Body composition and hepatic steatosis as precursors for fibrotic liver disease

McCullough, Arthur J.; Falck‐Ytter, Yngve

doi:10.1002/hep.510290451

Cited by 64 publications

(39 citation statements)

References 48 publications

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“…The observation that obesity (BMI Ͼ 30 kg/m 2 ) is a risk factor for progression of fibrosis is consistent with the results of 3 recently published studies. [23][24][25] Although the mechanisms responsible for the effect of BMI on liver histology are unknown, 25 a practical recommendation to reduce body weight before starting therapy may be beneficial. This statement is strengthened by our observation of reduced fibrosis in the small proportion of nonresponders with the lowest BMI values.…”

Section: Discussionmentioning

confidence: 99%

Effect of peginterferon alfa-2a on liver histology in chronic hepatitis C: A meta-analysis of individual patient data

et al. 2004

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Multicenter randomized trials have shown that once-weekly pegylated interferon (peginterferon) alfa-2a is more efficacious than conventional interferon alfa-2a (IFN) in patients with chronic hepatitis C. We performed a meta-analysis of 1,013 previously untreated patients (from 3 randomized trials) with pretreatment and post-treatment liver biopsies to assess the differences between peginterferon alfa-2a and IFN in terms of their effects on liver histology. Reported values were standardized mean differences (SMD) between patients receiving peginterferon alfa-2a and those receiving IFN (post-treatment value minus baseline value for each group). We used a random-effects model to quantify the average effect of peginterferon alfa-2a on liver histology. Peginterferon alfa-2a significantly reduced fibrosis compared with IFN (SMD, ؊0.14; 95% CI: ؊0.27, ؊0.01; P ‫؍‬ .04). A reduction in fibrosis was observed among sustained virologic responders (SMD, ؊0.59; 95% CI: ؊0.89, ؊0.30; P < .0001) and patients with recurrent disease (SMD, ؊0.34; 95% CI: ؊0.54, ؊0.14; P ‫؍‬ .0007), whereas no significant reduction was observed among nonresponders (SMD, ؊0.

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Section: Discussionmentioning

confidence: 99%

Effect of peginterferon alfa-2a on liver histology in chronic hepatitis C: A meta-analysis of individual patient data

et al. 2004

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“…The observation that some obese individuals presented a liver disease histologically indistinguishable from alcoholic liver disease itself had long been recognized. [42][43][44][45][46][47][48][49] Interestingly, it has been recently demonstrated that obesity also increases the risk of liver disease induced by either alcohol 50 or chronic hepatitis C. [51][52][53] In a literature survey of 41 original articles comprising information on liver morphology in 1515 morbidly obese patients, liver biopsy was considered as normal in only 12% of the cases. 54 The most frequent abnormality reported was fatty changes present in 80% of the biopsies; portal inflammation was also common (33%) while portal or periportal fibrosis was observed in 29%.…”

Section: The Association Of Nash With Obesitymentioning

confidence: 99%

Obesity and liver disease

Scheen

Luyckx

2002

Best Practice & Research Clinical Endocrinology & Metab

118

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Non-alcoholic steatohepatitis (NASH) is a disease of emerging identity and importance. It is frequently associated with obesity, especially visceral fat, and is intimately related to fatty liver and markers of the insulin resistance syndrome. Both the prevalence and the severity of liver steatosis are related to body mass index, waist circumference, hyperinsulinaemia, hypertriglyceridaemia and impaired glucose tolerance or type 2 diabetes. The identification of obese patients who may progress from steatosis to NASH and from NASH to fibrosis/cirrhosis is an important clinical challenge. Substantial weight loss is accompanied by a marked attenuation of insulin resistance and related metabolic syndrome and, concomitantly, by a remarkable regression of liver steatosis in most patients, although increased inflammation may be detected in some subjects. Thus, NASH may be considered as another disease of affluence, as is the insulin resistance syndrome, and perhaps being part of it, especially in obese patients.

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“…In addition, this BMI effect was independent of hepatic steatosis. Before discussing the potential mechanisms and clinical implications of these observations, it is important to revisit a number of issues, previously discussed in this journal, 6 that relate to the accuracy and interpretation of studies involving body composition.…”

mentioning

confidence: 99%

Obesity and its nurturing effect on hepatitis C

McCullough

2003

Hepatology

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Body composition and hepatic steatosis as precursors for fibrotic liver disease

Cited by 64 publications

References 48 publications

Effect of peginterferon alfa-2a on liver histology in chronic hepatitis C: A meta-analysis of individual patient data

Effect of peginterferon alfa-2a on liver histology in chronic hepatitis C: A meta-analysis of individual patient data

Obesity and liver disease

Obesity and its nurturing effect on hepatitis C

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