Etiopathogenesis of Nonalcoholic Steatohepatitis
By S. Chitturi, G. Farrell. Seminars in liver disease (Print), 2001
669 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/85dc33eb555a1ba03f55e1405d0349e4c871ab9e
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Citations in the corpus
- The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice. (2003, neutral): “Fatty liver disease is a common finding in patients and various animal models with obesity, insulin resistance, diabetes, and dyslipidemia (60).”
- NASH and insulin resistance: Insulin hypersecretion and specific association with the insulin resistance syndrome (2002, methodology): “16 as follows: (1) a liver biopsy specimen showing steatosis, lobular inflammation, and hepatocellular degeneration, irrespective of the presence of fibrosis or Mallory bodies; (2) exclusion of patients with secondary causes of NASH; and (3) exclusion of other liver disorders (alcoholic liver diseas”
- Gene expression of tumor necrosis factor α and TNF‐receptors, p55 and p75, in nonalcoholic steatohepatitis patients (2001, background): “(3) No evidence of drug-induced liver disease, and no evidence of drug-induced liver injury on liver biopsy; (4) no long-term consumption of corticosteroids, amiodarone, tamoxifen, or tetracyclins; (5) seronegativity for hepatitis B surface antigen, hepatitis delta antigen (HDAg), hepatitis delta an”
- Non-alcoholic fatty liver disease (NAFLD): a review of pathophysiology, clinical management and effects of weight loss (2022, background): “lipodystrophy or cachexia or intestinal bypass surgery) [13, 14].”