Cited by 212Hepatocellular Carcinoma Treatment and PrognosisLiver Disease Diagnosis and TreatmentLiver physiology and pathology

Does nonalcoholic fatty liver disease predispose patients to hepatocellular carcinoma in the absence of cirrhosis?

Guzman, Grace, Brunt, Elizabeth M., Petrovic, Lydia M., Chejfec, Gregorio, Layden, Thomas J., Cotler, Scott J.·2008·Archives of Pathology & Laboratory Medicine

Abstract

Context. —Hepatocellular carcinoma (HCC) is recognized as a complication of cirrhosis related to nonalcoholic fatty liver disease (NAFLD). Diabetes and the metabolic syndrome are also associated with HCC. However, it is not clear whether NAFLD predisposes patients to HCC in the absence of cirrhosis. Objective. —To seek evidence that HCC can develop in NAFLD unaccompanied by cirrhosis. Design. —Retrospective case study was performed on cases from 2004 to 2007 at the University of Illinois at Chicago Medical Center, using the key words hepatocellular carcinoma, liver explant , and liver resection. The diagnosis of HCC was identified and confirmed by hematoxylin-eosin–stained slides in 50 cases. Cause of liver disease was determined by review of liver histology, clinical history, and laboratory data. Results. —Three patients presented with advanced HCC with features of metabolic syndrome, including an elevated body mass index. Each patient had bland steatosis on liver biopsy, without fibrosis or cirrhosis. None of the 3 patients had evidence of any cause for liver disease other than NAFLD. Conclusions. —The cases presented here suggest that NAFLD may predispose patients to HCC in the absence of cirrhosis. Further studies are needed to confirm this potentially important observation.

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Crossref · 10.5858/132.11.1761

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38 of 38 references verified0 citation errors · 0 not checkable

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  • NASH and advanced fibrosis increase HCC risk by 15-fold and 25-fold in humans, respectively.

    “NASH and advanced fibrosis increase HCC risk by 15 and 25 folds in humans, respectively (Guzman et al., 2008; Hashimoto et al., 2009).”

    From Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis (2016) · cites this paper as Guzman et al., 2008

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Authors
Guzman, G., Brunt, E. M., Petrovic, L. M., Chejfec, G., Layden, T. J., & Cotler, S. J.
Affiliations
University of Southern California (US)
Venue
Archives of Pathology & Laboratory Medicine
Published
2008-11
Volume
132
Issue
11
Pages
1761-1766
ISSN
  • 0003-9985 (ISSN-L)
  • 1543-2165
OpenAlex
W2168535299
Cited by
212
References
38
Citations by year
2025: 2 · 2024: 3 · 2023: 3 · 2022: 5 · 2021: 12 · 2020: 12 · 2019: 13 · 2018: 21 · 2017: 15 · 2016: 16 · 2015: 20 · 2014: 16 · 2013: 13 · 2012: 11
FWCI
12.24
Type
journal article
Language
en
Open access
closed
Locations
  • Archives of Pathology & Laboratory Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Archives of Pathology & Laboratory Medicine
Topics
  • Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
non-alcoholic fatty liver disease, hepatocellular carcinoma, non-cirrhotic liver cancer, metabolic syndrome, diabetes mellitus, hepatic steatosis, liver fibrosis, liver biopsy, hepatectomy, liver explants
MeSH terms
Aged, Biopsy, Fatty Liver, Female, Carcinoma, Hepatocellular, Humans, Liver, Liver Neoplasms, Male, Middle Aged, Obesity, Retrospective Studies, Risk Factors, Causality, Metabolic Syndrome

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