A study conducted 15-year ago showed that only 13.5% of chronic alcoholics developed alcohol-induced liver damage, which misled some people to believe a lack of relationship between the amount of alcohol and the occurrence of liver disease. However, it is true that a significant correlation exists between per capita consumption and the prevalence of cirrhosis. Alcoholic fatty liver is observed in most of chronic alcoholics even though the severity is not uniform. Abstinence remains the cornerstone of therapy for alcoholic liver disease (ALD). There is also consensus for the use of corticosteroids and pentoxifylline in severe alcoholic hepatitis maintaining good nutritional status to treat comorbidities in all forms of ALD, and liver transplantation in the end-stage ALD patients who can stop drinking for 6 months pre-transplantation period. Several clinical trials targeting tumor necrosis factor (TNF-alpha) and reducing oxidative stress have not been successful at this time. There is still a large field of alcohol research to explore in order to go farther in the area of pathophysiology. We need to understand a role of various cytokines and immune cells in the development of ALD to have more treatment tools to cope with ALD.
Alcohols/metabolism ; Cytochrome P-450 CYP2E1/metabolism ; Fatty Liver, Alcoholic/pathology/therapy ; Humans ; Liver Cirrhosis, Alcoholic/pathology/therapy ; Liver Diseases, Alcoholic/*etiology/pathology/therapy ; Oxidative Stress

Humans ; Non-alcoholic Fatty Liver Disease/drug therapy* ; Hypoglycemic Agents/therapeutic use* ; Liver Cirrhosis/pathology* ; Biopsy ; Patients ; Liver/pathology* ; Fibrosis

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing rapidly with the obesity and diabetes mellitus epidemics. It is rapidly becoming the most common cause of liver disease worldwide. NAFLD can progress to serious complications such as cirrhosis, hepatocellular carcinoma and death. Therefore, it is important to recognise this condition so that early intervention can be implemented. Lifestyle modifications and strict control of metabolic risk factors are the mainstay of treatment. As disease progression is slow in the majority of NAFLD patients, most can be managed well by primary care physicians. NAFLD patients with advanced liver fibrosis should be referred to specialist care for further assessment.
Carcinoma, Hepatocellular ; pathology ; Diet ; Disease Progression ; Humans ; Life Style ; Liver ; pathology ; Liver Cirrhosis ; pathology ; Liver Neoplasms ; pathology ; Metabolic Syndrome ; complications ; Non-alcoholic Fatty Liver Disease ; diagnosis ; therapy ; Obesity ; complications ; Prevalence ; Risk Factors ; Treatment Outcome

Liver fibrosis is a slow, insidious process involving accumulation of extracellular matrix protein in the liver. The stage of liver fibrosis in chronic liver disease (CLD) determines overall morbidity and mortality; the higher the stage, the worse the prognosis. Noninvasive composite scores can be used to determine whether patients with CLD have significant or advanced fibrosis. Patients with low composite scores can be safely followed up in primary care with periodic reassessment. Those with higher scores should be referred to a specialist. As the epidemic of diabetes mellitus, obesity and non-alcoholic fatty liver diseases is rising, CLD is becoming more prevalent. Easy-to-use fibrosis assessment composite scores can identify patients with minimal or advanced fibrosis, and should be an integral part of decision-making. Patients with cirrhosis, high composite scores, chronic hepatitis B with elevated alanine aminotransferase and aspartate aminotransferase, or deranged liver panel of uncertain aetiology should be referred to a specialist.
Alanine Transaminase ; blood ; Aspartate Aminotransferases ; blood ; Decision Making ; End Stage Liver Disease ; complications ; diagnosis ; therapy ; Hepatitis B ; complications ; Humans ; Liver ; pathology ; Liver Cirrhosis ; complications ; diagnosis ; therapy ; Non-alcoholic Fatty Liver Disease ; complications ; diagnosis ; therapy ; Prognosis ; Referral and Consultation ; Treatment Outcome

No abstract available.
Antiviral Agents/therapeutic use ; Ascites/diagnosis/prevention & control/therapy ; Cholagogues and Choleretics/therapeutic use ; Fatty Liver/diagnosis/diet therapy ; Fatty Liver, Alcoholic/diagnosis/drug therapy ; Hemorrhage/prevention & control/therapy ; Hepatic Encephalopathy/diagnosis/prevention & control/therapy ; Hepatitis B, Chronic/diagnosis/drug therapy ; Hepatitis C, Chronic/diagnosis/drug therapy ; Humans ; Liver Cirrhosis/*diagnosis/drug therapy/pathology/*therapy ; Liver Cirrhosis, Biliary/drug therapy ; Vasodilator Agents/therapeutic use

OBJECTIVETo investigate the therapeutic effect of Corbrin shugan capsule for treatment of alcoholic hepatic fibrosis in rats.

METHODSThe rat model of alcoholic hepatic fibrosis was induced by intragastric administration of alcohol repeatedly. The serum procollagen III (PC III), laminin (LN) and tissue inhibitors of metalloproteinase-1 (TIMP-1) levels were measured with ELISA, and the content of hydroxyproline (Hyp) in liver tissue were determined with colorimetric method. Collagen deposition in liver tissue was observed with Masson's staining, and the fibrosis area was measured with digital medical image analysis system (Motic Med 6.0).

RESULTSCompared with the model control group, the serum TIMP-1 and LN levels and hepatic fibrosis area in liver tissue significantly decreased in Corbrin shugan capsule groups with doses of 0.09,0.27 and 0.45 g*kg(-1), and the serum PC III and the Hyp contents in liver tissue also decreased of Corbrin shugan capsule groups with doses of 0.27 and 0.45g*kg(-1).

CONCLUSIONCorbrin shugan capsule can decrease serum PC III, TIMP-1 and LN levels and Hyp levels in liver tissue and hepatic fibrosis area in rats, indicating it may have therapeutic effect on alcoholic hepatic fibrosis.

Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; therapeutic use ; Hydroxyproline ; metabolism ; Laminin ; blood ; Liver ; metabolism ; pathology ; Liver Cirrhosis, Alcoholic ; drug therapy ; metabolism ; pathology ; Male ; Procollagen ; blood ; Rats ; Tissue Inhibitor of Metalloproteinase-1 ; blood

OBJECTIVETo observe the apoptosis of hepatic stellate cell (HSC) and hepatocyte and the effect of Qinggan Huoxue Recipe (QHR) on it in alcoholic liver fibrosis (ALF) rats.

METHODSRats were divided into six groups: the normal group, the model group, the QHR low dose (4.75 g/(kg x d)], medium dose (14.25 g/(kg x d)] and high dose (28.5 g/(kg x d)) groups, and the Essentiale (66.5 mg/(kg x d)] group. They were treated with respective drugs through gavage for 2 weeks, while the normal and model groups were given normal saline instead. The serum levels of ALT, AST and gamma-GT were measured by chromatometry, the degree of inflammation and fibrosis was observed by HE staining and Masson staining, and the apoptosis of hepatocyte and HSC were detected by TUNEL and TUNEL-alpha-SMA double immunolabeling respectively.

RESULTSCompared with those before treatment, the serum levels of ALT, AST and gamma-GT obviously decreased (P < 0.05), inflammation and fibrosis relieved (P < 0.05), and the apoptosis of hepatocyte reduced (P < 0.05), while that of activated HSC increased in the QHR groups after treatment (P <0.05).

CONCLUSIONQHR can effectively relieve hepatic fibrosis, decrease hepatocyte apoptosis caused by alcohol and induce activated HSC apoptosis in ALF rats.

Actins ; analysis ; Animals ; Apoptosis ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Hepatic Stellate Cells ; drug effects ; metabolism ; pathology ; Hepatocytes ; drug effects ; metabolism ; pathology ; Immunohistochemistry ; In Situ Nick-End Labeling ; Liver ; drug effects ; metabolism ; pathology ; Liver Cirrhosis, Alcoholic ; drug therapy ; metabolism ; pathology ; Male ; Muscle, Smooth ; chemistry ; Phytotherapy ; Rats ; Rats, Wistar