Steatohepatitis: comparison of alcoholic and non-alcoholic subjects with particular reference to portal hypertension and hepatic complications.
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Obesity is the most important risk factor associated with non-alcoholic steatohepatitis, which is caused by to impaired insulin activity, overflow of portal triglycerides, and production of inflammatory cytokines; all of these are deleterious to hepatocytes. These phenomena facilitate disruptions in hepatic physiology, as observed in alcoholic hepatitis; however, consumption of this substance is absent. Non-alcoholic steatohepatitis has had a great impact due to the fact that previously, main cases of cryptogenic cirrhosis actually were attributed to this disease. Despite advances in understanding the pathophysiologic process of the disease, there is no better treatment than weight reduction (a combination of diet and exercise). In this issue, we describe the most important topics with regard to non-alcoholic steatohepatitis and the obesity-related process.
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<i>Background and Aims:</i> Alcoholic liver disease continues to be a major health problem with respect to both morbidity and mortality. To understand the clinical syndromes of alcoholic liver disease, this review highlights the papers on both clinical and basic research of alcoholic liver disease, especially on steatosis, alcoholic hepatitis and fibrosis. <i>Methods:</i> The various forms of alcoholic liver disease are described, and knowledge about the clinical and pathophysiological features of different stages of alcoholic liver disease are summarized. <i>Results:</i> Clinical studies combined with basic research have established a spectrum of alcoholic liver disease from steatosis to steatohepatitis, fibrosis, and cirrhosis. New insights into the pathogenesis of alcoholic liver disease include the key roles of the excess production of cytokines, reactive oxygen species, and the shortage of protective mediators, including adiponectin. <i>Conclusion:</i> These new insights will lead to new specific therapies for the treatment of alcoholic hepatitis and alcoholic liver fibrosis.
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Fatty liver diseases, non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) are the most common causes of chronic liver disease around the world. NAFLD and ALD can progress towards a more severe form of the disease, including as non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH). In both instances central pathogenic events include hepatocyte death, liver inflammation, pathological angiogenesis, and fibrosis, followed by cirrhosis and cancer. Over the last few years, extracellular vesicles (EVs) have been identified as effective cell-to-cell communicators that contain a cell- and stress-specific cargo from the cell of origin and are capable of transferring this cargo to a target or acceptor cell. In this review, we focus on the growing evidence supporting a role for EVs in the pathophysiology of NASH and ASH as well as their potential roles as targets for novel biomarkers for these conditions.
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Non-alcoholic steatohepatitis (NASH) is a disease of unknown origin characterized histologically by alcoholic-like liver injury in the absence in the absence of significant alcohol intake. This study was conducted to assess the clinical and pathological features of NASH patients in Iran. Patients with elevated liver transaminases, negative serologic markers of viral or autoimmune hepatitis and no findings in favor of metabolic liver disease were enrolled. A careful history was taken with special attention to alcohol intake and ultrasonography and liver biopsy were performed in those with no evidence of significant alcohol intake. A histology showing moderate to gross macrovesicular fatty change with inflammation (lobular or portal), with or without Mallory bodies, fibrosis, or cirrhosis, was considered diagnostic for NASH. Patients with mild steatosis were rechecked for the presence of hepatitis C virus (HCV) infection. Fifty-three patients who met the above criteria entered the study. Thirty-two patients (60.4%) were male and 21 (39.6%) were female with the mean age of 37.8±11.3 years. Twenty-six patients (55.3%) were diabetic. Mean AST to ALT ratio was 0.95±0.52; 65.3%of patients had a ratio below than 1, and 95.9% were below of 2. Ultrasonography was abnormal in 32 (76.2%) patients. Liver biopsy showed mild steatosis in 35.7% moderate steatosis in 53.6% and severe forms in 10.7%. In 80.2% of patients, portal inflammation was present, and 15.1% had some degrees of fibrosis. The amount of increase in liver enzymes bore no relationship with the presence of fibrosis, portal inflammation, and degree of steatosis (P>0.05). The patients wee somewhat younger than other studies, and most of them were male which might be due to the low rate of alcohol consumption in our country. Most of the patients had body mass index (BMI) higher than normal. Our findings show that NASH must not be considered a disease confined to high-risk groups only, and its impact be larger than what is generally considered.
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Mechanisms for non-alcoholic steatohepatitis (NASH) development are under investigation in an era of increased prevalence of obesity and metabolic syndrome. Previous findings have pointed to the role of adipose tissue, adipose tissue macrophages and their secretory products in the development of a chronic inflammatory status inducing insulin resistance and a higher risk of liver steatosis called non-alcoholic fatty liver disease. The activation of resident macrophages [Kupffer cells (KC)] and the recruitment of blood derived monocytes/macrophages into the diseased liver have now been identified as key elements for disease initiation and progression. Those cells could be activated through gut flora modifications and an altered gut barrier function but also through the internalization of toxic lipid compounds in adjacent hepatocytes or in KC themselves. Due to the role of activated KC in insulin resistance, fibrosis development and inflammation amplification, they became a target in clinical trials. A shift towards an anti-inflammatory KC phenotype through peroxisome proliferator activator-receptorδ agonists, an inhibition of macrophage recruitment through anti-C-C chemokine receptor 2 action and a specific blocking of internalization of toxic lipoxidation or glycation compounds into KC by galectin-3 receptor inhibitors are now under investigation in human NASH.
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Objective
To investigate the expression and significance of Golgi protein 73 (GP73) in alcoholic cirrhosis.
Methods
From March 2015 to August 2017, 163 patients with alcoholic liver disease in the No.541 General Hospital were selected, including 51 patients with alcoholic fatty liver, 62 patients with alcoholic hepatitis, 50 patients with alcoholic liver cirrhosis, and 70 healthy volunteers were selected as control group.The liver function and the level of GP73 were detected.
Results
The GP73 level in the alcoholic liver cirrhosis group was (210.16±40.11)ng/mL, which was higher than that of the control group[(46.24±12.24)ng/mL], alcoholic fatty liver group [(85.10±20.43)ng/mL] and alcoholic hepatitis group[(160.18±32.05)ng/mL] (t=15.822, 30.022, 23.212, all P 0.05). After treatment, the GP73 levels of effective patients in the alcoholic fatty liver group, alcoholic hepatitis group and alcoholic liver cirrhosis group were (54.16±11.18)ng/mL, (104.11±28.46)ng/mL, (122.03±30.54)ng/mL, respectively, which were lower than that of the ineffective patients (t=-4.600, -5.081 and -4.100, all P<0.05).
Conclusion
The GP73 level is significantly elevated in alcoholic liver disease.In alcoholic cirrhosis, GP73 level is the highest, has a certain relationship with the liver function index GGT, Alb and the therapeutic effect.
Key words:
Golgi apparatus; Liver cirrhosis, alcoholic; Fatty liver, alcoholic; Hepatitis, alcoholic; Aspartate aminotransferases; Alkaline phosphatase; gamma-Glutamyltransferase; Bilirubin
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The aim of the study was to compare the features of immune response in patients with alcoholic liver disease and non-alcoholic steatohepatitis.There was investigated immune status of 46 patients with alcoholic liver disease and 34 patients with non-alcoholic steatohepatitis.It was found the resemblance of the immune regulation of pathogenesis in both diseases. It was also established that in the history of alcoholic liver disease necrosis starts earlier because of loosing immune regulation of programmed cell death. This leads to forming liver cirrhosis in younger age.
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Alcoholic Hepatitis
Pathogenesis
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Steatohepatitis
Steatosis
Hyperlipidemia
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