Nonalcoholic steatohepatitis

By B. Mulhall, Z. Younossi. Current treatment options in gastroenterology, 2004

1,297 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/ed0534fe49bc52298e2e1382ba4cc43948004125

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. S. Friedman
2. Q. Anstee
3. M. Pinzani
4. A. Sanyal
5. J. Clark
6. Robert D. Goldin
7. E. Brunt
8. R. Loomba

In Hepatology

1. S. Friedman
2. J. Clark
3. M. Pinzani
4. R. Loomba
5. Q. Anstee
6. Robert D. Goldin
7. Shira Zelber-Sagi
8. R. Oren

In Pathology and Forensic Medicine

1. J. Clark
2. Q. Anstee
3. Robert D. Goldin
4. Shira Zelber-Sagi
5. R. Oren
6. E. Santo
7. M. Webb
8. Z. Halpern

Citations in the corpus

• Updated Definitions of Healthy Ranges for Serum Alanine Aminotransferase Levels (2002, background): “Therefore, the donors more likely to be found in the right side of the ALT distribution curve were typically overweight and had hyperlipidemia or glucose intolerance, a pattern of abnormalities closely resembling that of nonalcoholic fatty liver disease (8, 10).”
• Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. (2002, neutral): “The men also did not have serological evidence of hepatitis A, B, or C or autoimmune hepatitis nor did they have clinical signs or symptoms of inborn errors of metabolism or a history of use of toxins, other than less than moderate amounts of alcohol ( 20 g/d), or drugs associated with steatosis (16”
• Diagnostic value of a computerized hepatorenal index for sonographic quantification of liver steatosis. (2009, methodology): “For patients with nonalcoholic fatty liver disease, the extent of liver steatosis and the degree of fibrosis and necroinflammatory activity were assessed histologically according to the Brunt [23, 24] criteria.”
• Gut microbiome based metagenomic signature for non-invasive detection of advanced fibrosis in human nonalcoholic fatty liver disease (2017, neutral): “Determination of histological features from centrally reviewed biopsy using the NASHClinical Research Network Scoring System (Kleiner et al., 2005) Ballooning classification: few indicates rare but definite ballooned hepatocytes, as well as cases that are diagnostically borderline”
• Liver enzyme alteration: a guide for clinicians (2005, background): “Suspicion of nonalcoholic fatty liver disease is increased by the presence of conditions linked to the metabolic syndrome and insulin resistance (increased body mass index, diabetes, hyperlipemia, hypertension), although the disease may occur in patients without these associated factors.(48,49) The ”
• Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Diagnosis of NASH requires histological assessment in the context of suspected NAFLD and is typically characterized by the presence of steatosis, lobular inflammation, and ballooning with or without perisinusoidal fibrosis (Kleiner et al., 2005).”
• Vitamin E and vitamin C treatment improves fibrosis in patients with nonalcoholic steatohepatitis (2003, background): “In fact, recent studies have demonstrated that fibrosis or cirrhosis is evident on initial biopsy in 15%–50% of NASH patients (13).”
• Nonalcoholic fatty liver disease: pathology and pathogenesis. (2010, background): “When present, they are considered by most pathologists to be a useful morphologic finding (37) and are related to higher necroinflammatory activity (35).”
• INCREASED HEPATIC SYNTHESIS AND DYSREGULATION OF CHOLESTEROL METABOLISM IS ASSOCIATED WITH THE SEVERITY OF NONALCOHOLIC FATTY LIVER DISEASE (2012, methodology): “Fatty liver and steatohepatitis were diagnosed using standard criteria used before (Kleiner et al., 2005).”
• Defining high-fat-diet rat models: metabolic and molecular effects of different fat types. (2006, background): “…active tissues such as liver, muscle and pancreas, build the pathophysiologic basis of the metabolic syndrome (McPherson & Jones 2003, Unger 2003, Carr et al. 2004), and hepatic steatosis is now often added to the classical components mentioned above (Brunt 2004, den Boer et al. 2004).”
• Obesity accelerates epigenetic aging of human liver (2014, methodology): “Increased BMI is the primary risk factor for nonalcoholic fatty liver disease (NAFLD), which ranges from simple liver steatosis to nonalcoholic steatohepatitis (NASH).”