Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapy by pegylated interferon-alpha (PEG-IFN-alpha), lamivudine and adefovir have significantly improved treatment perspectives for patients with chronic hepatitis B. New nucleos(t)ide analogues should permit the development of more effective combination therapies. In autoimmune hepatitis, if there is no response or an intolerance to therapy with prednisone and imurek, administration of mycophenolate mofetil should be envisaged. Ursodeoxycholic acid (UDCA) therapy, at a dosage of 13-15 mg/ kg/day, remains the treatment of choice for primary biliary cirrhosis and should be administered at an early stage to improve patients' survival. In the treatment of nonalcoholic fatty liver disease, thiazolidinediones show considerable promise, but further clinical studies are required in order to prove their efficacity and safety.
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PMID:[Hepatology]. 1649 65

Liver steatosis is highly prevalent in chronic hepatitis C virus (HCV) infection, especially in patients infected with genotype 3 virus, but its significance for the outcome of antiviral treatment is not fully understood. We have monitored steatosis in liver biopsies from 231 patients with chronic HCV infection who received pegylated recombinant interferon-alpha and ribavirin in a phase III study (DITTO trial). The degree of steatosis, along with relevant metabolic parameters, was correlated with the early disappearance of virus and with the final outcome of treatment. Our data suggest that the presence of steatosis impairs the early reduction of viral load during treatment in patients infected with HCV genotype 3 and non-3. Steatosis negatively affected the final outcome of treatment mainly in patients infected with HCV genotype non-3 virus. Based on these findings, we propose that interventions aiming at reducing hepatic steatosis prior to the onset of antiviral therapy may be of benefit to patients infected with HCV of the non-3 genotypes. Patients infected with genotype 3, on the other hand, should be offered early antiviral treatment.
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PMID:Impact of hepatic steatosis on viral kinetics and treatment outcome during antiviral treatment of chronic HCV infection. 1721 41

Clinical progression of chronic hepatitis C depends on several cofactors, which also have a negative affect on the rate of response to interferon-alpha-based therapy. Given the current worldwide prevalence of the metabolic syndrome, the impact of obesity and insulin resistance, and of their histopathological correlate, hepatic steatosis, on the natural history and management of chronic hepatitis C is undoubtedly very important. We will review some of the current knowledge on the clinical consequences of overweight/obesity, steatosis and insulin resistance on chronic hepatitis C, and discuss how this issue may be dealt with in clinical practice.
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PMID:Impact of obesity, steatosis and insulin resistance on progression and response to therapy of hepatitis C. 1973 24

Infection with hepatitis C virus (HCV) primarily causes chronic liver disease with characteristic histopathologic features, including hepatic steatosis. Moreover, chronic hepatitis C is also closely related to insulin resistance (IR) and an increased risk of type 2 diabetes mellitus (DM). This review summarizes the available clinical evidence for a linkage of chronic HCV infection and developing IR or DM that comprises (i) retro- and prospective clinical studies, (ii) the excess risk of chronic hepatitis C patients to develop DM compared to hepatitis B patients, (iii) a preferential relationship of IR with HCV type-1, -2 or -4 infections, (iv) a correlation between IR, viral load and responsiveness to antiviral treatment and (v) a decreased incidence of DM in chronic hepatitis C after sustained virological response. This review further refers to the clinical evidence of a preferential relationship between hepatic steatosis and HCV type-3 infection, and that two distinct genotype-specific pathogenic mechanisms underlie steatosis in hepatitis C. In HCV type-3 infections, steatosis is related to viral load but not to metabolic factors, and, thus, is termed 'viral steatosis'. In HCV type-1, -2 or -4 infections, steatosis appears to be secondary to IR and regarded as 'metabolic steatosis'. In conclusion, multiple lines of clinical evidence support a linkage of HCV infection and both hepatic carbohydrate and lipid metabolism. The extent to which targeting the host's metabolism by drugs or by lifestyle change translates into an improvement of health or in a better response to interferon-alpha will provide further valuable insights into virus-host interactions, and is topic which is currently addressed in clinical studies.
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PMID:Hepatitis C virus, diabetes and steatosis: clinical evidence in favor of a linkage and role of genotypes. 2046 Sep 24