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)

Obesity and the metabolic syndrome have hepatic manifestations, including steatosis and progression of fibrosis. In individuals with chronic hepatitis C, obesity is associated with inflammation, insulin resistance, steatosis, progression of fibrosis, and nonresponse to treatment with interferon or peginterferon alpha and ribavirin. Patients with both hepatitis C and obesity-related nonalcoholic fatty liver disease are at greater risk for more advanced liver disease. We review the mechanisms by which obesity may be associated with decreased efficacy of interferon-based therapies in individuals with chronic hepatitis C and the therapeutic strategies that may increase the effectiveness of these therapies in obese individuals.
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PMID:Impact of obesity on treatment of chronic hepatitis C. 1672 27

Hepatitis C infection is associated with the development of hepatocellular carcinoma, and progress has been made in a number of areas. Transgenic mice lines expressing the hepatitis C core protein develop hepatic steatosis, adenomas, and hepatocellular carcinomas, with no significant hepatitis or fibrosis. This implies that hepatitis C can lead directly to malignant transformation. A new lesion, irregular regeneration, has been described in chronic hepatitis C infection and is associated with a 15-fold increase in the relative risk of developing hepatocellular carcinoma. A minority of patients with hepatitis C-related hepatocellular carcinoma have intense lymphocytic infiltration of the cancer, a feature associated with a better prognosis. Several studies have confirmed the association between large cell dysplasia and hepatocellular carcinoma. However, large cell dysplasia may not be a premalignant lesion and instead may be a marker for premalignant alterations elsewhere in the liver. Oral contraceptives previously have been linked to an increased risk of hepatocellular carcinoma. A large multicenter European case-control study has shown minimal increased risk of hepatocellular carcinoma with use of steroidal contraception. Tamoxifen had shown promise in the management of advanced hepatocellular carcinoma. However, a randomized placebo-controlled study of 477 patients with hepatocellular carcinoma found no benefit from tamoxifen. In a preliminary study, however, octreotide has shown improved survival and quality of life in patients with advanced hepatocellular carcinoma. Finally, interferon treatment continues to be linked to a reduced risk of hepatocellular carcinoma in patients with hepatitis C. These studies generally are not randomized, and a randomized prospective study is required to address this issue.
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PMID:Hepatocellular carcinoma. 1702 53

Both diabetes and chronic hepatitis C virus (HCV) infection are common conditions that often coexist in the same subject. Studies seem to confirm the presence of an association between them. Mechanisms leading to HCV-induced insulin resistance and glucose intolerance are beginning to be elucidated. Insulin resistance in the setting of chronic HCV infection could be related etiologically to viral factors but is also often seen with concomitant nonalcoholic fatty liver disease, the hepatic manifestation of the metabolic syndrome. Insulin resistance decreases the likelihood of response to interferon-based therapies and may be an independent risk factor for the progression of HCV-related liver disease.
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PMID:Mechanisms of glucose intolerance in patients with chronic hepatitis C: implications for treatment. 1732 47

Recurrence of hepatitis C virus (HCV) following liver transplantation (LT) is universal. A subset of these patients develop advanced fibrosis and cirrhosis and it is believed that this leads to increased posttransplantation mortality. The specific aims of this study were to determine the incidence of advanced fibrosis and those factors associated with this process, and to evaluate causes for mortality in patients with recurrent HCV. A total of 227 patients who underwent LT with chronic HCV were monitored prospectively. The mean age of this group at LT was 49.5 yr; 76% were male and 85% were Caucasian. Fibrosis progression was monitored by protocol liver biopsy, initially performed 6 months after LT and then at 6- to 24-month intervals. Advanced fibrosis, defined as the bridging fibrosis or cirrhosis, developed in 1%, 11%, 25%, and 41% of patients after 1, 3, 5, and 6-10 yr, respectively. Acute cellular rejection hepatic steatosis, a persistent elevation in serum alanine aminotransferase and donor-race were associated with the development of advanced fibrosis. In contrast, the development of advanced fibrosis was not affected by the use of interferon prior to undergoing LT, cytomegalovirus disease, or donor age. A total of 60 patients (26%) died over 15 yr of follow-up. Although graft failure accounted for 45% of deaths in patients with advanced fibrosis, this represented only 8% of all deaths in patients with recurrent HCV. Sepsis was the most common cause of death and this was observed with similar frequency in patients who developed advanced fibrosis (45%) and in those with less advanced fibrosis (47%). In conclusion, approximately 41% of patients with recurrent HCV developed advanced fibrosis 6-10 yr after LT. However, complications associated with sepsis, not recurrent cirrhosis, was the most common cause of death in patients with recurrent HCV and this was similar in patients with or without advanced fibrosis.
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PMID:A prospective evaluation of fibrosis progression in patients with recurrent hepatitis C virus following liver transplantation. 1760 Mar 60

Latinos are the largest minority in the USA and have higher rates of HCV infection. The course of chronic hepatitis C in Latinos is more aggressive, with higher risk to develop cirrhosis than any other ethnic group or race. Available information suggests that more rapid progression of liver disease is aggravated by decreased efficacy to treatment with available therapies. The causes for more aggressive progression and decreased efficacy of treatment are complex. Factors related to metabolic syndrome, insulin resistance, and hepatic steatosis are important, as well as genetic differences, not only for metabolic syndrome but for immune responses to interferon. In addition, there are substantial barriers for Latinos to access medical care. Language, cultural differences, and socioeconomic factors, including lack of medical insurance, more frequent use of alcohol, and possible medical care provider bias, are significant obstacles to diagnosis and treatment. The severity of the liver disease and the association to metabolic syndrome medical conditions justify that Latinos be considered a special population with urgent need of intervention strategies. In this article we present all the available evidence on epidemiology, natural history of chronic hepatitis C, and efficacy of anti-HCV therapy in Latinos infected with HCV.
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PMID:Latinos and chronic hepatitis C: a singular population. 1845 93

Steatosis is a common feature of many liver diseases, namely non-alcoholic steatohepatitis (NASH) and hepatitis C virus (HCV) infection, but the pathogenic mechanisms differ. Insulin resistance (IR), a key feature of metabolic syndrome, is crucial for NASH development, associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to fibrosis. This may have potential implications for new drug therapy. In HCV-related disease, steatosis impacts both fibrosis progression and response to treatment. Steatosis in HCV-related disease relates to both viral factors (HCV genotype 3), and host factors (alcohol consumption, overweight, hyperlipidemia, diabetes). Among others, IR is a recognized factor. Hepatic steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its receptors. Thus, hepatic steatosis should not be considered a benign feature, but rather a silent killer.
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PMID:Hepatic steatosis: a benign disease or a silent killer. 1863 54

Emerging attention has been paid to metabolic syndrome, which comprises several metabolic disorders including visceral obesity, diabetes mellitus, dyslipidemia, and hypertension. Whether the severity of each disease is mild to moderate, the comorbidity of these metabolic disorders has a serious impact on the development of atherosclerosis. Nonalcoholic fatty liver disease (NAFLD) is the major hepatic disorder in patients with metabolic syndrome, and indeed it is the most common cause of abnormal liver function tests in the working population in industrialized countries. In recent years, it has become recognized that NAFLD is no longer just a trivial disease, and a rather considerable proportion of the patients develop liver cirrhosis. Furthermore, chronic infection of hepatitis C virus also develops a pathological feature of steatohepatitis, and extended hepatic steatosis has a serious impact not only on the progression of hepatic fibrosis but also on the antiviral efficacy of interferon therapy. Emerging lines of studies indicated that insulin resistance, abnormal lipid metabolism, and dysregulation of cytokines/adipokines (e.g., tumor necrosis factor-alpha, adiponectin, and leptin) are profoundly involved in the pathogenesis of NAFLD. This review aims to integrate the reported evidence and to provide the current point of view for comprehensive understanding of the pathophysiology of steatohepatitis.
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PMID:Liver diseases and metabolic syndrome. 1864 37

Chronic hepatitis C virus (HCV) infection is common in HIV-infected individuals, especially if the route of infection is intravenous (e.g. intravenous drug use or blood transfusion). Prognosis is poorer in patients with HCV and HIV coinfection than in those with HCV monoinfection, mainly due to the immunodepression caused by HIV infection and probably also to a direct effect of HIV on the liver. Moreover, although antiretroviral therapy can cause liver damage, there is little doubt about the net benefits obtained with triple therapy in coinfected individuals, since suppression of HIV replication and immune recovery help to halt liver damage. However, not all antiretroviral agents are equal and those with the lowest hepatotoxicity and best metabolic profile should be used in coinfected patients, since hepatic steatosis accelerates progression of hepatic fibrosis and insulin resistance hampers the success of treatment with interferon and ribavirin. Tenofovir is currently one of the safest nucleos(t)ide analogues, due to its low hepatotoxicity and its lack of negative interference on treatment of HCV infection.
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PMID:[Role of tenofovir in HIV and hepatitis C virus coinfection]. 1919 36

There has been a marked increase in the number of babies born by elective CS (Caesarean section). Following CS, the lack of normal stimuli that occur at birth alters the thermogeneic response, but any effects on hepatic metabolism have not been identified. In the present study, we compared the effect of delivery on hepatic metabolism in piglets, born either by CS or VD (vaginal delivery) and fed by TPN (total parenteral nutrition), by measuring lipid metabolism and enzyme activity coupled with metabolomic and genomic approaches. Hepatic lipid in the CS piglets at 7 days post-partum was in excess of 5 mg/g of liver consistent with hepatic steatosis, whereas in the VD piglets the amount of lipid was markedly lower (3 mg/g of liver) and below the threshold for a diagnosis of steatosis. Metabolomic analysis indicated that CS resulted in higher hepatic glycerol and lower glycerol phosphate dehydrogenase activity, suggesting that CS causes a decrease in hepatic gluconeogenesis from glycerol. CS also resulted in altered cholesterol handling and gene expression, despite the same dietary intake for 7 days post-partum. Furthermore, the CS piglets had a lower expression of interferon-responsive genes, but a higher expression of markers of immature hepatocytes. In conclusion, the results suggest that VD promotes normal liver maturation and hepatic metabolism, thereby reducing the accumulation of hepatic lipid.
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PMID:Delivery by Caesarean section, rather than vaginal delivery, promotes hepatic steatosis in piglets. 1944 54

Hepatic steatosis seems a frequent histological alteration seen in chronic hepatitis C virus infected patients. There is still a lot to learn about the exact mechanism of effect of liver steatosis and its influence on the progression of liver diseases. Our study involved 96 chronic hepatitis C genotype 1 infected Hungarian patients who received pegylated interferon and ribavirin treatment for the first time. Degree of steatosis, viral and host factors influencing its development and its effect on the efficiency of antiviral treatment were determined. In 61 (64%) of patients the liver tissue showed varying degree of steatosis, which did not show relationship with level of alcohol consumption (p = 0.5792), diabetes mellitus (p = 0.5925) or body mass index (p = 0.9685) in type 1 chronic hepatitis C patients. Degree of steatosis and virus titer showed strong relationship (OR = 2.1). Significant relationship was also found between degree of hepatic steatosis and stage (p = 0.0119), as well as between therapeutic response to combined pegylated interferon + ribavirin treatment and steatosis (p = 0.0012). Our results demonstrated that steatosis has clinical significance in hepatitis C virus genotype 1 infected patients.
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PMID:Effect of liver steatosis on therapeutic response in chronic hepatitis C virus genotype 1 infected patients in hungary. 1975


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