Clinical and Molecular Hepatology

"Nonalcoholic steatohepatitis"

Correspondence

Steatotic liver disease

Correspondence to editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”: Hayeon Kim, Min Jeong Park, Myeong Gyu Kim, Kyungim Kim; Clin Mol Hepatol 2024;30(4):989-991.
Published online August 27, 2024; DOI: https://doi.org/10.3350/cmh.2024.0705

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Reply to correspondence on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
Clinical and Molecular Hepatology.2024; 30(4): 1039. CrossRef

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Editorials

Hepatic neoplasm

Hepatocellular carcinoma surveillance in non-alcoholic fatty liver disease – who and how?: Margaret LP Teng, Darren Jun Hao Tan, Cheng Han Ng, Daniel Q. Huang; Clin Mol Hepatol 2023;29(2):404-407.
Published online March 14, 2023; DOI: https://doi.org/10.3350/cmh.2023.0069

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Steatotic liver disease

Lean vs. obese phenotypes of nonalcoholic fatty liver disease: similar or different?: Ho Soo Chun, Minjong Lee; Clin Mol Hepatol 2023;29(2):377-380.
Published online March 9, 2023; DOI: https://doi.org/10.3350/cmh.2023.0061

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Original Article

Steatotic liver disease

Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: A network meta-analysis: Min Jeong Park, Hayeon Kim, Myeong Gyu Kim, Kyungim Kim; Clin Mol Hepatol 2023;29(3):693-704.
Published online March 9, 2023; DOI: https://doi.org/10.3350/cmh.2022.0330

Background/Aims
Previous studies have revealed that glucagon-like peptide-1 receptor agonist (GLP-1RA) and thiazolidinedione (TZD) can improve nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steatohepatitis (NASH). However, comprehensive research comparing the effects of GLP-1RA and TZD is limited. Thus, this study aimed to compare the effects of GLP-1RA and TZD on NAFLD or NASH through a network meta-analysis.
Methods
The PubMed, Embase, Web of Science, and Scopus databases were searched for randomized controlled trials (RCTs) that explored the efficacy of GLP-1RAs or TZDs in adult patients with NAFLD or NASH. The outcomes were liver biopsy-based (NAFLD activity score [NAS], fibrosis stage, and NASH resolution), noninvasive technique-based (liver fat content on proton magnetic resonance spectroscopy [¹H-MRS] and controlled attenuation parameter [CAP]), biological, and anthropometric indicators. A random effects model was used to calculate the mean difference (MD) and relative risk with 95% confidence interval (CI).
Results
Twenty-five RCTs with 2,237 overweight or obese patients were included. GLP-1RA was significantly superior in reducing liver fat content evaluated using ¹H-MRS (MD –2.42, 95% CI –3.84 to –1.00), body mass index (MD –1.60, 95% CI –2.41 to –0.80), and waist circumference (MD –4.89, 95% CI –8.17 to –1.61) than TZD. In liver biopsy-based evaluation and liver fat content assessment using CAP, GLP-1RA tended to surpass TZD, albeit not significantly. Sensitivity analysis showed consistent results with the main results.
Conclusions
Compared with TZD, GLP-1RA had better effects on liver fat content, body mass index, and waist circumference in overweight or obese patients with NAFLD or NASH.

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Correspondence to editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
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Reply to correspondence on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
Clinical and Molecular Hepatology.2024; 30(4): 1039. CrossRef
Incretin-based therapy in the management of metabolic dysfunction-associated steatotic liver disease (MASLD): one piece of the puzzle: Editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fa
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Reviews

Steatotic liver disease

Pharmacological advances in the treatment of nonalcoholic fatty liver diseases : focused on global results of randomized controlled trials: Jihyun An, Joo Hyun Sohn; Clin Mol Hepatol 2023;29(Suppl):S268-S275.
Published online December 20, 2022; DOI: https://doi.org/10.3350/cmh.2022.0437

Abstract
PDF

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease globally, and its prevalence is rapidly increasing. Nonalcoholic steatohepatitis (NASH), a progressive form of NAFLD, is characterized by hepatocellular injury, inflammation, and fibrosis. Patients with NASH or severe fibrosis should be treated according to international NAFLD guidelines. Currently, regulatory agencies have not approved any pharmaceutical treatment for NAFLD. Vitamin E and pioglitazone are efficacious for NASH resolution; however, their benefits must be weighed against the reported risks. In a phase 2 trial, a glucagon-like peptide-1 agonist commonly used for diabetes and obesity was found to improve liver histology in patients with NASH. Furthermore, therapeutic agents targeting NASH pathogenesis, including bile acid signaling, insulin resistance, and lipid metabolism, are in various phases of clinical development. In this article, we review the benefits and drawbacks of current pharmacotherapy and the efficacy of upcoming treatments for NASH.

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Steatotic liver disease

Surveillance of the progression and assessment of treatment endpoints for nonalcoholic steatohepatitis: Yi-wen Shi, Jian-Gao Fan; Clin Mol Hepatol 2023;29(Suppl):S228-S243.
Published online December 14, 2022; DOI: https://doi.org/10.3350/cmh.2022.0401

Abstract
PDF

Nonalcoholic steatohepatitis (NASH) is an aggressive form of nonalcoholic fatty liver disease (NAFLD) characterized by steatosis-associated inflammation and liver injury. Without effective treatment or management, NASH can have life-threatening outcomes. Evaluation and identification of NASH patients at risk for adverse outcomes are therefore important. Key issues in screening NASH patients are the assessment of advanced fibrosis, differentiation of NASH from simple steatosis, and monitoring of dynamic changes during follow-up and treatment. Currently, NASH staging and evaluation of the effectiveness for drugs still rely on pathological diagnosis, despite sample error issues and the subjectivity associated with liver biopsy. Optimizing the pathological assessment of liver biopsy samples and developing noninvasive surrogate methods for accessible, accurate, and safe evaluation are therefore critical. Although noninvasive methods including elastography, serum soluble biomarkers, and combined models have been implemented in the last decade, noninvasive diagnostic measurements are not widely applied in clinical practice. More work remains to be done in establishing cost-effective strategies both for screening for at-risk NASH patients and identifying changes in disease severity. In this review, we summarize the current state of noninvasive methods for detecting steatosis, steatohepatitis, and fibrosis in patients with NASH, and discuss noninvasive assessments for screening at-risk patients with a focus on the characteristics that should be monitored at follow-up.

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Steatotic liver disease

Genetics in non-alcoholic fatty liver disease: The role of risk alleles through the lens of immune response: Silvia Sookoian, Carlos J. Pirola; Clin Mol Hepatol 2023;29(Suppl):S184-S195.
Published online December 5, 2022; DOI: https://doi.org/10.3350/cmh.2022.0318

The knowledge on the genetic component of non-alcoholic fatty liver disease (NAFLD) has grown exponentially over the last 10 to 15 years. This review summarizes the current evidence and the latest developments in the genetics of NAFLD and non-alcoholic steatohepatitis (NASH) from the immune system’s perspective. Activation of innate and or adaptive immune response is an essential driver of NAFLD disease severity and progression. Lipid and immune pathways are crucial in the pathophysiology of NAFLD and NASH. Here, we highlight novel applications of genomic techniques, including single-cell sequencing and the genetics of gene expression, to elucidate the potential involvement of NAFLD/NASH-risk alleles in modulating immune system cells. Together, our focus is to provide an overview of the potential involvement of the NAFLD/NASH-related risk variants in mediating the immune-driven liver disease severity and diverse systemic pleiotropic effects.

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Repurposing drugs to target nonalcoholic steatohepatitis: Auranofin, a gold-organic molecule complex for the treatment of a specifc complex trait: Carlos J. Pirola, Silvia Sookoian; Clin Mol Hepatol 2022;28(4):806-809.
Published online August 19, 2022; DOI: https://doi.org/10.3350/cmh.2022.0208

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Personalized medicine in nonalcoholic fatty liver disease: Carlos J. Pirola, Silvia Sookoian; Clin Mol Hepatol 2022;28(4):935-938.
Published online June 24, 2022; DOI: https://doi.org/10.3350/cmh.2022.0175

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A crystal ball to forecast treatment responsiveness in nonalcoholic fatty liver disease: Seonghwan Hwang, Won Kim; Clin Mol Hepatol 2022;28(3):478-480.
Published online June 16, 2022; DOI: https://doi.org/10.3350/cmh.2022.0143

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Review

Nonalcoholic fatty liver disease versus metabolic-associated fatty liver disease: Prevalence, outcomes and implications of a change in name: Cheng Han Ng, Daniel Q. Huang, Mindie H. Nguyen; Clin Mol Hepatol 2022;28(4):790-801.
Published online May 11, 2022; DOI: https://doi.org/10.3350/cmh.2022.0070

Abstract
PDF

Nonalcoholic fatty liver disease (NAFLD) affects about a third of the world’s adult population and is a major public health concern. NAFLD is defined by the presence of hepatic steatosis and the absence of other causes of liver disease. As NAFLD is closely associated with the presence of the metabolic syndrome, several experts have called for a change in nomenclature from NAFLD to metabolic-associated fatty liver disease (MAFLD) to better reflect the underlying pathophysiology of NAFLD as a metabolically driven disease and shift to a “positive” diagnostic criteria rather than one of exclusion. Recent studies have suggested that the global prevalence of MAFLD is higher than that of NAFLD, and patients with MAFLD have more metabolic comorbidities compared to those with NAFLD. Emerging data also suggest that all-cause and cardiovascular mortality may be higher in MAFLD compared with NAFLD. In this synopsis, we discuss differences in clinical features, prevalence and clinical outcomes between NAFLD and MAFLD. In addition, we highlight the advantages and disadvantages of a name change from NAFLD to MAFLD from the perspective of the scientific community, care providers and patients.

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Original Article

Steatotic liver disease

Serum lipocalin-2 is a potential biomarker for the clinical diagnosis of nonalcoholic steatohepatitis: Gang Xu, Yu-Min Wang, Miao-Miao Ying, Sui-Dan Chen, Zong-Rui Li, Hong-Lei Ma, Ming-Hua Zheng, Jian Wu, Chunming Ding; Clin Mol Hepatol 2021;27(2):329-345.
Published online January 20, 2021; DOI: https://doi.org/10.3350/cmh.2020.0261

Background/Aims
Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis. We aimed to investigate the usefulness of a key biomarker, lipocalin-2 (LCN2), for the detection of NASH progression.
Methods
A mouse NASH model was established using a high-fat diet and a high-sugar drinking water. Gene expression profile of the NASH model was analyzed using RNA sequencing. Moreover, 360 NAFLD patients (steatosis, 83; NASH, 277), 40 healthy individuals, and 87 patients with alcoholic fatty liver disease were recruited.
Results
Inflammatory infiltration, focal necrosis in the leaflets, steatosis, and fibrosis were documented in the mouse liver. In total, 504 genes were differentially expressed in the livers of NASH mice, and showed significant functional enrichment in the inflammation-related category. Upregulated liver LCN2 was found to be significantly interactive with various interleukins and toll-like receptors. Serum LCN2 levels were significantly increased in NAFLD patients. Serum LCN2 levels were correlated with steatosis, intralobular inflammation, semiquantitative fibrosis score, and nonalcoholic fatty liver disease activity score. The area under the curve of serum LCN2 was 0.987 with a specificity of 100% and a sensitivity of 93.5% for NASH diagnosis, and 0.977 with almost the same specificity and sensitivity for steatosis.
Conclusions
LCN2 might be involved in the transition from NAFL to NASH by mediating inflammation. Serum LCN2 levels might be a novel biomarker for the diagnosis of NASH.

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Review

Steatotic liver disease

Recent research trends and updates on nonalcoholic fatty liver disease: Jeong-Ju Yoo, Won Kim, Moon Young Kim, Dae Won Jun, Sang Gyune Kim, Jong-Eun Yeon, Jin Woo Lee, Yong Kyun Cho, Sang Hoon Park, Joo Hyun Sohn, On behalf of the Korean Association for the Study of the Liver (KASL)-Korea Nonalcoholic fatty liver Study Group (KNSG); Clin Mol Hepatol 2019;25(1):1-11.
Published online August 8, 2018; DOI: https://doi.org/10.3350/cmh.2018.0037

Abstract
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Nonalcoholic fatty liver disease (NAFLD), together with metabolic syndrome and obesity, has shown a rapid increase in prevalence worldwide and is emerging as a major cause of chronic liver disease and liver transplantation. Among the various phenotypes of NAFLD, nonalcoholic steatohepatitis (NASH) is highly likely to progress to development of end-stage liver disease and cardiometabolic disease, resulting in liver-related and non-liver–related mortality. Nonetheless, there is no standardized pharmacotherapy against NASH and many drugs are under development in ongoing clinical trials. To develop a successful anti-NASH drug, it is necessary to select an appropriate target population and treatment outcomes depending on whether the mode of action is anti-metabolic, anti-inflammatory or anti-fibrotic. Recently, innovative surrogate markers have been investigated to replace hard outcomes such as liver histology and mortality and reduce the clinical trial duration. Currently, several drugs with fast track designation are being tested in phase III clinical trials, and many other drugs have moved into phase II clinical trials. Both lean NAFLD and typical obese NAFLD have been extensively studied and genetic variants such as PNPLA3 and TM6SF2 have been identified as significant risk factors for lean NAFLD. In the near future, noninvasive biomarkers and effective targeted therapies for NASH and associated fibrosis are required to develop precision medicine and tailored therapy according to various phenotypes of NAFLD.

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Original Article

Steatotic liver disease

Serum matrix metalloproteinase-1 level represents disease activity as opposed to fibrosis in patients with histologically proven nonalcoholic steatohepatitis: Wataru Ando, Hiroaki Yokomori, Nobuhiro Tsutsui, Eigoro Yamanouchi, Yutaka Suzuki, Masaya Oda, Yutaka Inagaki, Katsuya Otori, Isao Okazaki; Clin Mol Hepatol 2018;24(1):61-76.
Published online November 20, 2017; DOI: https://doi.org/10.3350/cmh.2017.0030

Background/Aims
Nonalcoholic steatohepatitis (NASH) is prevalent in both economically developed and developing countries. Twenty percent of NASH progresses to cirrhosis with/without hepatocellular carcinoma, and there is an urgent need to find biomarkers for early diagnosis and monitoring progression of the disease. Using immunohistochemical and immunoelectron microscopic examination we previously reported that expression of matrix metalloproteinase-1 (MMP-1) increased in monocytes, Kupffer cells and hepatic stellate cells in early stage NASH. The present study investigated whether serum MMP-1 levels reflect disease activity and pharmaceutical effects in NASH patients.
Methods
We measured the serum levels of MMPs, tissue inhibitors of metalloproteinases (TIMPs), and several cytokines/ chemokines in patients with histologically proven early and advanced stages of NASH and compared them with those in healthy controls.
Results
Serum MMP-1 levels in stage 1 fibrosis, but not in the more advanced fibrosis stages, were significantly higher than in healthy controls (P=0.019). There was no correlation between serum MMP-1 level and fibrosis stage. Serum MMP- 1 levels in NASH patients represented disease activity estimated by serum aminotransferase values during the followup period. In contrast, MMP-2, MMP-9 and TIMPs did not change with disease activity. Consistent with the finding that MMP-1 is expressed predominantly in monocytes and Kupffer cells, serum levels of monocyte chemotactic protein-1 and granulocyte-colony stimulating factor were significantly increased in NASH with stage 1 fibrosis.
Conclusions
These results suggest that serum MMP-1 levels represent disease activity and may serve as a potential biomarker for monitoring the progression of NASH.

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Case Report

Steatotic liver disease

Severe steatohepatitis with hepatic decompensation resulting from malnutrition after pancreaticoduodenectomy: Eun Hui Sim, Jung Hyun Kwon, Se Young Kim, Seung Min Jung, Lee-So Maeng, Jeong Won Jang, Kyu Won Chung; Korean J Hepatol 2012;18(4):404-410.
Published online December 21, 2012; DOI: https://doi.org/10.3350/cmh.2012.18.4.404

Abstract
PDF

The most common finding related to nonalcoholic steatohepatitis is obesity, but a status of severe malnutrition can also induce the steatohepatitis. The authors report a rare case of steatohepatitis leading to hepatic decompensation caused by malnutrition after pancreaticoduodenectomy. A 68-year-old female patient who had been previously diagnosed with pancreatic cancer and had undergone pancreaticoduodenectomy 5 months previously presented with abdominal distension. Routine CT performed 3 months after the surgery revealed severe fatty liver without evidence of tumor recurrence. After undergoing pancreaticoduodenectomy her food intake had reduced, and as a result she had lost 7 kg of body weight over 2 months. At this admission, CT revealed moderate amounts of ascites without tumor recurrence. Furthermore, her albumin and lipid profile levels were markedly decreased, and she had a flapping tremor and slurred speech suggestive of hepatic encephalopathy. Her liver biopsy findings were consistent with steatohepatitis and disclosed macrovesicular steatosis without definite fibrosis. After careful nutritional control, her symptoms disappeared and her laboratory findings improved.

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Original Article

Validity and reliability of the nonalcoholic fatty Liver diseases activity score (NAS) in Korean NAFLD patients and its correlation with clinical factors: Kyung-Hun Lee, M.D., Sang Hoon Park, M.D., Yu Jin Kim, M.D., Kyung Rim Huh, M.D., Kwang Seon Min1, M.D., Sun-Young Jun1, M.D., Kyoung Oh Kim, M.D., Cheol Hee Park, M.D., Taeho Hahn, M.D., Kyo-Sang Yoo, M.D., Jong Hyeok Kim, M.D., Myung-Seok Lee, M.D., Choong Kee Park, M.D.; Korean J Hepatol 2010;16(1):29-37.
Published online March 26, 2010; DOI: https://doi.org/10.3350/kjhep.2010.16.1.29

Abstract
PDF

Background
/Aim: Nonalcoholic steatohepatitis (NASH) is commonly diagnosed using the semi-quantitative grading and staging system proposed by Brunt et al. in 1999. The Pathology Committee of the NASH established the nonalcoholic fatty liver diseases (NAFLD) activity score (NAS) in 2005. The aim of this study was to elucidate the validity and reliability of the NAS in Korean NAFLD patients. Methods: Fifty-six patients on whom sonography-guided liver biopsy for well-defined NAFLD was performed between 1999 and 2007 were identified retrospectively. Two pathologists evaluated each biopsy sample. NAFLD was evaluated using both the grading system developed by Brunt et al. and the NAS. Each pathologist was blinded to the patients` clinical data and scored independently. We evaluated the body mass index (BMI), liver enzymes, lipid profile, peripheral insulin resistance, leptin, insulin/c-peptide ratio, ferritin, and fasting blood glucose. Results: The patients were aged 32.1±12.5 years (mean±SD) and comprised 44 males (78.6%). Patients with different grades at the two grading systems had mild steatosis or ballooning changes with fibrosis, and 36.6% of them were borderline cases (NAS of 3 or 4). The interobserver agreement on diagnostic category was 0.748 (P<0.001) for the NAS (using weighted κ statistics). Elevated fasting glucose, ALT, and triglyceride were associated with the NAS. Conclusions: The simple and reproducible NAS was found to be a useful pathologic grading system in Korean NAFLD patients. However, the proportion of borderline cases based on the NAS was high. The "wait and see" strategy is necessary for evaluating the long-term prognosis. (Korean J Hepatol 2010;16:29-37)

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Published online December 31, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.S6.S34

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Review

Pathology of nonalcoholic steatohepatitis: Yoon Mi Jeen , So Young Jin; Korean J Hepatol 2009;15(2):122-130.
Published online June 30, 2009; DOI: https://doi.org/10.3350/kjhep.2009.15.2.122

Abstract
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Nonalcoholic steatohepatitis (NASH), one of the NAFLDs (nonalcoholic fatty liver diseases), is regarded as a hepatic manifestation of metabolic syndrome. NASH can progress to cirrhosis, and possibly to hepatic malignancy. Currently, liver biopsy is the only reliable method of assessing the presence or absence of NASH and the stage of fibrosis. The finding of steatosis with evidence of hepatocyte injury such as inflammation, ballooning, degeneration, and/or fibrosis, is generally essential for making a diagnosis of NASH. However, its diagnostic criteria have not yet been established. The pathologic findings of NASH and related diseases, and the grading system currently in use are reviewed herein. (Korean J Hepatol 2009;15:122-130)

Citations

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Original Articles

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.

Abstract
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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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Relationship between the Severity of Liver Damage and the Serum Leptin Level for Nonalcoholic Fatty Liver Disease: Kyoung Oh Kim, M.D., Sang Hoon Park, M.D., Cheol Hee Park, M.D., Tai Ho Han, M.D., Kyo-Sang Yoo, M.D., Jong Hyeok Kim, M.D., Myung Seok Lee, M.D., Dong Jun Kim, M.D., Choong Kee Park, and Hyun-Deuk Cho, M.D.1; Korean J Hepatol 2005;11(1):51-58.

Abstract
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Background/Aims
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of conditions that are mainly characterized histologically by macrovesicular hepatic steatosis. There are two histologic patterns of NAFLD: simple steatosis alone and steatohepatitis. The factors leading from simple steatosis to nonalcoholic steatohepatitis (NASH) are still obscure. The datas from several studies have suggested that leptin could be involved in the progression from hepatic steatosis to steatohepatitis including the fibrosis. We evaluated serum leptin levels in patients with NAFLD to determine whether any relationships existed between the leptin levels and the severity of hepatic inflammation or fibrosis. Methods: We studied 62 patients with NAFLD who were diagnosed at the Hallym University Sacred Heart Hospital from July 2001 to May 2004. We measured the serum leptin level in all cases and liver biopsy samples were obtained from 31 cases. The liver biopsy specimens were graded according to methods described by Brunt. Spearman rank correlations were used to detect the associations between the serum leptin and the various anthropometric and biochemical variables. The relationship between the histologic severity and the serum leptin level was evaluated with logistic regression analysis. Results: Serum leptin levels correlated with insulin, c-peptide, ALT and homeostasis model assessment insulin resistance, but not with BMI, age and gender. Serum leptin level also correlated with hepatic fibrosis, but not with hepatic steatosis or inflammation. However, the serum leptin level was not a significant independent predictor of the grade of hepatic steatosis, inflammation and fibrosis on the univariate analysis. Conclusions: The serum leptin level was not an independent predictor of the severity of liver damage in NAFLD. (Korean J Hepatol 2005;11:51-58)

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Antioxidant Status in Nonalcoholic Steatohepatitis: Kyung Sik Park, M.D., Byoung Kuk Jang, M.D., Ki Min Kwon, M.D., Woo Jin Chung, M.D., Kwang Bum Cho, M.D., Jae Seok Hwang, M.D., Sung Hoon Ahn, M.D., Kyo Cheol Mun, M.D.1 and Young Hwan Kim, M.D.2; Korean J Hepatol 2005;11(2):135-143.

Abstract
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Background/Aims
Nonalcoholic steatohepatitis (NASH) is chronic liver disease that can potentially progress to end stage liver disease. Oxidative stress to the vulnerable fatty liver has been reported as a key mechanism in development of NASH. Several antioxidant pathways have been identified, but reports that involved quantitative analysis of each antioxidant systems are rare, and these reports have shown various results. So, we investigated antioxidant status and the degree of oxidative stress by measuring several antioxidant enzymes, the total antioxidant status (TAS), and the metabolites of superoxide in NASH patients. Methods: Nineteen NASH patients who were confirmed by liver biopsy and fifteen controls were involved in this study. The levels of body mass index (BMI), AST, ALT, superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase, TAS, hydrogen peroxide (H₂O₂), and malondialdehyde (MDA) were compared between both groups. The relationship between the histologic severity and the levels of each antioxidants were analyzed in the NASH group. Results: The activities of SOD and catalase were lower in the NASH group. The concentrations of TAS and H₂O₂ were higher in NASH group. The level of GPx and MDA showed no significant differences between both groups. There were no significant relationships between the above variables and the pathological severity. Conclusions: The disturbed metabolism of superoxide due to the decreased activities of SOD and catalase seem to be important in the pathogenesis of NASH. Further investigations about the nonenzymatic secondary antioxidant mechanism are necessary because the TAS was higher for the NASH group. The lack of difference between both groups for the concentration of MDA indicates that mechanisms other than lipid peroxidation also may be important in the pathogenesis of NASH. (Korean J Hepatol 2005;11:135-143)