Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cirrhosis is the end-stage consequence of fibrosis progression in patients with chronic hepatitis C. The median time from infection to cirrhosis is 30 years, with a high inter-individual variability, which is now better understood. Several factors have been clearly shown to be associated with fibrosis progression rate: duration of infection, age, male gender, alcohol consumption, HIV co-infection and low CD4 count. Metabolic conditions such as steatosis, being overweight and diabetes are emerging as independent co-factors of fibrogenesis. The recent validation of non-invasive biomarkers should facilitate the study of fibrosis progression in large populations.
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PMID:Natural history and predictors of disease severity in chronic hepatitis C. 1635 83

Nonalcoholic fatty liver disease (NAFLD) is likely to reach epidemic proportions in children worldwide in the next decade. NAFLD may be the hepatic aspect of the metabolic syndrome in adults and children. The entire range of liver involvement characterizing NAFLD can occur in children: hepatic macrovesicular steatosis without inflammation, steatosis with inflammation or fibrosis, and cirrhosis. NAFLD may be more severe in children from certain ethnic groups or in association with metabolic disorders characterized by abnormalities in insulin receptor structure and function. Treatment strategies focus on modifying risk factors because specific drug treatments are lacking. Overweight/obesity should be identified as early as possible. Comprehensive clinical management to normalize weight should be instituted immediately to avoid hepatic and nonhepatic complications.
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PMID:Nonalcoholic fatty liver disease in children. 1637 97

Nonalcoholic steatohepatitis (NASH) once considered a benign process is now known to lead to progressive fibrosis and cirrhosis. NASH is frequently associated with the metabolic syndrome. Gradual weight reduction and increased physical activity are always recommended in overweight patients, but not always effective in reversing NASH. Promising pharmacological treatments have been demonstrated with antioxidants, insulin sensitizers, hepatoprotectants, lipid-lowering agents, and antihypertensive drugs. The similar histological features and natural histories of alcoholic steatohepatitis (ASH) and NASH suggest that common pathogenic mechanisms might be involved in these two conditions. Therapeutic strategies targeting the common mechanisms may also have promising potential. A larger randomized-controlled trial is needed to definitively determine the efficacy of pharmacological treatments for NASH.
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PMID:[Drug therapy for non-alcoholic steatohepatitis]. 1676 23

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of liver disease whose hallmark is the accumulation of large-droplet fat in hepatocytes. This metabolic disorder occurs mainly in overweight or obese individuals. The disease mechanism involves hyperinsulinemia and hepatic insulin resistance, not ethanol abuse. NAFLD may be the hepatic manifestation of the "metabolic syndrome" classically associated with type 2 diabetes mellitus and cardiovascular disease. NAFLD ranges from simple steatosis, which is the least rapidly progressing disorder, to nonalcoholic steatohepatitis to cirrhosis, which can evolve to chronic liver failure. The high prevalence of NAFLD in children has been recognized only in the past 5 to 10 years, as rates of childhood obesity have soared. Accordingly, the best strategies for diagnosis and treatment of childhood NAFLD are a work in progress and remain controversial. Weight reduction through a healthy diet and regular medium-intensity exercise is the mainstay of current treatment. Few research data are available to guide pharmacologic therapy. Certain points regarding management of childhood NAFLD require emphasis: It is a serious liver disease that requires detailed clinical investigation. Other liver diseases causing fatty liver and/or abnormal liver tests, notably Wilson disease and chronic viral hepatitis, need to be excluded. Liver biopsy can provide critical diagnostic and staging information. Associated genetic or endocrine disorders need to be identified. Treatment should begin with a low-glycemic index diet that provides adequate nutrients but is low in harmful fats and eliminates foods causing postprandial hyperglycemia. Initially, this can target two to three problem foods so that it is easy for the adolescent to follow. Regular exercise suited to the capabilities and interests of the teenager should be added to the daily routine. Where possible, a team approach, including a dietician and psychologist, should be utilized, as adolescents do better in a supportive atmosphere. Optimal drug treatment requires further research: current front-runners are vitamin E and metformin. The roles of drugs that alter appetite and bariatric surgery for adolescents with NAFLD have not been determined.
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PMID:Nonalcoholic Fatty Liver Disease (NAFLD): Approach in the Adolescent Patient. 1694 68

Although population prevalence is very difficult to establish, nonalcoholic fatty liver disease (NAFLD) is probably the most common cause of liver disease in the preadolescent and adolescent age groups. There seems to be an increase in the prevalence of NAFLD, likely related to the dramatic rise in the incidence of obesity during the past 3 decades. Despite an increase in public awareness, overweight/obesity and related conditions, such as NAFLD, remain underdiagnosed by health care providers. Accurate diagnosis and staging of nonalcoholic steatohepatitis (NASH) requires liver biopsy. The development of noninvasive surrogate markers and the advancements in imaging technology will aid in the screening of large populations at risk for NAFLD. Two distinct histological patterns of NASH have been identified in the pediatric population, and discrete clinical and demographic features are observed in children with these 2 patterns. The propensity for NASH to develop in obese, insulin-resistant pubertal boys of Hispanic ethnicity or a non-Hispanic white race may provide clues to the pathogenesis of NAFLD in children. The natural history of pediatric NASH has yet to be defined, but most biopsies in this age group demonstrate some degree of fibrosis. In addition, cirrhosis can be observed in children as young as 10 years. While the optimal treatment of pediatric NAFLD has yet to be determined, lifestyle modification through diet and exercise should be attempted in children diagnosed with NAFLD. A large, multicenter trial of vitamin E and metformin is underway as part of the NASH clinical research network.
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PMID:Pediatric nonalcoholic fatty liver disease: a critical appraisal of current data and implications for future research. 1703 14

Insulin resistance is more often seen in hepatitis C than in other liver diseases, including non-alcoholic steatohepatitis. The Homeostasis Model for Assessment [HOMA= fasting insulin (mUI/ml) * fasting glucose (mmol/L) / 22.5] has proved useful in the measurement of insulin sensitivity in euglycemic patients. Cross-sectional and case-cohort studies support a role for hepatitis C as a factor implied in the development of type-2 diabetes in high-risk patients (male patients, older than 40 years, and overweight). In transgenic mice models the HCV core protein has been found to induce insulin resistance via TNF production. Insulin resistance has been associated with steatosis development and fibrosis progression in a genotype-dependent manner. In genotype-1 patients, the mechanisms by which insulin resistance promotes fibrosis progression include: a) steatosis; b) hyperleptinemia; c) increased TNF production; and d) impaired expression of PPARg receptors. Indeed, insulin resistance has been found as a common denominator to the majority of features associated with difficult-to-treat patients. Patients with cirrhosis, obesity, coinfected with HIV, and Afro-American, all of them showed insulin resistance. Insulin resistance strongly influences sustained response rates, at least in genotype-1 patients. Insulin resistance decreases during and after treatment in patients that achieved virus C clearance. Moreover, the incidence of type-2 diabetes seems to be lower in responders than in non-responders. In summary, hepatitis C promotes insulin resistance and insulin resistance induces steatosis, fibrosis, and interferon resistance. The treatment of insulin resistance by decreasing hyperinsulinemia could improve sustained response rates in patients with chronic hepatitis C treated with peginterferon plus ribavirin.
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PMID:Hepatitis C and insulin resistance: steatosis, fibrosis and non-response. 1704 97

There are limited data on nonalcoholic fatty liver disease (NAFLD) from India. The clinicopathological profile of Indian patients with NAFLD may be different from that of Western patients. One hundred NAFLD patients with increased liver enzymes were prospectively evaluated for clinical presentation, associated diseases, overweight/obesity, central obesity (n=54), presence of diabetes mellitus, lipid abnormalities, insulin resistance (n=39), metabolic syndrome (n=54), serum iron, serum ferritin, and transferrin saturation (n=60), and HFE gene mutations (n=30). Risk factors for the grade and stage of the disease on histology were studied in 38 biopsy-proven patients. Patients were treated with lifestyle modifications and ursodeoxycholic acid (UDCA). Seventeen nonresponder patients were treated with metformin. The majority of patients were males (n=70). Twenty percent of patients were overweight, 68% had obesity, and 78% had central obesity. Abnormal cholesterol, HDL, and triglycerides were present in 36%, 66%, and 53% of patients, respectively. Twelve percent of patients had diabetes mellitus and 16% patients had various associated diseases. All 22 (100%) patients studied by ITT and all but 1 (98%) studied by HOMA-IR were found to have reduced insulin sensitivity and 50% were found to have metabolic syndrome by the modified ATP III criteria. Two (3%) patients were found to have high serum iron, 4 (7%) patients had high ferritin, 5 (8%) patients had increased transferrin saturation, and 4 (13%) patients were found to be heterozygotes for H63D HFE gene mutation. Twenty patients of 38 (53%) had histological evidence of NASH (class 3=6, class 4=14). The other 18 (47%) qualified for class I (n=1) or class II (n=17) NAFLD. Four (10.5%) patients had bridging fibrosis and none had evidence of cirrhosis liver. Seventy-four (74%) patients achieved a biochemical response to lifestyle modification and UDCA. All 17 patients treated with metformin had a reduction in ALT level and 10 (59%) of them had normalization of their enzymes. We conclude that the clinicopathological profile of NAFLD in Indian patients is different from that in the West.
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PMID:The clinicopathological profile of Indian patients with nonalcoholic fatty liver disease (NAFLD) is different from that in the West. 1742 Sep 51

Obesity has emerged as a significant global health problem in the pediatric population. Pediatric liver disease is a serious complication of childhood obesity. Non-alcoholic steatohepatitis (NASH) is an entity in the spectrum of non-alcoholic fatty liver disease (NAFLD) ranges from fat in the liver--simple steatosis, NASH/ steatohepatitis--fat with in.ammation and/or fibrosis to advanced fibrosis and cirrhosis when fat may no longer be present. NASH is associated with obesity, diabetes, insulin resistance (IR), and hypertriglyceridemia. Children get NAFLD, and the incidence of this pediatric liver disease is rising as childhood obesity becomes increasingly prevalent. Although much remains to be learned about pediatric NAFLD, it is already evident that children with NASH risk progressive liver damage, including cirrhosis. Liver biopsy is required for definitive diagnosis, and other causes of fatty liver in childhood must be excluded. Gradual weight loss through increased regular exercise and a low-fat, low-refined carbohydrate diet appears to be effective. Drug treatments are being developed. The important message is that childhood obesity poses important health problems, including but not limited to potentially severe chronic liver disease. Early diagnosis of children who are only overweight is a worthy goal so that strategies to limit obesity can be instituted as early as possible. Identification of genetic risks is important, but management will invariably require changes in environmental factors. In addition to individual treatment, a multifaceted, societal initiative is required for solving the childhood obesity epidemic.
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PMID:Non-alcoholic fatty liver disease and childhood obesity. 1747 88

The two most frequent endocrine complications of hemochromatosis are diabetes mellitus and hypogonadotrophic hypogonadism. Other endocrine disorders related to this disease are very rare and are described especially in the most severe and earliest posttransfusion iron overloads. Endocrine complications are evidence of advanced hemochromatosis, often already associated with cirrhosis. Given the low frequency of HFE mutations in type 2 diabetes, routine genetic testing in this population does not seem reasonable. Testing for iron overload is recommended in subjects with atypical type 2 diabetes (for example, patients who are not overweight) and in cases of hypogonadism, characteristic pigmentation, or cirrhosis. Phlebotomy plays an important role in the management of endocrine complications of hemochromatosis, especially when diagnosis is early. In all cases of hypogonadotrophic hypogonadism, primary hemochromatosis must be considered.
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PMID:[Endocrine consequences of hemochromatosis]. 1752 8

Nonalcoholic fatty liver disease (NAFLD) is an emerging clinical entity. There is limited data on NAFLD from India. The objective of this article was to review all the published literature on NAFLD from India. The epidemiological studies including prevalence ofNAFLD amongst special groups like in those with unexplained rise in transaminases, diabetes mellitus and cryptogenic cirrhosis, studies on pathogenesis including insulin resistance, iron abnormalities, and studies available for the treatment of such patients have been reviewed. In addition some of the differences between Indian patients and those from the West have been highlighted. Available literature show that majority of Indian patients with NAFLD have overweight or obesity as per Asian Pacific criteria even though they do not have the kind of morbid obesity as seen in patients from the West. Other differences between Indian patients and those from the West include less of metabolic syndrome including its components like diabetes mellitus and hypertension, less of iron abnormalities and HFE gene mutations and mild histological disease at presentation in Indian patients. More data is required to substantiate these findings and to prove if NAFLD patients in India are different at presentation.
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PMID:Nonalcoholic fatty liver disease in India--is it different? 1754 90


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