Nonalcoholic Steatohepatitis: A Proposal for Grading and Staging The Histological Lesions

Brunt, Elizabeth M.; Janney, Christine G.; Bisceglie, Adrian M. Di; Neuschwander‐Tetri, Brent A.; Bacon, Bruce R.

doi:10.1111/j.1572-0241.1999.01377.x

Cited by 3,300 publications

(951 citation statements)

References 19 publications

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“…33 Two studies 25,26 used the chronic hepatitis C validated METAVIR classification system, 34 in which steatosis is considered mild if present in 1%-10% of the hepatocytes, moderate in 11%-30%, and severe when in more than 30%. Necroinflammation and fibrosis were graded or staged by METAVIR 20,21,23,25,26 or Ishak classifications.…”

Section: Resultsmentioning

confidence: 99%

Hepatic steatosis in patients coinfected with human immunodeficiency virus/hepatitis C virus: A meta-analysis of the risk factors

2010

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Hepatic steatosis (HS) is frequent in patients with hepatitis C virus (HCV) infection, occurring in 40%-80%, associating with metabolic and virus-related factors, namely, genotype 3 and viral load. Human immunodeficiency virus (HIV) infection and antiretroviral treatment seem to be risk factors for HS. Several studies addressed this issue in coinfected patients, with discrepant results. A meta-analysis was performed on the HS risk factors in coinfected patients. Eligible studies were identified through structured keywords including coinfection, HCV, HIV, and steatosis in relevant databases including PubMed. Pooled odds ratios (ORs) and confidence limits (CIs) were obtained with the random-effects model and the DerSimonian-Laird method. Twelve studies, including 1,989 coinfected patients, were selected. Twenty percent were infected with HCV genotype 3. The overall prevalence of HS was 50.8% (23%-72%). Four studies also included 1,540 HCV monoinfected patients, not showing an increased risk for HS in coinfected patients (OR 1.61, 95% CI 0.84-3.10, P 5 0.151). In coinfected patients, HS was associated with higher body mass index (OR 1.13, 95% CI 1.07-1.19, P < 0.001), diabetes mellitus (OR 2.32, 95% CI 1.32-4.07, P 5 0.003), elevated alanine aminotransferase levels (OR 1.28, 95% CI 1.02-1.61, P 5 0.035), necroinflammatory activity (OR 1.72, 95% CI 1.11-2.67, P 5 0.016), and fibrosis (OR 1.67, 95% CI 1.20-2.34, P 5 0.003). No associations were found between HS and gender, other metabolic factors (dyslipidemia, glucose, metabolic syndrome), HCV-related factors (genotype, viral load), or HIV-related factors (viral load, CD4 count, antiretroviral therapy, and class of medication). Conclusion: In coinfected patients, HS does not seem to be more frequent than in HCV monoinfected patients and is mostly associated with metabolic factors, such as increased weight, diabetes mellitus, and more severe liver disease. The fact that no associations with HCV factors were found may be due to the small percentage of genotype 3-infected patients. (HEPATOLOGY 2010;52:71-78)

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Section: Resultsmentioning

confidence: 99%

Hepatic steatosis in patients coinfected with human immunodeficiency virus/hepatitis C virus: A meta-analysis of the risk factors

2010

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“…[19] Steatosis was defined and graded according to Brunt and colleagues. [20] Liver sections were stained with Hematoxylin and Eosin (H and E) and with special stains, namely reticulin (for reticular fibers) and periodic acid-Schiff (PAS) (for glycogenated nuclei) before being examined.…”

Section: Methodsmentioning

confidence: 99%

Insulin resistance, steatosis, and fibrosis in Egyptian patients with chronic Hepatitis C virus infection

Ahmed

Hassan

Abd‐Elsayed

et al. 2011

Saudi J Gastroenterol

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Background/Aim:Both nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C virus (HCV) infection are common in Egypt, and their coexistence is expected. There is controversy regarding the influence of NAFLD on chronic HCV disease progression. This study evaluates the effect of NAFLD on the severity of chronic hepatitis C (CHC) (necroinflammation and fibrosis) and assesses the relative contribution of insulin resistance syndrome to the occurrence of NAFLD in patients with chronic HCV infection.Patients and Methods:Untreated consecutive adults with chronic HCV infection admitted for liver biopsy were included in this study. Before liver biopsy, a questionnaire for risk factors was completed prospectively, and a blood sample was obtained for laboratory analysis.Results:Our study included 92 male patients. Their mean ± SD age and aspartate aminotransferase (AST) level were 42 ± 7.7 years (range 20-56) and 68 ± 41.7 U/L (range 16-214), respectively. The mean insulin level and insulin resistance index were 15.6 ± 18.3 mIU/mL (range 5.1-137.4) and 5.9 ± 15.2 (range 0.9-136.2), respectively. Fifty four percent of patients had steatosis and 65% had fibrosis. In multivariate analyses, steatosis was associated with insulin resistance and fibrosis was associated with high AST level, age ≥40 years, and steatosis.Conclusions:Steatosis is a histopathologic feature in >50% of patients with chronic HCV infection. Insulin resistance has an important role in the pathogenesis of steatosis, which represents a significant determinant of fibrosis together with high serum AST level and older age.

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“…All liver biopsy specimens were examined using haematoxylin-eosin and silver reticulin stain. A pathologist who was blinded to the patients' clinical condition and biochemical data scored each biopsy for steatosis, inflammation and fibrosis, using previously reported criteria [14,15]. Steatosis was scored as 0 (no steatosis), 1 (in less than 5% of the lobular parenchyma), 2 (in 5-25% of the lobular parenchyma), 3 (in 25-75% of the lobular parenchyma) or 4 (in more than 75% of the lobular parenchyma).…”

Section: Methodsmentioning

confidence: 99%

Genes for systemic vascular complications are differentially expressed in the livers of Type 2 diabetic patients

et al. 2004

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Aims/hypothesis. Type 2 diabetes is characterised by excessive hepatic glucose production and frequently leads to systemic vascular complications. We therefore analysed the relationship between the gene expression profile in the liver and the pathophysiology of Type 2 diabetes. Methods. Liver biopsy samples were obtained from twelve patients with Type 2 diabetes and from nine non-diabetic patients. To assay gene expression globally in the livers of both groups, we made complementary DNA (cDNA) microarrays consisting of 1080 human cDNAs. Relative expression ratios of individual genes were obtained by comparing cyanine 5-labelled cDNA from the patients with cyanine 3-labelled cDNA from reference RNA from the liver of a nondiabetic patient. Results. On assessing the similarities of differentially expressed genes, the gene expression profiles of the twelve diabetic patients formed a separate cluster from those of the non-diabetic patients. Of the 1080 genes assayed, 105 (9.7%) were up-regulated and 134 (12%) were down-regulated in the diabetic livers (p<0.005). The genes up-regulated in the diabetic patients included those encoding angiogenic factors such as vascular endothelial growth factor, endothelin and platelet-derived growth factor. They also included TGF superfamily genes such as TGFA and TGFB1 as well as bone morphogenetic proteins. Among the down-regulated genes in the diabetic patients were molecules defending against stress, e.g. flavin-containing monooxygenase and superoxide dismutase. Conclusions/interpretation. These findings suggest that livers of patients with Type 2 diabetes have gene expression profiles indicative of an increased risk of systemic vascular complications.

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Nonalcoholic Steatohepatitis: A Proposal for Grading and Staging The Histological Lesions

Cited by 3,300 publications

References 19 publications

Hepatic steatosis in patients coinfected with human immunodeficiency virus/hepatitis C virus: A meta-analysis of the risk factors

Hepatic steatosis in patients coinfected with human immunodeficiency virus/hepatitis C virus: A meta-analysis of the risk factors

Insulin resistance, steatosis, and fibrosis in Egyptian patients with chronic Hepatitis C virus infection

Genes for systemic vascular complications are differentially expressed in the livers of Type 2 diabetic patients

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