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

A patient with acute hepatitis associated with isoniazid therapy is described. The relevance fo isoniazid hepatotoxicity in Melanesian populations is discussed. Guidelines for recognition and management of INH-induced hepatitis are suggested.
 ...
PMID:Isoniazid-associated hepatitis in a Melanesian. 27

The occurrence of anti-HBcAg antibodies in the blood as determined by indirect immunofluorescence and its relation to the occurrence of HBsAg in the cytoplasm and of HBcAg and IgG in the nuclei of hepatocytes were studied in the following groups of patients (total of 123 biopsies): I. 64 HBAg-negative patients with various liver diseases; II. 51 HBAg-positive patients without therapeutical immunosuppression (6 acute hepatitis, 10 nonspecific reactive and 10 chronic persistent hepatitis, 19 chronic aggressive hepatitis, 6 "Hippie"-hepatitis); III. 8 kidney transplant recipients. It could be shown that nuclear IgG is found only if both parameters can be demonstrated at the same time: HBcAg in liver cell nuclei and anti-HBcAg antibodies in the serum in titers higher than 1:64. Accordingly, all types of hepatitis with excess formation of nuclear HBcAg (early phase of acute hepatitis, chronic aggressive hepatitis and chronic non-aggressive forms with generalized core formation, i.e. carrier state or chronic persistent hepatitis of the HBc type) may show nuclear fluorescence for IgG. All forms of hepatitis B without detectable core formation (acute hepatitis in the elimination phase, chronic non-aggressive hepatitis with isolated HBsAg expression, i.e. carrier state or chronic persistent hepatitis of the HBs type, posthepatitic phase) do not present nuclear IgG despite eventual anti-HBcAg formation. Finally, lack of anti-HBcAg or very low titers associated with lack of IgG in hepatocytic nuclei do not exclude generalized core formation in liver cell nuclei in chronic persistent hepatitis of effectively immunosuppressed patients. Although the demonstration of nuclear IgG has several diagnostic and prognostic consequences in common with the demonstration of HBcAg, a specific search for the core antigen in the tissue is needed for the correct appraisal of the HBcAg- and HBsAg tissue expression pattern and the associated disease.
 ...
PMID:Nuclear fluorescence of liver cells for IgG in viral hepatitis B: significance and relation to hepatitis B-core and anti-hepatitis B-core formation. 32 65

Transmission of Hepatitis B virus from mother to infant can cause a severe type of neonatal hepatitis. Comparing chronic carrier mothers with mothers who have acute hepatitis in pregnancy we find that the latter group present the greater risk to their infants. Differences in the presence of Hepatitis B core and Hepatitis B e antigen and antibody in the acute case and in the carrier state may expoain the differences observed in the transmission rates of two groups. In countries where the prevalence of the carrier state is high it appears that vertical transmission of the carrier state is also common. This pattern may be explained by differences in the geographical distribution of carriers of Hep B e antigen, which has been recently described as a virulance factor.
 ...
PMID:Vertical transmission of hepatitis-B surface antigen. 32 29

Papular acrodermatitis of childhood (PAC) is characterized by papular eruption of skin, lymphadenopathy, and acute hepatitis B surface antigen (HBsAg)-positive anicteric hepatitis. To study the course of hepatitis B virus infection we followed 16 patients with PAC, 2 to 7 years of age, for periods ranging from 6 to 46 months. All patients tested developed hepatitis B surface antigenemia subtype ay, and produced antibody to hepatitis B core antigen with the highest incidence after 3 to 5 months. Half of the children investigated developed antibody to hepatitis B surface antigen 4 to 18 months (mean, 6.5) after the onset of PAC. At the end of the investigation, 31% of the children were still HBsAg-positive, 50% were antibody to hepatitis B core antigen-positive, and in 43% the activity of serum aminotransferases was abnormal. Liver biopsy repeated in 2 children showed chronic aggressive hepatitis. The pattern of antibody response to hepatitis B virus is similar in both HBsAg-positive hepatitis and PAC. The frequent development of HBSAg carrier state and the high proportion of children with liver abnormalities at the end of the investigation suggest an impaired clearance of hepatitis B virus and a tendency to chronicity.
 ...
PMID:Immune response to hepatitis B virus in children with papular acrodermatitis. 33 78

The classification of chronic hepatitis introduced in 1968 is still current, but has been modified. The concept of bridging hepatic necrosis has been incorporated, and is recognised as an important feature of both acute and chronic aggressive (active) hepatitis (CAH). In the pathogenesis of the latter, piecemeal necrosis is, however, thought to be the more important factor. The histological picture of CAH varies widely. Several causes of CAH have been identified, including hepatitis B virus. Recognition of surface and core components of the virus in tissue sections has facilitated study of the relationship between host response and pathological lesion in chronic hepatitis. CAH and primary biliary cirrhosis share histological features, and a mixed form has been postulated. Staining for copper sometimes helps to distinguish the two lesions. A third histological category, chronic lobular hepatitis, comprises patients with histological lesions like those of acute hepatitis, but with a chronic or recurrent course.
 ...
PMID:Liver biopsy in chronic hepatitis: 1968-78. 35 68

Intravenous glucose tolerance tests were performed in 10 patients with acute virus hepatitis. The assimilation coefficient of glucose and the level of insulin and C-peptide in serum were determined before and in the course of the glucose tolerance tests. In comparison to healthy normal weight persons C-peptide concentration in patients with acute hepatitis increased twice as high whereas the pattern of insulin secretion did not differ significantly. The higher levels of C-peptide indicate an increase of the beta-cell secretion in acute hepatitis. One could suppose an increased hepatic destruction of insulin in acute hepatitis, because there is no significant difference among the insulin levels. More likely, there is a reactive increase of secretion of the beta-cell due to a reduction of insulin sensitivity and this is indicated much better by C-peptide- than insulin levels because of the longer half live of the the C-peptide molecule.
 ...
PMID:[Concentration of C-peptide and insulin in serum of patients with acute virus hepatitis (author's transl)]. 36 78

Smooth-muscle antibodies (SMA) were investigated by the indirect immunofluorescence method and serum immunoglobulin (Ig) concentrations measured by radial immunodiffusion in 15 patients with hepatitis B antigen (HBAg)-positive and 20 patients with HBAg-negative acute hepatitis. In both types of hepatitis the serum IgM and IgG concentrations were significantly higher than in 55 controls, while the IgA levels were the same in patients and controls. IgM-SMA in titres of 10--80 occurred in 11 (55%) patients with HBAg-negative acute hepatitis, and this was significantly higher than in controls (P = 10(-8), whereas IgM-SMA were found in only 2 (13%) patients with HBAg-positive acute hepatitis. IgG-SMA occurred in 3 (15%) HBAg-negative and in 4 (27%) HBAg-positive patients. In HBAg-negative hepatitis the serum IgM concentrations were significantly higher in IgM-SMA-positive (mean: 439 mg/dl) than in IgM-SMA-negative (mean: 216 mg/dl) cases (P = 0.028). It was not possible to demonstrate a similar rleationship in HBAg-positive acute hepatitis. No correlation between the occurrence of IgG-SMA and the IgG levels could be demonstrated in acute hepatitis. It is assumed that IgM-SMA may account for a minor part of the elevated IgM levels in HBAg-negative acute hepatitis, but the reason for formation of SMA in acute viral hepatitis is not known.
 ...
PMID:Correlation between serum immunoglobulin concentrations and smooth-muscle antibodies in acute viral hepatitis. 37 86

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.
 ...
PMID:Hepatitis B core antigen immune complexes in the liver of hepatitis B patients. 38 86

Hypertriglyceridaemia occurring in patients with liver disease has been studied by measuring hepatic triglyceride lipase (H-TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H-TGL with specific antibodies. Lipid analysis, determination of lecithin-cholesterol-acyltransferase (LCAT) activity, and liver function tests were performed in parallel in fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty with cirrhosis of the liver. Total post-heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H-TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridaemia disappeared with a concomitant increase of H-TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.
 ...
PMID:Secondary hypertriglyceridaemia in patients with parenchymal liver disease. 41 76

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
 ...
PMID:Patterns of hepatic injury induced by methyldopa. 42 37


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>