Systematic review of risk factors for fibrosis progression in non-alcoholic steatohepatitis

Argo, Curtis K.; Northup, Patrick G.; Al‐Osaimi, Abdullah; Caldwell, Stephen H.

doi:10.1016/j.jhep.2009.03.019

Cited by 494 publications

(416 citation statements)

References 88 publications

(114 reference statements)

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“…In that group, 37% showed progressive fibrosis. 76 It is important to mention, however, that in two other studies, 18% of patients showed a drop in their fibrosis score on a mean follow-up of 5.7 years and in another, 29% of patients had regression of fibrosis on a mean follow-up of 3.2 years. 22,77 Despite a lower risk of progression than alcohol-induced liver disease, NASH must be considered a risk factor for cirrhosis and increased liverrelated mortality.…”

Section: Cirrhosis and Liver-related Mortalitymentioning

confidence: 83%

Epidemiology and Natural History of Non-alcoholic Fatty Liver Disease

Mishra¹,

Younossi²

2012

Journal of Clinical and Experimental Hepatology

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Non-alcoholic fatty liver disease (NAFLD) is an important cause of liver disease burden across the world. By definition, although the histopathologic features of NAFLD are identical to that of alcoholic liver disease, its diagnosis requires absence of significant alcohol use and absence of other causes of chronic liver disease. We now know that NAFLD is not simply a disease of the Western world. It is manifested across the world, in varying rates, across gender, across varying ethnicities, and in its association with other host factors. In this review article, the definition of NAFLD, its spectrum, ranging from mild steatosis to hepatocellular injury and inflammation defined as non-alcoholic steatohepatitis (NASH) is discussed. Mild steatosis is generally a stable disease whereas NASH can be progressive. Based on current published literature, current incidence and prevalence of NAFLD and NASH are discussed. It is also accepted that these processes will continue to increase in prevalence with the rise of obesity, type II diabetes, and associated metabolic syndrome. Some of the risk factors have been well-established and are discussed. In addition, this review also presents emerging associations with other risk factors for NAFLD. Natural history of NAFLD is variable depending upon the histologic subtypes and other underlying comorbidities and is discussed in this review as well. (J CLIN EXP HEPATOL 2012;2:135-144)

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Section: Cirrhosis and Liver-related Mortalitymentioning

confidence: 83%

Epidemiology and Natural History of Non-alcoholic Fatty Liver Disease

Mishra¹,

Younossi²

2012

Journal of Clinical and Experimental Hepatology

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“…This may have several explanations: the slower progression rate (0.1-0.2 stages per year) of fibrosis [127] may require larger and longer RCTs to show fibrosis regression, and the encouraging results of TZDs on fibrosis progression are consistent with this view; alternatively, hepatic fibrogenesis may involve different molecular mechanisms from those involved in dysmetabolism, steatosis and inflammation. Within this context, antifibrotic agents targeting directly hepatic stellate cell activation and collagen deposition/remodelling, including toll-like receptor-4, tissue inhibitors of metalloproteinases (TIMPs) and FXR, are under development and phase III RCTs are eagerly awaited [128].…”

Section: Implications For Future Researchmentioning

confidence: 99%

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

et al. 2012

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Aims/hypothesis Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH): NAFLD causes an increased risk of cardiovascular disease, diabetes and liverrelated complications (the latter confined to NASH). The effect of proposed treatments on liver disease, glucose metabolism and cardiovascular risk in NAFLD is unknown. We reviewed the evidence for the management of liver disease and cardiometabolic risk in NAFLD. Methods Publications through November 2011 were systematically reviewed by two authors. Outcomes evaluated though standard methods were: histological/radiological/biochemical features of NAFLD, variables of glucose metabolism and cardiovascular risk factors. Seventy-eight randomised trials were included (38 in NASH, 40 in NAFLD): 41% assessed post-treatment histology, 71% assessed glucose metabolism and 88% assessed cardiovascular risk factors. Lifestyle intervention, thiazolidinediones, metformin and antioxidants were most extensively evaluated. Results Lifestyle-induced weight loss was safe and improved cardio-metabolic risk profile; a weight loss ≥7% improved histological disease activity, but was achieved by <50%

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“…A current systematic review of ten studies has examined risk factors for progression from NASH to advanced fibrosis (63) . Using multivariate analysis the review has found that only age and the presence of inflammation on initial biopsy are independent predictors of progression in 221 patients over a 5 .…”

Section: Proceedings Of the Nutrition Societymentioning

confidence: 99%

Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome

2010

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Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease in both adults and children worldwide. As a disease spectrum, NAFLD may progress from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. An estimated 20-35% of the general population has steatosis, 10 % of whom will develop the more progressive non-alcoholic steatohepatitis associated with markedly increased risk of cardiovascular-and liver-related mortality. Development of NAFLD is strongly linked to components of the metabolic syndrome including obesity, insulin resistance, dyslipidaemia and type 2 diabetes. The recognition that NAFLD is an independent risk factor for CVD is a major public health concern. There is a great need for a sensitive non-invasive test for the early detection and assessment of the stage of NAFLD that could also be used to monitor response to treatment. The cellular and molecular aetiology of NAFLD is multi-factorial; genetic polymorphisms influencing NAFLD have been identified and nutrition is a modifiable environmental factor influencing NAFLD progression. Weight loss through diet and exercise is the primary recommendation in the clinical management of NAFLD. The application of systems biology to the identification of NAFLD biomarkers and factors involved in NAFLD progression is an area of promising research.

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Systematic review of risk factors for fibrosis progression in non-alcoholic steatohepatitis

Cited by 494 publications

References 88 publications

Epidemiology and Natural History of Non-alcoholic Fatty Liver Disease

Epidemiology and Natural History of Non-alcoholic Fatty Liver Disease

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

Non-alcoholic fatty liver disease: the hepatic consequence of obesity and the metabolic syndrome

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