publishing Ltd
                ISSN (Print): 0269-2813
                ISSN (Electronic): 1365-2036
                Publication date (Print): March 2011
                Publication date (Electronic): 29 December 2010
                Volume: 33
                Issue: 5
                Pages: 525-540
                Affiliations
                [* ]simpleCentre for Liver Research, 5th floor, Institute of Biomedical Research, University of Birmingham Edgbaston, Birmingham B15 2TT, UK
                [† ]simpleThe Liver Unit, Queen Elizabeth Hospital Birmingham Edgbaston, Birmingham B15 2TH, UK
                [‡ ]simpleCentre for Endocrinology, Diabetes and Metabolism, University of Birmingham Edgbaston, Birmingham B15 2TT, UK
                Author notes
                Dr J. K. Dowman, Centre for Liver Research, 5th floor, Institute of Biomedical Research, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. E-mail: j.k.dowman@ 123456bham.ac.uk

                This uncommissioned systematic review was subject to full peer-review.

                Re-use of this article is permitted in accordance with the Terms and Conditions set out at http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms

                Article
                DOI: 10.1111/j.1365-2036.2010.04556.x
                PMC ID: 3080668
                PubMed ID: 21198708
                SO-VID: bb4eea20-95a7-4669-9797-bf0d4c54f2a3
                Copyright © Copyright © 2011 Blackwell Publishing Ltd
                License:

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

                History
                Date received : 07 September 2010
                Date revision received : 27 September 2010
                Date revision received : 02 December 2010
                Date accepted : 06 December 2010
                Categories
                Subject: Systematic Review

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

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