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

Chronic hepatitis may develop after acute B-hepatitis or acute non A-non B-hepatitis, as well as after toxic liver damage. Microscopic examination after biopsy allows to differentiate between chronic persistent (CPH) and chronic active (CAH) hepatitis. CPH needs not to be treated, but just to be controlled. Immunosuppressive therapy with steroids, eventually combined with azathioprine, is recommended nowadays in HBsAg-negative CAH. It has been shown, that survival rates are higher in patients, when this therapy is applied during the early stage of the disease, than in patients without therapy; the development of cirrhosis of the liver however does not seem to be influenced by this therapy. Immunosuppressive treatment of HBsAg-positive CAH is still controversial. Antiviral therapy (anti-HBs-antibodies, interferon, adenine-arabinoside) or therapy using immunostimulation (transfer-factor, levamisole, BCG) are also still in an experimental state.
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PMID:[Therapy of chronic hepatitis (author's transl)]. 616 69

36 patients with acute sporadic non-A, non-B viral hepatitis were prospectively followed up. Study parameters included biochemical and immunological (hepatitis A/B) data, histology of the acute and chronic stage of the disease and immunohistology for hepatitis B markers. The mean follow-up period for the patients with complete remission was 8.5 months, and 30.5 months for the patients with progression to chronic liver disease. 13 (36%) patients developed histologically confirmed chronic hepatitis (6 CPH, 7 CAH). In the chronic stage of the disease, the transaminases showed a markedly fluctuating course in 8 of the 13 patients. Two of the 6 patients with CPH showed complete remission after 25 and 58 months respectively; in the 4 others the disease remained unchanged. In the 7 patients with CAH no remission occurred, but in 2 patients complete cirrhotic transformation of the liver was demonstrated after 36 and 38 months respectively. Hence the prognosis of chronic sporadic non-A, non-B hepatitis seems to be worse than the prognosis of chronic posttransfusion non-A, non-B hepatitis.
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PMID:[Long-term course of sporadic non-A, non-B hepatitis: a biochemical, immunologic and histologic follow-up study]. 644 91

In a retrospective study a total of 754 sera from 397 hepatitis patients were assayed for delta antigen and antibody by radioimmunoassay. The study included patients of all age groups (3 months up to 85 years) whose first serum sample, taken from 1978 until January 1984, was positive for HBsAg. Clinically the patients could be subdivided into three major groups: 311 sera were from 181 patients with acute hepatitis, 296 from 135 CPH/CAH patients, including a few cases of liver cirrhosis and 3 cases of HCC, and 147 sera were from 81 asymptomatic carriers. Delta markers were found in 30 patients (7.6%). 20 of these were under the age of 30, and 13 presented with acute, often fulminant hepatitis or (in a minority of cases) exacerbations of preexisting HBV infection. Only two symptomless carriers had anti-delta. It seems of particular interest that all 10 cases where delta antigen could be demonstrated in the first serum sample presented with acute, often fulminant hepatic disease and 9 had anti-HBc-IgM antibodies. Where a second sample could be tested (5 cases), seroconversion to anti-delta was always demonstrated. Delta superinfection could be shown in 2 cases where anti-delta antibodies appeared more than a year after HBsAg positivity was first detected.
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PMID:[Delta hepatitis in Switzerland. Determination of delta antigens and delta antibodies in 397 HBsAg-positive patients (1978-1984)]. 647 32

The prevalence of autoantibodies against the liver membrane antigen LSP (anti LSP) has been studied in acute and chronic non-B hepatitis. Anti LSP autoantibodies were detected in five of eight patients with type A and in two of 18 patients with type non-A, non-B (NANB) acute hepatitis. No statistically significant difference was observed between the group of anti LSP positive and anti LSP negative cases of acute non-B hepatitis concerning age, serum glutamic pyruvic transaminase (SGPT), and serum bilirubin levels. In hepatitis A SGPT and bilirubin levels were significantly higher as compared to type NANB acute hepatitis. Sera which were positive for anti LSP in the acute phase were negative within 2 months from onset although the two anti LSP positive patients hepatitis (CPH). None of 27 patients with chronic NANB hepatitis displaying the morphology of CPH were anti LSP positive; in contrast, six of nine patients with autoimmune type chronic hepatitis were anti LSP positive, displaying the morphology of chronic active hepatitis. In conclusion, in acute hepatitis anti LSP autoantibodies are a consequence of liver cell destruction rather than being involved in the mechanism of liver cell necrosis. Anti LSP autoantibodies are unlikely to play an important role in the development of chronic NANB hepatitis.
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PMID:Studies on anti LSP autoantibodies in acute and chronic non-B hepatitis -- evidence for the lack of anti LSP in non-A, non-B (NANB) viral hepatitis. 678 2

Between 1975 and 1980, 10 children with acute and 8 children with chronic hepatitis type Non A, NON B (NANB) were seen in our hospital. Parenteral inoculation was probable in 10 cases. Hepatitis NANB was diagnosed in about 11% of all children with acute viral hepatitis who were admitted over this period. Children with parenterally acquired disease were more frequently anicteric and had less pronounced transaminase elevation than "sporadic" cases. An uncomplicated outcome was observed in only three of the ten children. Two patients died from acute liver failure, chronic hepatitis developed in three other children. The 9 children with chronic hepatitis NANB are representing 17% of all patients with chronic hepatitis who were seen in our clinic between 1975 and 1980. In six children with CPH a benign course was observed whereas three children with CAH were severely ill including portal hypertension. Immunosuppressive therapy was tried in two cases without success. In children as well as in adult patients, acute hepatitis NANB apparently has more frequently a prolonged course or progression to chronic liver disease than acute hepatitis of other etiology. It seems that CPH NANB shows a similarly benign course as chronic persistent hepatitis B. CAH NANB in our patients, however, had a poorer prognosis than CAH type B.
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PMID:[Non A, non B-hepatitis in children]. 681 83

For an early identification of chronic courses of hepatitis virus B infections a statistical prediction model based on simple biochemical parameters and immunofluorescence microscopy for the investigation of virus HBs and HBc antigen expression in liver tissue is established. As early as 3 weeks after maximum liver cell damage it is possible to identify chronic virus B infections and to predict the further course of hepatitis (CPH, CAH).
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PMID:[Prognostic validity of biochemical data and immunofluorescence microscopy in acute hepatitis B (author's transl)]. 701 Aug 69

This paper gives the results for HBeAg and anti-HBe titers in chronic HBsAg carriers and patients with type B hepatitis using a "solid-phase" radioimmunoassay. In tumor and hemodialysis patients the HBeAg titers are statistically significant higher compared to the group of HBsAg positive CAH or CPH. High anti-HBe titers are a characteristic finding in "healthy" HBsAg carriers. On the other hand, there is a subgroup of HBsAg positive CAH with anti-HBe; although there are signs of an ongoing virus B replication these cases of CAH proceed sometimes to cirrhosis.
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PMID:Quantitation of HBeAG and anti-HBe by RIA in sera of chronic HBsAG carriers and individuals with type B hepatitis. 725 42

The terms chronic active hepatitis (CAH), chronic persistent hepatitis (CpH), and chronic lobular hepatitis (CLH) have become obsolete, and their use without further specifications should be discontinued. This recommendation has become necessary because these names have changed from descriptive terms, intended for grading, to terms that are used either as morphologic diagnoses or disease designations or both, depending on individual preferences. Because this practice has caused serious misunderstandings, many authors and two international groups have recommended the use of a clear etiologic terminology. For the reporting practice of pathologists, we recommend that the pathologist routinely sign out biopsy samples with features of chronic hepatitis by indicating etiology, grade, and stage. An example would be autoimmune hepatitis, severe, stage 3. The stage in this case would indicate the presence of well-developed septal fibrosis but no nodular regeneration. Obviously, for the etiologic diagnosis, morphologic findings must be integrated with clinical and laboratory data. If this information is not available, clear morphologic diagnoses should be reported. Thus, instead of CPH, the diagnosis should be portal hepatitis, cause undetermined. This reporting practice eliminates ambiguous terminology and avoids the risk of inappropriate treatment as might occur, for example, when a term such as CAH is used to describe Wilson's disease and is misunderstood to mean autoimmune hepatitis. For a transitional period and to facilitate relearning, the terms CAH, CPH, and CLH can be reported in parentheses behind the etiologic diagnosis.
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PMID:Chronic hepatitis. An update on terminology and reporting. 750 62

In the search for parameters that can indicate changes in the behaviour of liver tissue from normal to chronic to neoplastic disease, DNA content by FCM (ploidy and percent of 4N cells) and morphobiological characteristics were investigated in fresh liver specimens of 16 patients with normal liver, 21 with persistent hepatitis (CPH), 23 with chronic active hepatitis (CAH), 17 with cirrhosis, and 13 with hepatocellular carcinoma (HCC). Aneuploidy was mostly found in HCC specimens (54%), whereas the percentage of 4N peak decreased in chronic hepatitis and cirrhosis patients but increased to 11.09% in HCC samples (r = -0.02; p = 0.05). Finally, the binuclearity rate decreased gradually from normal to flogistic to HCC specimens. The 4N peak and the binuclearity rate were closely correlated in non-HCC (p = 0.0006, by T-test) but not in HCC samples. Only DNA ploidy and the binuclearity rate have been confirmed as being significantly and independently related to the histology of liver tissue by multivariate regression analysis.
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PMID:Flow cytometry DNA content and morphobiological characteristics in chronic and neoplastic human liver disease. 779 88

The classification of chronic hepatitis distinguishing benign chronic persistent hepatitis from severe chronic active hepatitis was constructed without knowledge of well-defined aetiological factors. Better understanding of the different hepatitis-viruses has shed new light on this subject. Chronic viral hepatitis B and C each show typical histological patterns. The validity of the conventional classification has been evaluated by a comparative study of chronic viral hepatitis B and C. 130 biopsies from 110 patients with chronic hepatitis C (CH-C) proven serologically by antibodies (second generation testing) were compared with 105 biopsies from 73 patients with chronic hepatitis B (CH-B). These were scored semi-quantatively. In CH-C, lymphoid follicles and/or aggregates were found in 88.5%, fatty degeneration in 51%, bile duct lesions in 46.2%, and Mallory body-like material in the hepatocytes in 9.2%. The portal lymphocytic infiltration generally predominated over the necro-inflammatory lesions of the parenchyma. Chronic persistent hepatitis (defined by the presence of portal hepatitis) was present exclusively in CH-C. Chronic lobular hepatitis was found exclusively in CH-B. We conclude that the histological criteria described for CH-C are highly suggestive of the diagnosis, that the artificial subdivision of chronic hepatitis into CPH and CAH is obsolete and that the histological assessment of chronic hepatitis should consist of a grading of inflammatory activity (minimal, mild, moderate, severe) and staging of fibrosis (extent of distortion of architecture). The final diagnosis should be based on the demonstration of the aetiological agent.
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PMID:Chronic viral hepatitis B and C: an argument against the conventional classification of chronic hepatitis. 781 6


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