Nonalcoholic steatohepatitis

Elizabeth M. Brunt

doi:10.1055/s-2004-823098

Cited by 481Liver Disease Diagnosis and TreatmentLiver Diseases and ImmunityLiver physiology and pathology

Nonalcoholic steatohepatitis

Elizabeth M. Brunt·2004·Seminars in Liver Disease

DOI 10.1055/s-2004-823098

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Abstract

Nonalcoholic fatty liver disease (NAFLD) is being increasingly recognized as a common liver disorder that represents the hepatic manifestation of the metabolic syndrome, a variably defined aggregate of disorders related to obesity, insulin resistance, type II diabetes, hypertension and hyperlipidemia. Nonalcoholic steatohepatitis (NASH) is the progressive form of liver injury that carries a risk for progressive fibrosis, cirrhosis, and end-stage liver disease. Hepatocellular carcinoma (HCC) is a documented complication in an as yet unknown percentage of cases of NASH cirrhosis. The diagnosis of nonalcoholic steatohepatitis requires histopathologic evaluation because the lesions of parenchymal injury and fibrosis cannot be detected by imaging studies or laboratory tests. This article will briefly discuss prevalence studies and the pathophysiology of NAFLD and focus on current discussions related to the specific lesions in the pathology of NASH, including the challenges of pediatric NASH and NASH-related cirrhosis.

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Adipose tissue can synthesize and release proinflammatory cytokines and adipokines, including leptin, adiponectin, and resistin; and these factors make up one of the driving mechanisms of insulin resistance.
“Adipose tissue can synthesize and release proinflammatory cytokines and adipokines, including leptin, adiponectin, and resistin; and these factors make up one of the driving mechanisms of IR (Brunt, 2004).”
From <i>Akkermansia muciniphila</i> alleviates <scp>high‐fat‐diet</scp> ‐related metabolic‐associated fatty liver disease by modulating gut microbiota and bile acids (2023) · cites this paper as Brunt, 2004
The assessment and severity of NASH is made histologically based on the patterns and degrees of hepatic steatosis, inflammation, and injury, in the absence of significant alcohol consumption.
“The assessment and severity of NASH is made histologically based on the patterns and degrees of hepatic steatosis, inflammation, and injury, in the absence of significant alcohol consumption.8”
From Leptin reverses nonalcoholic steatohepatitis in patients with severe lipodystrophy† (2005) · cites this paper as [8]

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Authors: Brunt, E. M.
Affiliations: Saint Louis University Hospital (US)
Corresponding author: Elizabeth M. Brunt
ORCID: Elizabeth M. Brunt
Venue: Seminars in Liver Disease
Publisher: Georg Thieme Verlag KG
Published: 2004-01
Volume: 24
Issue: 1
Pages: 3-20
ISSN: 0272-8087 (ISSN-L)
1098-8971
DOI: 10.1055/s-2004-823098
OpenAlex: W3149847267
Cited by: 481
References: 0
Citations by year: 2026: 2 · 2025: 2 · 2024: 9 · 2023: 8 · 2022: 4 · 2021: 6 · 2020: 13 · 2019: 4 · 2018: 18 · 2017: 14 · 2016: 24 · 2015: 25 · 2014: 26 · 2013: 22 · 2012: 31
FWCI: 29.48
Type: journal article
Language: en
Open access: closed
Locations: Seminars in Liver Disease (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: nonalcoholic steatohepatitis, non-alcoholic fatty liver disease, metabolic syndrome, liver fibrosis, liver cirrhosis, hepatocellular carcinoma, histopathology, pathophysiology, prevalence, insulin resistance, obesity
MeSH terms: Adolescent, Adult, Child, Fatty Liver, Fatty Liver, Alcoholic, Carcinoma, Hepatocellular, Humans, Liver Cirrhosis, Liver Neoplasms, Prevalence, Metabolic Syndrome

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