Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic steatohepatitis (NASH) is a condition characterized by hepatomegaly, elevated serum aminotransferase levels, and a histologic picture similar to alcoholic hepatitis in the absence of alcohol abuse. Most patients with NASH are obese women, and many have diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia. NASH has also been associated with a number of metabolic conditions, surgical procedures, and drug treatments. Most patients are asymptomatic. The most common sign of NASH is hepatomegaly. Stigmata of chronic liver disease are rare. Laboratory abnormalities include a 2-4-fold elevation of serum aminotransferase levels; other liver function test results are usually normal. Histologically, there is moderate to severe macrovesicular steatosis and lobular hepatitis with necrosis or ballooning degeneration and/or fibrosis. The pathogenesis of NASH is poorly understood, but lipid peroxidation and oxidative stress are the leading culprits. The natural history of NASH is unknown, but NASH seems to be a stable disease in most patients. Treatment of NASH is unproven, but weight reduction is recommended in obese patients. Small pilot studies of several drugs have shown promise, but large randomized clinical trials are awaited. Orthotopic liver transplantation is the treatment of choice for end-stage liver disease secondary to NASH.
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PMID:Nonalcoholic steatohepatitis. 1152 55

TT virus is a recently discovered virus, of which the pathogenetic potential is still uncertain. The present paper describes the histopathological features of a case of TT virus-related acute recurrent hepatitis. The patient is a 28-year-old woman with no history of drug or alcohol abuse, presenting with repeated episodes of hypertransaminasemia evidenced during the last 4 years. No other markers of viral or autoimmune disease were found. On histological analysis, the liver parenchyma showed a preserved architecture. The histological features were those of a mild acute hepatitis. The clinicopathological findings suggest th
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PMID:TT virus-related acute recurrent hepatitis. Histological features of a case and review of the literature. 1178 46

The National Institute on Alcohol Abuse and Alcoholism and the Office of Rare Diseases, National Institutes of Health, sponsored a satellite symposium on "Cellular and Molecular Mechanisms of Alcoholic Hepatitis" at the 24th Annual Scientific Meeting of the Research Society on Alcoholism, Montreal, Quebec, Canada, June 2001. Alcohol intake is a major cause of hepatitis that may lead to alcoholic cirrhosis-a major cause of death in the United States. In up to one third of heavy drinkers alcoholic hepatitis develops, which is characterized by liver cell death and infiltration of leukocytes in hepatic parenchyma. Although leukocytes have been implicated in the pathogenesis of alcoholic hepatitis, the underlying cellular and molecular mechanisms by which leukocytes migrate to hepatic parenchyma and initiate tissue injury are not clear. For this symposium, 10 speakers were invited to address the following aspects of the mechanisms of alcoholic hepatitis: role of Kupffer cells in initiating the process of alcoholic hepatitis; types of leukocytes involved in the pathogenesis of alcoholic hepatitis; chemokines that are responsible for the attraction of leukocytes; adhesion molecules that promote the attachment of leukocytes to the endothelial cells and hepatocytes; mechanisms of leukocyte transmigration to hepatic parenchyma; mechanisms by which leukocytes initiate tissue injury; and interactive effects of alcohol and hepatitis viral proteins on liver injury. This article provides an introduction to the problem and a summary of the 10 scientific presentations delivered at the symposium.
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PMID:Cellular and molecular mechanisms of alcoholic hepatitis: introduction and summary of the symposium. 1206 29

Two patients developed acute cholestatic hepatitis during treatment with propafenone. Viral infections, alcohol abuse, hepatotoxicity by other drugs, and biliary obstruction were excluded as causes. In one patient, liver biopsy showed changes consistent with a drug-associated injury. Another patient had autoimmune antibodies (ANA) in the serum. Following propafenone withdrawal, the clinical and biochemical profiles of both patients improved. Hepatic toxicity from the antiarrhythmic drug propafenone is highly uncommon. Moreover, the drug produces hepatocellular injury by an unknown mechanism. Most of the seven cases reported here had acute cholestatic hepatitis after a latency period of two to four weeks.
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PMID:Propafenone hepatotoxicity: report of two new cases. 1264 15

The aim of the study was to investigate present and past morbidity in drug addicts, 25 years after hospitalisation for acute hepatitis B or hepatitis nonA-nonB. The hospital records for 214 consecutively admitted patients were analysed, and a follow-up study on 66 of the 144 patients still alive was performed. At follow-up, 1 of 54 (1.8%) hepatitis B patients was still HBsAg positive. Twelve patients originally diagnosed as hepatitis nonA-nonB were all among 54 found to be anti-hepatitis C virus (anti-HCV) positive, and the total anti-HCV prevalence was 81.8%. Twelve (22.2%) of the HCV cases were unknown before the follow-up examination. Four (6.1%) participants were anti-human immunodeficiency virus positive, only 1 was on antiretroviral therapy, and none had developed AIDS. Other chronic somatic diseases were a minor problem, whereas drug users reported skin infections as a frequent complication. Forty-three patients (65%) had abandoned addictive drugs since the hospital stay. Serious mental disorders were reported by 19 patients (28.8%), and 17 (25.8%) regarded themselves as present (9) and former (8) compulsive alcohol drinkers. A large proportion of the participants were granted disability pension (39%), a majority because of psychiatric disorders, drug and alcohol abuse.
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PMID:A 25-year follow-up study of drug addicts hospitalised for acute hepatitis: present and past morbidity. 1264 34

Pancreatitis is clearly associated with alcohol abuse, but only a relatively small percentage of people who abuse alcohol develops obvious pancreatitis. These observations have led to the concept that the development of alcoholic pancreatitis requires cofactors. Although diet and smoking have been studied, a clear cofactor has not been identified. The study results presented in this paper were obtained to determine whether viral infection of the pancreas would be a cofactor for alcoholic pancreatitis similar to the role of hepatitis virus infections in the development of alcoholic liver disease. To test this hypothesis, mice were fed ethanol with a liquid diet protocol and infected with coxsackievirus B3 (CVB3). It was found that consumption of alcohol alone did not result in pancreatitis as determined by serum levels of amylase or histologic changes in the pancreas. Two strains of CVB3 that are tropic for the pancreas were used; a virulent and an avirulent strain. Infection of alcohol-fed animals with the virulent CVB3 strain 28 resulted in a more severe pancreatitis than the pancreatitis noted in control animals. Alcohol-fed mice infected with the avirulent strain (GA) showed severe pancreatitis, whereas the infection of control mice did not result in obvious pathologic effects in the pancreas. This model allows mechanistic studies to define the role of viral infection as a cofactor for alcoholic pancreatitis.
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PMID:Animal model of alcoholic pancreatitis: role of viral infections. 1457 91

Nonalcoholic steatohepatitis (NASH) is a condition characterized histologically by macrovesicular steatosis and lobular hepatitis with necrosis or ballooning degeneration and/or fibrosis--a picture resembling alcoholic hepatitis, in the absence of alcohol abuse. Most patients with NASH are asymptomatic, and the disease is detected incidentally. The most common signs of NASH are hepatomegaly and laboratory abnormalities, which include a 2-4-fold elevation of serum aminotransferase levels, while other liver function test results are usually normal. Most patients with NASH are obese, many have diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia. NASH has also been associated with a number of metabolic derrangements, conditions, surgical procedures, and drug treatments. The pathogenesis of NASH is poorly understood, but lipid peroxidation and oxidative stress seem to be the leading culprits. The natural history of NASH is unknown, but it seems to be a stable disease in most patients. Still, the progress to cirrhosis is possible. There is no established treatment for NASH. Treatment is usually directed towards optimizing body weight, and pharmacologic agents are mostly experimentally used. Orthotopic liver transplantation is the treatment of choice for end-stage liver disease secondary to NASH.
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PMID:[Non-alcoholic steatohepatitis]. 1458 65

A variety of carcinogens, in particular smoking, alcohol abuse and infections, are associated with an increased risk for the development of cancer of the upper gastrointestinal tract. Cancer prevention should start here, in particular since cessation of nicotine abuse, only moderate consumption of alcohol, and weight loss also have other positive effects on health. Where the indication is appropriate, H. pylori eradication, vaccination against hepatitis B and avoidance of exposure to hepatitis are well-founded prophylactic measures. Further screening measures make good sense only in high-risk groups, and are based on recommendations. It has, however, not yet been demonstrated that the screening of patients with Barrett's esophagus, liver cirrhosis, chronic hepatitis or gastric risk diseases actually can lower cancer-related deaths.
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PMID:[Esophagus, stomach, liver, pancreas carcinoma. What recommendations for prevention?]. 1460 99

Increased oxidative stress and lipid peroxidation (LPO) are implicated in multistage carcinogenesis. Recent studies have shown that LPO-derived reactive hydroxyalkenals can form promutagenic exocyclic etheno-DNA adducts in vivo. Such DNA damage was found to be increased in the liver of patients with metal storage diseases and in colon adenomas of familial adenomatous polyposis patients. We now have investigated the levels of 1,N(6)-ethenodeoxyadenosine (epsilon dA) in human liver samples obtained from a group of patients diagnosed with hepatitis, fatty liver, fibrosis and cirrhosis, primary hemochromatosis and Wilson's disease. Using an immunohistochemical method, the relative mean pixel intensity of randomly selected nuclei was measured by imaging software; positively stained cell nuclei (arbitrary mean pixel intensity > or =0.5) were counted. Prevalence of epsilon dA (%) was calculated from the ratio of a number of positively stained cell nuclei over a total number of cells counted. When compared with normal livers (3.1%), the percent prevalence (means) was significantly higher in specimens of alcoholic fatty liver (15%) and fibrosis patients (50%) but not in samples with hepatitis (induced by various factors) (6.2%). The percent prevalence in alcohol fibrosis was as high as in the liver from Wilson's disease (50.7%) and hemochromatosis (33%) patients. This is the first demonstration of increased epsilon dA in human liver diseases due to alcohol abuse. We conclude that excessive hepatic DNA damage, as assessed by miscoding etheno-DNA adduct in the nuclei of liver biopsies, is probably caused by alcohol-induced oxidative stress and LPO. In cancer-prone liver diseases (fatty liver, cirrhosis/fibrosis) such damage may act as a driving force towards malignancy.
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PMID:Immunohistochemical detection of 1,N6-ethenodeoxyadenosine in nuclei of human liver affected by diseases predisposing to hepato-carcinogenesis. 1474 17

Ten percent of patients who undergo resection for hepatocellular carcinoma (HCC) associated with chronic liver disease have no detectable cause for this underlying liver disease. Recent studies have shown that patients with cryptogenic chronic liver disease frequently have risk factors for nonalcoholic fatty liver disease (NAFLD). This study examines the incidence of risk factors for NAFLD in patients with chronic liver disease who underwent resection for HCC. Among 210 patients with chronic liver disease who underwent resection for HCC, 18 (8.6%) had no identifiable cause for the underlying liver disease. These patients were assessed for obesity, diabetes mellitus, and histological features of the tumor and the adjacent liver parenchyma. Comparisons were made with matched patients with alcohol- and chronic-viral-hepatitis-related HCC. The prevalence of obesity (50% vs. 17% vs. 14%), diabetes (56% vs. 17% vs. 11%), aspartate aminotransferase/alanine aminotransferase ratio<1 (50% vs. 19% vs. 17%), and steatosis>20% (61% vs. 17% vs. 19%) was significantly higher in patients with cryptogenic liver disease than in patients with alcohol abuse and chronic viral hepatitis (P<0.0001 for each). Well-differentiated tumors were significantly more common in patients with cryptogenic liver disease (89% vs. 64% in patients with alcohol-related HCC vs. 55% in patients with chronic viral hepatitis-related HCC, P<0.0001). In conclusion, the hypothesis that obesity and diabetes mellitus may be important risk factors for cryptogenic chronic liver disease in patients with HCC is supported by the analysis of surgically treated patients. Whether HCC is primarily related to obesity and diabetes mellitus or secondarily to a NAFLD-like parenchymal lesions remains to be clarified.
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PMID:Obesity and diabetes as a risk factor for hepatocellular carcinoma. 1476 43


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