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)

Whereas the histologic findings in clinically "chronic" autoimmune hepatitis have been well established, with piecemeal necrosis as a hallmark lesion, the histologic findings of clinically "acute" or recent-onset autoimmune hepatitis remain undefined. The goal of this study was to define more fully the liver histomorphology in patients with recent-onset autoimmune hepatitis. Twenty-six patients were identified at our institution who had well-characterized autoimmune hepatitis and had undergone a liver biopsy within 6 months of clinical presentation. A detailed histologic evaluation revealed evidence of chronic liver disease in 25 (of 26) patients despite the lack of correlating clinical chronicity. The histologic evidence of chronicity included, in addition to a portal lymphoplasmacytic infiltrate, bridging (septal) fibrosis (11 patients) and overt cirrhosis (four patients). Eighteen of these 25 cases with evidence of chronicity also showed zone 2 and 3 lobular hepatitis, including disarray and hepatocyte necrosis. A single case showed lobular hepatitis with confluent hepatocyte necrosis (submassive hepatocellular necrosis), but no evidence of chronic liver disease. Although autoimmune hepatitis remains in the differential diagnosis of lobular hepatitis, these data show that most patients with autoimmune hepatitis who undergo biopsy early in its clinical course will have histologic evidence of chronic liver disease. Most of these patients probably have a lobular "flare" in disease activity, which likely precipitated the clinical presentation. The findings herein reinforce the concept that autoimmune hepatitis is by definition a chronic disease and supports the proposal that the modifier "chronic" be eliminated from autoimmune hepatitis.
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PMID:Recent-onset autoimmune hepatitis. Biopsy findings and clinical correlations. 775 56

Chronic diseases of the liver were found to be associated with microsomal hydroxylation reactions inhibition, this inhibition depending on the disease activity and stage. Chronic cholestatic hepatitis and primary biliary cirrhosis are associated with a more marked suppression of these reactions, the degree of inhibition being in proportion with the cholestatic syndrome severity. Demethylation process was found inhibited in active liver cirrhosis and primary biliary cirrhosis. The authors believe that assessment of the rate of microsomal oxidation in a liver biopsy specimen will help objectively assess the first phase of cytochrome P-450 effected biotransformation (hydroxylation) in patients with chronic disease.
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PMID:[Cytochrome P-450-dependent hydroxylation in liver tissue of patients with hepatobiliary diseases]. 803 24

Plasma DNA increases where cell death occurs in vivo. To investigate its significance in elderly patients, plasma DNA was assayed in 79 institutionalized patients over 68 years of age. The patients were divided into two groups: group I comprises 39 patients suffering from various acute or chronic illnesses; group II comprises 40 patients without chronic disease, and free of any clinical or biological symptoms of any infectious or inflammatory process. Plasma DNA was higher in group I than in group II (p < 0.0001) and in group II than in a control group of middle-aged subjects (p < 0.05). In group I, increase in plasma DNA concentration was found in various pathological situations associated with cell death phenomena, including infections, cancers with metastasis, hepatitis, irreversible cardiac failure, severe respiratory insufficiency and thrombophlebitis. Plasma DNA concentrations were not correlated with erythrocyte sedimentation rate, fibrinogen concentration, hemoglobin concentration or leukocyte count. In group I, as well as in the overall population, survival after 1 month was significantly reduced in patients with increased concentrations of plasma DNA. In conclusion, plasma DNA as a marker of cell death phenomena occurring in vivo, could be helpful for follow-up and management of elderly patients.
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PMID:Plasma DNA as cell death marker in elderly patients. 824 49

To assess whether the risk of chronic disease in patients with acute non-A, non-B/type C (NANB/C) hepatitis after transfusion could be reduced by treatment with interferon, patients were randomised to receive 3 million units interferon (IFN) alfa-2b three times a week for three months or no therapy. At the end of treatment, IFN had significantly reduced the number of patients with abnormal alanine aminotransferase activities compared with untreated patients but this difference was not maintained during a 15 month follow up. Treatment with IFN alfa-2b was considered safe and was well tolerated.
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PMID:Multicentre randomised controlled trial of recombinant interferon alfa-2b in patients with acute non-A, non-B/type C hepatitis after transfusion. 831 83

After the discovery of HDV there have been significant advances in the understanding of the biology and disease of HDV infection. Analyses at the molecular level have revealed several fascinating features (ribozyme activity, RNA-dependent RNA polymerase activity of RNA polymerase II, HDAg isoprenylation, and RNA editing) that are of significant interest. Intensive investigation of the ribozyme elements has yielded important insights in both functional and structural features. However, there is information lacking about other aspects of the HDV replication cycle including the specific nature of the interaction between HDAg and HDV RNA, the function of HDAg in HDV RNA replication, transcription by RNA polymerase II, and the mechanisms of HDV RNA editing and its regulation. Further study of these and other aspects of the HDV replication cycle will continue to enrich our understanding of basic biology. Evaluation of the mechanisms of HDV disease remains an important goal in the study of this agent. Although both acute and chronic disease are commonly associated with unfavorable outcomes, it is clear that chronic infection is associated with a broad spectrum of disease. The interactions between HDV, HBV, and the host are necessarily complex, and it is likely that each contribute factors that influence disease and outcome. Recent analyses of HDV genotypes have suggested that disease variations may be associated with viral genetic factors. Consistent with the obligate role of HBV in the HDV life cycle, HBV replication is also an important determinant of HDV disease. It is still unclear if interactions between specific genotypes or variants of HBV and HDV influence disease. Recent data also suggest that infection with multiple hepatitis viruses (HBV, HDV, and HCV) can influence the severity of disease. It remains to be seen whether coinfection with the recently discovered hepatitis G virus is associated with altered disease patterns. Further advances in our understanding HDV disease and possible therapeutic approaches will rely on a combination of additional studies at the molecular, genetic, epidemiologic, and clinical levels. These studies will continue to elaborate the model of HDV infection and disease that can ultimately be tested by experimental infection of chimpanzees and woodchucks.
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PMID:Hepatitis delta virus. Genetics and pathogenesis. 879 82

From the original records of the Italian Central Institute of Statistics (ISTAT) alcohol-related deaths in Italy during the 1980-1990 period were estimated applying alcohol-attributable fractions (AAFs), derived from the national and international literature, to a list of alcohol-related diagnoses. Age-adjusted mortality rates direct method) were computed for each year sex and geographic region. Alcohol-related years of potential life lost (YPLL) to age 70 were estimated only for 1990. In 1990 overall alcohol-related deaths were 18,033 (males: 12,937; females: 5,096), accounting for 3.3% of all deaths in Italy (males: 4.6%: females 2.0%. Over 200,000 YPLL (males: 162,318; females 38,367) to age 70 were attributable to alcohol-related causes each death contributing on average with 11.1 YPLL (males: 12.5; females: 7.5). Among individual causes of death, chronic disease (malignant neoplasms and liver diseases) represent 65% of ARM, while intentional and unintentional injuries account for almost 35% of ARM According to the decreasing temporal trend of alcohol intake in Italy, during the 1980-1990 period, ARM decreased by 17% in both sexes (from 51.3 x 100,000 to 42.4 in males from 18.1 to 15.2 in females). Geographic variability of ARM in Italy suggests that in Central regions some protection factors concomitant with alcohol and hepatitis viruses exposure (diet, type of alcoholic beverage, pattern of alcohol make genetic factors) could account for the reduced risk of alcohol-induced biologic damage.
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PMID:[Geographic variability of alcohol-related mortality in Italy in the period 1980-1990]. 904 96

The relationship between hepatitis virus invasion and emergence of liver-specific autoantibodies against asialoglycoprotein receptor (anti-ASGPR) and the occurrence patterns, prognostic value, and specificity of these autoantibodies toward polypeptides of host ASGPR were investigated in experimental viral hepatitis in the woodchuck system. Sequential sera (n = 231) obtained before and after inoculation with woodchuck hepatitis virus (WHV) from animals which resolved acute infection (n = 7) or developed chronic hepatitis (n = 6) were tested for anti-ASGPR using radio and enzyme-immunodetection assays. In addition, the outcome of WHV hepatitis was analyzed in 30 other woodchucks whose preinoculation sera were tested for anti-ASGPR. The receptor subunit specificity of virus-induced anti-ASGPR was determined by Western blotting and compared with that of anti-ASGPR raised in woodchucks challenged with a heterologous (rabbit) receptor. The results revealed that WHV infection triggered anti-ASGPR in all except one of the initially autoantibody nonreactive animals (eight of nine; 89.9%). Once induced, anti-ASGPR were detectable throughout the entire follow-up independent of histological severity of liver damage or the outcome of hepatitis. In healthy WHV-naive woodchucks, anti-ASGPR occurred at low titers in approximately one third of the animals. Importantly, woodchucks reactive for anti-ASGPR before WHV inoculation developed chronic hepatitis with a significantly greater frequency (55.5%) than those autoantibody negative (15.6%; P < .05). In contrast to anti-ASGPR elicited by immunization with a heterologous receptor, which initially recognized only the ASGPR 40-kd polypeptide, anti-ASGPR emerging after virus invasion reacted with both the ASGPR 40- and 47-kd subunits from the moment of their appearance. This study provides the first direct evidence that hepatitis virus in the natural host triggers autoantibodies against a unique hepatocyte antigen and shows that anti-ASGPR autoimmunity existing before virus infection is associated with a high rate of progression to chronic disease in experimental hepadnaviral hepatitis.
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PMID:Virus-induced anti-asialoglycoprotein receptor autoimmunity in experimental hepadnaviral hepatitis. 904 20

The hepatitis C virus (HCV) genome was isolated during the late 1980s using molecular cloning techniques. It is recognized as the cause of most cases of percutaneously transmitted non-A, non-B hepatitis. Prevalence of antibodies to HCV(anti-HCV) in the general Australian population is 0.3%. However, among regular intravenous drug users the prevalence exceeds 90%. The predominant risk factors for HCV are intravenous drug use, tattoos, exposure to blood products, occupational risk and ethnicity. In contrast to hepatitis B, sexual spread and vertical transmission of HCV from mother to neonate are relatively uncommon. The risk of acquiring HCV from a single HCV-contaminated needlestick accident is about 5%. Most cases of acute HCV infection are asymptomatic, but 50 to 80% progress to chronic disease. The percentage of those with chronic HCV progressing to cirrhosis is not accurately known, but is probably 20%. Treatment strategies for HCV, utilizing recombinant interferons, are proving useful in patients with mild to moderate liver disease, but fare less well in patients with cirrhosis. Currently, there is no vaccine for hepatitis C, so pre-exposure prophylaxis is not possible. Equally, no post-exposure intervention, for example with gamma globulin, has been shown to be beneficial, though there may be a role for early interferon therapy.
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PMID:Hepatitis C. 913 92

Chronic viral hepatitis is a leading cause of death worldwide. Four of the six identifiable hepatitis viruses are associated with chronic disease. Until recently, the only accepted treatment has been injected interferon alfa. New antiviral medications currently hold promise in the treatment of hepatitis B. Hepatitis C remains more difficult to treat than hepatitis B, but involving the patient in selecting the treatment and identifying patients with better responses to interferon may help the physician direct the management of such patients more successfully.
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PMID:Management of chronic viral hepatitis. 919 59

On March 11-12, 1996, a workshop on how to implement new adolescent immunization (AI) recommendations was held in Atlanta, Ga. Sponsored by the Centers for Disease Control and Prevention, it was a collaborative effort of the National Immunization Program, the Division of Adolescent and School Health/National Center for Chronic Disease Prevention and Health Promotion, and the Hepatitis Branch/National Center for Infectious Diseases. The workshop brought together organizations and individuals interested in adolescent health and immunizations so they could address how new AI recommendations can be implemented most effectively. This article offers an overview of their discussions and suggestions, including issues of cooperation, education, legislation, and AI program development among health provider organizations, health department, schools, community groups and various other agencies relating to adolescent health services.
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PMID:Adolescent immunization: focus on implementation. 935 91


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