Autoimmune HEPATITIS (AIH) is one of causes of chronic liver diseases. It is an unresolving inflammation of liver tissue and characterized by elevated transaminases, hypergammaglobulinemia, and circulating autoantibodies. The disorder occurs mostly in females (F:M ratio is 3.6 to 1) and is a relatively uncommon disorder with point prevalence of 8-16.8 per 100 000 population in western countries. Hiostologic hallmarks are interface HEPATITIS (also called piecemeal necrosis), and portallymphoplasmacytic infiltration.Dignostic criteria are based on excluding other etiologies of chronic liver disease,such as viral hepatic (A, B, C), metabolic disorders eg Wilson disese,drug induced HEPATITIS and ALCOHOLIC liver disease. Conventional autoantibodies are Antinuclear antibody (ANA), Smooth muscle antibody (SMA) and Anti liver kidney microsomal 1 (Anti LKM1).Some cases have combined clinical, laboratory or histologic features of Primary Biliary Cirrhosis (PBC) or Primary Sclerosing Cholangitis (PSC) with AIH and are known as overlap syndrome. Standard treatments of AIH as the most successful treated form of chronic HEPATITIS are based on immunosuppression with corticosteroids alone or in combination with azathioprine.

The term "Non- ALCOHOLIC SteatoHEPATITIS (NASH)" is applied when sonographic and pathologic view of liver shows ALCOHOLIC HEPATITIS changes without history of alcohol consumption. Radiologic findings can easily make the diagnosis and liver biopsy confirms the initial suspicion. It is showed that up to 43.5% of patients with asymptomatic abnormal liver transferases levels have some degrees of NASH, which suggest the importance of being familiar with the issue and how to approach and treat it. NASH is commonly accompanied with diabetes mellitus (especially type II), obesity and hyperlipidemia. These findings support the theory in which insulin resistance is the mainstay of NASH pathophysiology. The natural history of NASH is unclear but surely it is far better than ALCOHOLIC related liver disease. It is estimated that up to 8% of patients would meet cirrhosis, considering risk factors such as obesity and features found in biopsy specimen. Steatosis, polymorphonuclear lobular inflammation, ballooning degeneration, hyaline- Mallory bodies and cirrhosis are among different pathologies seen in biopsy. It is important to rule out other chronic liver diseases including drug induced liver disease, chronic viral HEPATITIS, and metabolic and autoimmune liver diseases to establish the diagnosis of NASH. There is no definite treatment for NASH. Therapeutic measures are categorized as reducing risk factors and using hepatocellular protective agents. The former includes weight reduction, treating hyperinsulinemia and diabetes, control of hypertriglyceridemia and leptin. Protective agents are anti-oxidants like vitamin E and/ or C, probucol, silymarin, ursodeoxycholic acid, reducing iron load, N-acetyl cystein, food supplements and cytokines. Increasing rate of NASH is reported among children and adolescences, which could be due to growing amount of obesity in these age groups.

Background: Advanced hepatic fibrosis and cirrhosis has generally been considered to be irreversible. The aim of this study was to determine whether cirrhosis is reversible.Methods: Seven patients with autoimmune HEPATITIS with histologic evidence of cirrhosis were enrolled. After treatment, they had follow-up liver biopsy while in clinical and biochemical remission. Biopsy specimens were randomly coded in unpaired manner according to patient and were read independently by two pathologists using the modified HEPATITIS activity index (with a maximum stage of 6).Results: Three patients still had extensive fibrosis in the second liver biopsy. But four patients had almost total regression of their liver fibrosis. In the latter patients, the mean alanine aminotransferase level decreased from 776.3 U/L to 23 U/L. The mean bilirubin level decreased from 5.85 mg/dL, to 0.98 mg/dL. Extensive fibrosis or cirrhosis were present in all patients at diagnosis but were not present on follow-up liver biopsy. The mean fibrosis score decreased from 5.88 to 0.5 (P=0.0002), and the mean grading score from 11.38 to 2.5 (P=0.0008.).Conclusion: Frank cirrhosis due to autoimmune HEPATITIS may be reversible in some patients who respond to treatment.

Background: ALCOHOLIC HEPATITIS (AH) is an acute manifestation of ALCOHOLIC liver disease with high mortality rates.Objectives: Our aim was to study the molecular mechanisms of AH.Materials and Methods: The differentially expressed genes (DEGs) in liver between AH and control cases were identified by analyzing the GSE28619 microarray data using t-test. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) enrichment analyses were performed using DAVID online tool. The protein-protein interaction (PPI) network was constructed using Search Tool for the Retrieval of Interacting Genes (STRING) and the subnetwork was identified by BioNet. Both PPI network and subnetwork were visualized using the Cytoscape software.Results: Total 908 DEGs (551 up- and 357 down-regulated DEGs) were obtained. The up-regulated DEGs were significantly enriched in 15 pathways and 112 GO biological processes. The down-regulated DEGs were significantly enriched in 22 pathways and 84 GO biological processes. The PPI network with 608 nodes and 2878 interactions was constructed and the subnetwork with 53 nodes and 131 interactions was also identified. The hub DEGs (TSPO, PPIB, NME1 and NME2) were extracted in this subnetwork.Conclusions: TSPO might contribute to the liver damage and AH progression induced by mitochondrial dysfunction through oxidative stress of liver. TSPO interacted with PPIB might play important roles in liver damage in AH. The interaction between NME1 and NME2 might contribute to the transformation from AH to hepatocellular carcinoma.