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PubMed2006

[Mouse NASH model using retinoic acid receptor alpha].

To explore the role of retinoic acid (RA) in the liver, we developed transgenic mice expressing RA receptor a-dominant negative form (RARE) in hepatocytes using albumin promoter and enhancer. The RARE m ice developed microvesicular steatosis andspotty focal necrosis. Mitochondrial beta-oxidation activity of fatty acids and related enzymes were down-regulated, while peroxisomal beta-oxidation and related enzymes were up-regulated. Expression of cytochrome p4504a10, cytochrome p4504a12, and cytochrome p4504a14 was increased. Formation of H2O2 and 8-OHdG was increased. With age, these mice developed liver tumor. Feeding on a high-RA diet reversed histological and biochemical abnormalities and inhibited the occurrence of liver tumors. These results suggest that hepatic loss of RA function leads to the development of steatohepatitis and liver tumors.

Animals↗
PubMed2006

[Drug-induced NASH].

Steatohepatitis is pathologically characterized by zone 3-dominant hepatic steatosis with ballooned hepatocytes and Mallory bodies, zone 3 pericellular and perivenular fibrosis with or without bridging fibrosis, and lobular inflammatory cell infiltration. Alcoholic hepatitis is a prototype of this syndrome, but a variety of diseases such as obesity, diabetes mellitus, Wilson disease and hepatitis C could reveal very similar pathological changes in some occasions. Therefore, well defined diseases need to be excluded in the process of differential diagnosis of steatohepatitis. Pathways possibly involved in the development of drug-induced steatohepatitis were categorized into four and outlines of the possible mechanisms involved in the development of this syndrome were proposed in this article.

Amiodarone↗
PubMed1999

Non-alcoholic steatohepatitis and iron: increased prevalence of mutations of the HFE gene in non-alcoholic steatohepatitis.

BACKGROUND/AIMS: Non-alcoholic steatohepatitis (NASH) is increasingly recognized, and its pathogenesis is believed to involve increased oxidative stress. Elevated levels of serum ferritin and positive liver iron stains are often observed in patients with NASH, and the pathogenesis of liver injury due to iron is also thought to involve oxidative stress. The aim of this study was to determine whether there is an association of NASH and mutations in the HFE gene associated with hereditary hemochromatosis (HHC). METHODS: Clinical, laboratory, and histopathological data on all 57 subjects with a final diagnosis of NASH seen between August 1990 and August 1997 at our Liver Center were analyzed. Thirty-six Caucasian subjects (23 men) with NASH underwent mutational analyses of HFE gene mutations performed. The prevalence of HFE gene mutations was compared to that in 348 Caucasian normal controls. Data were analyzed by both parameteric and non-parametric methods with similar results. RESULTS: One subject (2.8%) with NASH was homozygous for the C282Y mutation and six (16.7%) were heterozygous, compared with 0%, and 11.2%, respectively, of controls. Two (5.6%) subjects with NASH were homozygous for the H63D mutation and 16 (44.4%) were heterozygous, whereas 2.9% and 26.4%, respectively, of controls had these genotypes. The prevalence of heterozygosity (61.1%) for either mutation was significantly higher in subjects with NASH than in controls (38%) (p = 0.008), and the prevalence of homozygosity or heterozygosity combined in NASH subjects (69.4%) was significantly higher than for controls (40.5%, p = 0.001). Sex (63-67% male) and age at diagnosis of NASH did not differ between those with or without HFE mutations, but men with NASH were significantly more likely than women to have the H63D mutation (15/23 vs. 3/13, p<0.05) Levels of serum ferritin, iron, transferrin saturation levels, and the degree of hepatic iron staining were significantly higher (p<0.05) in subjects with NASH who carried an HFE mutation than in those without. Differences in hepatic iron concentrations or hepatic iron indices between NASH subjects with and without HFE mutations were not significant. Those with C282Y mutations had significantly more hepatic fibrosis than those without (p<0.05). Those with HFE mutations had significantly higher levels of serum ALT (90+/-11 [mean +/- SE]) than those without (55+/-6; p = 0.02). CONCLUSION: The prevalences of the HFE gene mutations associated with hereditary hemochromatosis are increased among North American subjects with NASH.

Adult↗
PubMed2005

Difference and similarity between non-alcoholic steatohepatitis and alcoholic liver disease.

BACKGROUND: Non-alcoholic steatohepatitis (NASH) and alcoholic liver disease (ALD) are extremely similar in the pathologic findings and pathogenesis. This study aimed to elucidate the difference and similarity between these diseases. METHODS: Twenty-six patients with NASH and 26 with ALD including 11 with alcoholic hepatitis underwent clinico-pathologic analysis. The visceral fat area and liver/spleen ratio, an index of the hepatic fat content, were evaluated with computed tomography. The hepatic iron deposit and oxidative stress induced-lipid peroxidation were estimated by Prussian blue staining and 3-nitrotyrosine staining, respectively. RESULTS: The most prominent difference between NASH and ALD was the nutritional status, although elevation of AST/ALT ratio and gamma-GT is relatively characteristic of ALD. NASH was more frequently associated with diabetes mellitus as compared with ALD. The BMI and serum levels of total cholesterol and cholinesterase were higher in NASH than in ALD. Although the degree and distribution of fibrosis and necro-inflammatory reaction were similar in NASH and ALD, steatosis was more severe in NASH than in ALD. The liver/spleen ratio was lower and the visceral fat area was larger in NASH than in ALD, regardless of the coincidence of alcoholic hepatitis. Interestingly, the visceral fat area positively correlated with ALT and HOMA-IR in NASH, whereas these correlations were not observed in ALD. The hepatic iron deposit was less in NASH than in ALD, whereas lipid peroxidation in NASH was similar to that in ALD with alcoholic hepatitis and more advanced as compared with that in ALD without alcoholic hepatitis. CONCLUSIONS: NASH was characterized with over-nutrition and visceral fat type obesity as compared with ALD. The visceral fat accumulation was associated with hepatic inflammation and insulin resistance in NASH, but not in ALD. The difference in the nutritional status between NASH and ALD is not only reflected in the clinical features but also may closely associate with the mechanisms of hepatocellular damage in these diseases.

Abdomen↗
PubMed2005

Factors associated with the presence of nonalcoholic steatohepatitis in patients with chronic hepatitis C.

OBJECTIVES: The aim of this study was to identify factors associated with the presence of nonalcoholic steatohepatitis (NASH) in patients with chronic hepatitis C (CHC). METHODS: We studied 98 patients with CHC [47 with NASH (group HCV/NASH), 51 without NASH (group HCV)] and 85 with NASH not infected with hepatitis C virus (HCV) (group NASH). We determined factors associated with the presence of NASH in patients with hepatitis C. RESULTS: Group HCV/NASH patients resembled those with NASH. Body mass index (BMI) was higher in group HCV/NASH than in group HCV, but was similar to group NASH. Most HCV/NASH patients had risk factors for NASH. In patients infected with HCV, NASH and NASH-related lesions were independently associated with BMI, while steatosis score was associated with HCV genotype 3 and BMI. Fibrosis stage was independently associated with steatosis, necroinflammatory activity index, and NASH lesions. CONCLUSION: While HCV genotype 3 infection and BMI are associated with the presence of steatosis in CHC, BMI is the only factor independently associated with the presence of NASH in these patients. We suggest that overweight-related factors might induce NASH in CHC patients.

Adult↗
PubMed2001

Frequency of nonalcoholic steatohepatitis as a cause of advanced liver disease.

Although nonalcoholic steatohepatitis (NASH) has generally been considered a benign condition, the increasing prevalence and severity of obesity has heightened concerns about the frequency with which NASH progresses to end-stage liver disease. The aim of this study is to determine the frequency, clinical features, and posttransplantation history of decompensated liver disease secondary to NASH. The frequency of NASH as a cause of end-stage liver disease was prospectively determined in patients evaluated for liver transplantation. NASH was considered to be the primary cause of liver disease in patients who had histological evidence of steatohepatitis and in whom chronic liver diseases other than NASH were excluded. Posttransplantation histological characteristics were also determined in patients with NASH and compared with those of patients with pretransplantation diagnoses of cholestatic liver diseases, alcoholic disease, and hepatitis C. Of 1,207 patients evaluated for liver transplantation during the study period, 31 patients (2.6%) had NASH as the primary cause of liver disease. In the same period, 546 liver transplantations were performed, 16 of which (2.9%) were for end-stage disease secondary to NASH. Posttransplantation steatosis was seen in 60% of transplant recipients with NASH versus 5% of those with cholestatic disease, 15% of those with alcoholic disease, and 15% of those with hepatitis C. Steatohepatitis recurred in 33% of transplant recipients with NASH, with progression to cirrhosis in 12.5%. NASH can progress to end-stage liver disease in a minority of affected patients and was the primary cause of liver disease in 2.9% of patients evaluated for liver transplantation at our center. Recurrence of steatosis and NASH is frequent and can be severe after liver transplantation.

Adult↗
PubMed2004

Comparison of hepatocellular carcinoma patients with alcoholic liver disease and nonalcoholic steatohepatitis.

BACKGROUND: Alcoholic hepatitis and nonalcoholic steatohepatitis (NASH) show different clinical features with similar liver histology, but both disorders may progress to cirrhosis and hepatocellular carcinoma (HCC). HCC arising in alcoholic liver disease (ALD) or NASH, without hepatitis B or C virus infection, has been a rare observation, and there are no studies comparing the characteristics of ALD and NASH patients with HCC. Therefore, we compared the characteristics of ALD and NASH patients with HCC. METHODS: A total of 1202 patients received a diagnosis of HCC at Tokyo Women's Medical University from 1989 to 2003, and their clinical data were collected prospectively. A clinical diagnosis was made to diagnose ALD, and clinical and histological changes were required to diagnose NASH. Of these patients, 88 received a diagnosis of HCC arising from ALD. Among them, a biopsy specimen was obtained in 50 patients (ALD-HCC group). We compared the clinical and histological characteristics of 50 ALD and 8 NASH patients (NASH-HCC group) associated with HCC. They all were negative for hepatitis virus infection by serological methods. RESULTS: The most significant difference between these groups was sex. Women were significantly more common in the NASH-HCC group (6% vs. 63%; p < 0.0001). The median age was 65 years in the ALD-HCC group and 68 years in the NASH-HCC group. The risk factors for NASH all were high in the NASH-HCC group. However, liver function tests were similar in these groups. In the ALD-HCC group, 46 (92%) patients showed severe fibrosis; 2 had septal fibrosis and 44 had cirrhosis. All patients in the NASH-HCC group showed severe fibrosis, and seven had cirrhosis. CONCLUSIONS: Severe fibrosis might be an important risk factor for HCC. Patients who have ALD or NASH with cirrhosis may develop HCC. This seems to occur in a sufficient number of cases to warrant regular screening for this complication.

Adult↗
PubMed2003

Prevalence and predictors of asymptomatic liver disease in patients undergoing gastric bypass surgery.

BACKGROUND: Nonalcoholic steatohepatitis (NASH) is a form of fatty liver disease that is increasingly recognized. There are limited data on the prevalence of NASH and the role of risk factors for NASH among the morbidly obese. HYPOTHESIS: The prevalence of asymptomatic NASH among morbidly obese patients undergoing gastric bypass surgery is high, and there are identifiable risk factors for NASH. DESIGN: Prospective case study. SETTING: University hospital. PATIENTS: Forty-eight consecutive patients undergoing gastric bypass surgery who had a concurrent open liver biopsy. Exclusion criteria included current consumption of more than 2 alcohol beverages monthly and known cirrhosis. A hepatopathologist blinded to clinical data reviewed biopsy specimens. MAIN OUTCOME MEASURES: The presence of NASH or severe fibrosis, preoperative body mass index (BMI) (calculated as weight in kilograms divided by the square of height in meters), fasting triglyceride level, and presence of type 2 diabetes mellitus (DM). RESULTS: Patients (mean +/- SD age, 42 +/- 10 years; 33 women) had an initial mean BMI of 59.9 +/- 12. Thirty-one patients (65%) had moderate to severe steatosis. Only 6 (12%) had advanced fibrosis. Sixteen (33%) had evidence of NASH. There was no difference in mean age, sex, BMI, or fasting triglyceride level between patients with and without NASH or advanced fibrosis. The odds of NASH were 128 times greater (95% confidence interval [CI], 5.2-3137.0) and the odds of severe fibrosis 75 times greater (95% CI, 4.5-1247.0) in patients with DM than in those without DM. Preoperative BMI was not independently associated with NASH (odds ratio, 1.01; 95% CI, 0.9-1.1) or severe fibrosis (odds ratio, 0.9; 95% CI, 0.86-1.02) after adjustment for DM. CONCLUSIONS: Moderate to severe hepatic steatosis and NASH are common among individuals undergoing gastric bypass procedures. Diabetes mellitus but not BMI is associated with NASH and advanced hepatic fibrosis in these patients.

Adult↗