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"Nonalcoholic fatty liver disease (NAFLD)"

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"Nonalcoholic fatty liver disease (NAFLD)"

Original Articles

Viral hepatitis

Association between hepatic steatosis and the development of hepatocellular carcinoma in patients with chronic hepatitis B
Yun Bin Lee, Yeonjung Ha, Young Eun Chon, Mi Na Kim, Joo Ho Lee, Hana Park, Kwang-il Kim, Soo-Hwan Kim, Kyu Sung Rim, Seong Gyu Hwang
Clin Mol Hepatol 2019;25(1):52-64.
Published online October 23, 2018
DOI: https://doi.org/10.3350/cmh.2018.0040
Background/Aims
Nonalcoholic fatty liver disease (NAFLD) is becoming a worldwide epidemic, and is frequently found in patients with chronic hepatitis B (CHB). We investigated the impact of histologically proven hepatic steatosis on the risk for hepatocellular carcinoma (HCC) in CHB patients without excessive alcohol intake.
Methods
Consecutive CHB patients who underwent liver biopsy from January 2007 to December 2015 were included. The association between hepatic steatosis (≥ 5%) and subsequent HCC risk was analyzed. Inverse probability weighting (IPW) using the propensity score was applied to adjust for differences in patient characteristics, including metabolic factors.
Results
Fatty liver was histologically proven in 70 patients (21.8%) among a total of 321 patients. During the median (interquartile range) follow-up of 5.3 (2.9–8.3) years, 17 of 321 patients (5.3%) developed HCC: 8 of 70 patients (11.4%) with fatty liver and 9 of 251 patients (3.6%) without fatty liver. The five-year cumulative incidences of HCC among patients without and with fatty liver were 1.9% and 8.2%, respectively (P=0.004). Coexisting fatty liver was associated with a higher risk for HCC (adjusted hazards ratio [HR], 3.005; 95% confidence interval [CI], 1.122–8.051; P=0.03). After balancing with IPW, HCC incidences were not significantly different between the groups (P=0.19), and the association between fatty liver and HCC was not significant (adjusted HR, 1.709; 95% CI, 0.404–7.228; P=0.47).
Conclusions
Superimposed NAFLD was associated with a higher HCC risk in CHB patients. However, the association between steatosis per se and HCC risk was not evident after adjustment for metabolic factors.

Citations

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Steatotic liver disease

Serum bilirubin levels are inversely associated with nonalcoholic fatty liver disease
Min-Sun Kwak, Donghee Kim, Goh Eun Chung, Seung Joo Kang, Min Jung Park, Yoon Jun Kim, Jung-Hwan Yoon, Hyo-Suk Lee
Korean J Hepatol 2012;18(4):383-390.
Published online December 21, 2012
DOI: https://doi.org/10.3350/cmh.2012.18.4.383
Background/Aims

Serum bilirubin exerts antioxidant and cytoprotective effects. In addition, elevated serum bilirubin levels are associated with a decreased risk of metabolic and cardiovascular diseases. However, few studies have evaluated whether serum bilirubin is associated with non-alcoholic fatty liver disease (NAFLD), which is closely associated with other metabolic diseases. The aim of this study was thus to elucidate the association between serum total bilirubin levels and NAFLD.

Methods

A cross-sectional study of 17,348 subjects undergoing a routine health check-up was conducted. Subjects positive for hepatitis B or hepatitis C virus, or with other hepatitis history were excluded. NAFLD was diagnosed on the basis of typical ultrasonographic findings and an alcohol consumption of less than 20 g/day.

Results

The mean age of the subjects was 49 years and 9,076 (52.3%) were men. The prevalence of NAFLD decreased steadily as the serum bilirubin level increased in both men and women (P<0.001 for both). Multivariate regression analysis adjusted for other metabolic risk factors showed that serum bilirubin level was inversely associated with the prevalence of NAFLD [odds ratio (OR)=0.88, 95% confidence interval (CI)=0.80-0.97]. Furthermore, there was an inverse, dose-dependent association between NAFLD and serum total bilirubin levels (OR=0.83, 95% CI=0.75-0.93 in the third quartile; OR=0.80, 95% CI=0.71-0.90 in the fourth quartile vs. lowest quartile, P for trend <0.001).

Conclusions

Serum bilirubin levels were found to be inversely associated with the prevalence of NAFLD independent of known metabolic risk factors. Serum bilirubin might be a protective marker for NAFLD.

Citations

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    Darren M. Gordon, Samuel O. Adeosun, Somtochukwu I. Ngwudike, Christopher D. Anderson, John E. Hall, Terry D. Hinds, David E. Stec
    Archives of Biochemistry and Biophysics.2019; 672: 108072.     CrossRef
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    Somaya Albhaisi, Arun J. Sanyal
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    Hepatology.2018; 67(4): 1609.     CrossRef
  • Bilirubin in the Liver–Gut Signaling Axis
    Abdul-Rizaq Hamoud, Lauren Weaver, David E. Stec, Terry D. Hinds
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    Vikram L. Sundararaghavan, Sivjot Binepal, David E. Stec, Puneet Sindhwani, Terry D. Hinds
    Transplantation Reviews.2018; 32(4): 234.     CrossRef
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    American Journal of Physiology-Renal Physiology.2018; 315(2): F323.     CrossRef
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    Frontiers in Genetics.2018;[Epub]     CrossRef
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    Terry D. Hinds, Peter A. Hosick, Shujuan Chen, Robert H. Tukey, Michael W. Hankins, Andrea Nestor-Kalinoski, David E. Stec
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    David E. Stec, Kezia John, Christopher J. Trabbic, Amarjit Luniwal, Michael W. Hankins, Justin Baum, Terry D. Hinds, Hervé Guillou
    PLOS ONE.2016; 11(4): e0153427.     CrossRef
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    Kyong Yeun Jung, Sun Young Cho, Hyung Joon Kim, Suk Bae Kim, Il Han Song
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Liver Pathology

Nonalcoholic Steatohepatitis
So-Young Jin
Korean J Hepatol 2006;12(3):455-459.
  • 3,894 View
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Original Article
The Prevalence of Metabolic Syndrome in Patients with Nonalcoholic Fatty Liver Disease
Ki Won Moon, M.D., Joung Muk Leem, M.D., Sang Seok Bae, M.D., Ki Man Lee, M.D., Seok Hyung Kim, M.D.*, Hee Bok Chae, M.D., Seon Mee Park, M.D. and Sei Jin Youn, M.D.
Korean J Hepatol 2004;10(3):197-206.
Background/Aims
Nonalcoholic fatty liver disease (NAFLD) is associated with dyslipidemia, obesity, and insulin resistance, which are the main features of metabolic syndrome. First, we examined the prevalence of metabolic syndrome among patients with NAFLD . We then compared the prevalence of metabolic syndrome in simple steatosis with that in nonalcoholic steatohepatitis (NASH). Finally, we sought to identify clinical factors associated with the stage of liver fibrosis. Methods: From November 2002 to March 2004, we enrolled consecutive 25 patients with NAFLD from patients visiting outpatient clinic. The 17 controls were healthy persons w ho visited our health promotion center. We compared the clinical and biochemical data of the NAFLD group with those of the control group. Using histologic findings, we divided NAFLD into simple steatosis and NASH. We then compared the clinical and biochemical data of the simple steatosis group with those of the NASH group. Results: Fourteen patients (14/25, 56%) had metabolic syndrome in the NAFLD group. There was no difference in the prevalence of metabolic syndrome between the simple steatosis (5/10, 50%) and the NASH group (9/15, 60%). We found significant differences in cardiovascular risk factors between the two groups, but homeostasis model assessment insulin resistance w as the only significantly different factor between the simple steatosis group and the NASH group. In addition, no difference in histological features was found between NASH with metabolic syndrome and without metabolic syndrome. Conclusions: A considerable number of patients with NAFLD had metabolic syndrome. There was a close correlation between NAFLD and metabolic syndrome. We could not find any cardiovascular risk factors that could predict a severe fibrosis. (Korean J Hepatol 2004;10:197-206)
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