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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two women (aged 72 and 78 years) developed hepatitis due to clometacine. The main laboratory abnormalities were raised transaminases and blood eosinophil count. In one of these cases, in which the initial histological lesions had the appearance of aggressive chronic hepatitis, there was progression to cirrhosis despite the interruption of treatment. The mechanism of this hepatotoxicity is probably a hypersensitivity reaction.
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PMID:[Clometacine hepatitis. 2 cases (author's transl)]. 72 56

The probable etiology and outcome of bridging hepatic necrosis found on a liver biopsy performed within three months of the onset of clinical illness was evaluated in 42 consecutive patients with this finding. Eighteen of the patients (43%) had a probable drug etiology for their hepatitis. Ten patients had HBSAG-positive acute hepatitis. Fourteen patients had neither drug-induced disease nor proven HBSAg-positive hepatitis. One patient from the drug-induced group died, but the other 17 had complete clinical recovery. Eight of ten in the hepatitis B antigen-postive group cleared their antigen and had complete clinical recovery. Chronic hepatitis developed in two who remained persistently HGSAg positive. Eight of the patients in the group with unknown etiology recovered, while six developed evidence of active chronic liver disease. This incidence of active chronic liver disease is significantly greater than that found in the drug-induced group (P less than 0.02). We conclude that drug-induced hepatitiis accounts for a significant proportion of patients of acute hepatitis who have bridging hepatic necrosis on liver biopsy. However, in these drug-induced cases the finding of bridging hepatic necrosis does not appear to be associated with an increased risk of development of active chronic liver disease.
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PMID:Bridging hepatic necrosis. Etiology and prognosis. 73 15

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

To determine the clinical significance of serum bile acid measurements, changes in the serum bile acid composition in liver diseases and endogenous bile acid clearance due to test meal loads were investigated. In the case of changes in the serum bile acid composition, a characteristic pattern of a remarkable increase of chenodeoxycholic acid (CDCA) was found in fulminant hepatitis. In patients with acute hepatitis, increases in CDCA were somewhat greater than those of cholic acid (CA) and there was tendency for these changes to precede changes in other liver function tests. In cases of extrahepatic obstructive jaundice, the CA/CDCA ratio was a large value exceeding 1.0. In investigations of endogenous bile acid clearance, serum bile acid concentration two hours after the text meal load clearly reflected the hepatic disorder and it was useful in differentiating between active and inactive form in chronic hepatitis and compensation and decompensation in liver cirrhosis.
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PMID:Clinical significance of serum bile acid measurement in liver diseases. 74 93

Evidence of chronic hepatitis was found on histological examination in nine out of 15 patients positive for hepatitis-B surface antigen (HBsAg) who had either chronic renal failure or a functioning renal transplant. Cirrhosis had already developed in three of the patients, who deteriorated rapidly and died. Liver biopsies from the remaining 12 patients showed the features of chronic aggressive hepatitis in two, chronic persistent hepatitis in four, and minor histological lesions in six. The persistence of HBsAg in patients with renal failure or in those receiving immunosuppressive drugs after a transplant must indicate some impairment of the normal immune response to hepatitis-B viral antigens. Nevertheless, cellular or humoral immunity to HBsAg was detected in all eight patients with chronic hepatitis tested compared with only one out of five with minimal liver lesions, which suggests that the severity of the liver damage may be directly related to the degree of immunocompetence.
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PMID:Immune response to HBsAg and the spectrum of liver lesions in HBsAg-positive patients with chronic renal disease. 77 35

Chronic hepatitis was diagnosed on liver biopsy of 76 patients; 52 (68%)had HBsAg. Of the 52 patients with HBsAg, 23% had HBsAg shown by immunofluorescence on the liver, while it could not be detected with radioimmunoassay on the serum; 77% had HBsAg detectable in liver and in serum, and none had HBsAg in serum only. HBsAg was detected more frequently in chronic aggressive hepatitis and active cirrhosis than in chronic persistent hepatitis and cirrhosis with little activity. No correlation was found in the different forms of chronic hepatitis between the HBsAg status on the one hand, and levels of transaminases, gammaglobulins, and auto-antibodies on the other. Acute hepatitis was diagnosed on liver biopsy of 24 patients; 50% had HBsAg. Liver tissue positivity was very low in the fully developed stage compared to serum positivity. In 146 patients with other liver ailments, both liver and serum were negative for HBsAg.
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PMID:Hepatitis B surface antigen (HBsAg) in the liver of patients with hepatitis; a comparison with serological detection. 77 38

One hundred liver biopsies from 100 hepatitis patients were examined by the indirect immunofluorescent technique for the detection of HBsAg. Of the 60 positive specimens 52 were diagnosed as various types of chronic hepatitis and 8 were acute hepatitis. Four main distribution patterns of HBsAg were obtained: full cytoplasmic fluorescence with diffuse lobular distribution; cytoplasmic fluorescence with spotty distribution; peripheral fluorescence in the cell membrane and/or cell peripheries; and focal cytoplasmic positivity. There was an inverse relationship between the number of positive hepatocytes and the extent of liver cell necrosis. The distribution patterns of HBsAg were distinctive in each type of chronic hepatitis and in acute hepatitis. Homogeneous full cytoplasmic fluorescence, distributed diffusely in the whole liver lobule, was observed in chronic persistent hepatitis and in cirrhosis with little activity whereas peripheral liver cell membrane and/or peripheral cytoplasmic fluorescence associated with cytoplasmic positivity in a smaller number of hepatocytes was a characteristic finding in chronic aggressive hepatitis, active cirrhosis, and acute hepatitis with possible transition to chronicity. Focal cytoplasmic fluorescence was observed in acute hepatitis and a group of biopsies in chronic hepatitis in which HBsAg was detected in the liver but no antigen was detectable in the serum. The results show that the different patterns of distribution of HBsAg in the liver biopsy are helpful for the histological diagnosis of different types of HBAg positive viral hepatitis and are consistent with the hypothesis of the role of specific immune response in the pathogenesis of type B viral hepatitis.
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PMID:Distribution patterns of hepatitis B surface antigen (HBsAg) in the liver of hepatitis patients. 77 39

In confirmation of earlier descriptions by Huang et al. (Huang S-N, Millman I, O'Connell A, Aronoff A, Gault H, Blumberg BS: Am J Pathol 67: 453, 1972) nuclear eosinophilic inclusions due to excess HBcAg particles have been identified in cases of chronic hepatitis B virus infection. As the euchromatin space of affected nuclei is "sanded" by numerous core particles with concomitant dissolution of the chromatin network, spiky, finely granular, and eosinophilic inclusions without a limiting membrane become visible in hematoxylin and eosin-stained paraffin sections. These HBcAg inclusions stain greyish pink with chromotrope aniline blue and are negative for orcein, the periodic acid-Schiff reaction, and the Feulgen reaction for DNA. Sanded nuclei were detected, although not always and only few in number, exclusively in HBAg-positive patients when a focal (as in chronic aggressive hepatitis) or a generalized core formation (as in immunosuppressed kidney transplant recipients) could be demonstrated by electron microscopy or immunofluorescence. Therefore, the positive finding of sanded nuclei in a persistent hepatitis B virus infection indicates an excessive core formation the extent of which should be verified by specific methods.
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PMID:Sanded nuclei in hepatitis B: eosinophilic inclusions in liver cell nuclei due to excess in hepatitis B core antigen formation. 78 2

55 HBAg seropositive patients with chronic hepatitis B selected from a total of 217 liver biopsies were studied for the presence of HBcAg and HBsAg in the liver tissue and of Dane particles in blood by immunofluorescence and electron microscopy. Among 27 patients with non-aggressive chronic inflammation the following constellations were found: a) 19 patients (13 with nonspecific reactive hepatitis, 6 with chronic persistent hepatitis) had isolated HBsAg expression in the tissue (HBs type) and of these only 2 had rare Dane particles; b)4 patients (all with histologically very active chronic persistent hepatitis) with focal HBc- and HBsAg tissue expression (HBc+s type) and detectable Dane particles in blood; c)4 patients (1 with nonspecific reactive, 3 with chronic persistent hepatitis) with generalized HBcAg (and focal HBsAg) expression (HBc type) and multiple Dane particles in blood. Among 22 patients with aggressive inflammation (19 with chronic aggressive, 3 with "hippie"-hepatitis) focal HBcAg tissue expression (HBc+s type) was found in 17 cases and absence of HBcAg in 5 (3 with focal HBsAg, 2 completely negative by immunfluorescence), all 22 associated with Dane particles in blood, however. In a group of 6 immunosuppressed kidney transplant recipients exhibiting a high concentration of Dane particles in blood 5 patients had generalized HBcAg tissue expression (HBc type) in association with non-aggressive inflammation (1 nonspecific reactive and 4 chronic persistent hepatitis). One patient had chronic aggressive hepatitis in conjunction with focal HBcAg expression (HBc+s type). The consistent association of detectable HBcAg formation in the liver and presence of supposedly infectious Dane particles in blood has a bearing on the evaluation and classification of chronic hepatitis B. On the basis of a positive focal (HBc+s type) or generalized HBcAg tissue demonstration (HBc type and/or the direct identification of Dane particles in blood, discrimination of possibly highly infectious forms from those of low or even no infectivity has been rendered possible. This duality applies mainly to clinically and histologically benign non-aggressive forms of hepatitis presenting with a carrier state or chronic persistent hepatitis. On the basis of these and earlier findings a hypothetical concept of chronic hepatitis is presented which possesses proven diagnostic and prognostic applicability to routine liver biopsies. It is also capable of shedding new light on contradictory findings in the literature and serving as a basis for prospective epidemiologic studies.
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PMID:[Classification and infectiousness of chronic hepatitis B, defined by the Dane particle in the blood and virus components in the liver]. 79 97

The clinical course of acute viral hepatitis may vary from asymptomatic to fulminant, and the final outcome can be complete recovery, chronic hepatitis or cirrhosis. The two main challenges this generally benign, self limiting infection has presented for may years have been to understand 1) the progression to fulminant hepatitis, and 2) the progression to chronic hepatitis or cirrhosis. Fulminant hepatitis may appear infrequently (1-2 % of patients with clinical hepatitis) in both type A and type B infections. Nearly 10% of patients with acute viral hepatitis type B develop either chronic hepatitis or cirrhosis. The exact figures for progression to chronicity in patients with type A infections are probably less,but are still not fully known. During the acute phase of the disease, the patients with later progression to chronicity differ significantly from those with subsequent resolution in a number of serological, biochemical and morphological variables. Persistence of HBS antigenaemia for more than 13 weeks, a high concentration of circulating Dane particles, and the presence in the serum of the "e" antigenic determinant seem to be reliable prognostic markers for pregression to chronic hepatitis or cirrhosis. Such markers are prerequisites for therapeutic trials with potent drugs which are only justified for patients with fulminant hepatitis and patients with progression to chronicity. If the different outcome of viral hepatitis is a result of the individual T-cell function, these two categories of patients may represent the opposite extremes in lymphocytic function. Controlled clinical trials are required to evaluate the clinical effect of immunosuppression in fulminant hepatitis and immunostimulation in chronic hepatitis.
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PMID:Clinical course and prognosis of acute hepatitis. 79 97


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