Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1973 to 1989 five patients with hepatitis delta virus having anti-hepatitis delta antibodies continuously in the serum for more than 5 years were identified among 1019 hepatitis B virus carriers who were being followed-up for more than 3 years (mean 8.9 years). Of the five patients with antibodies, three had a history of blood transfusion, in two cases the transfusion was massive, and one patient had been addicted to narcotics given intravenously 35 years before. In the remaining patient, the route of superinfection could not be determined. Hepatitis delta antigen was detected in hepatocyte nuclei of one of the three patients in whom liver biopsies were performed and there was chronic persistent hepatitis detected by an indirect immunoperoxidase technique. During the follow-up, hepatocellular carcinoma developed in one case but the clinical prognosis was favourable in the remaining four cases.
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PMID:A long-term follow-up of five patients with hepatitis delta virus in Japan. 177 9

Overall 120 children with chronic liver diseases of HB-virus etiology were examined. In 78.3% of the patients, RIA was used to reveal anti-delta in blood serum, 33 children were diagnosed to have chronic persistent hepatitis, 44 chronic active hepatitis, and 43 liver cirrhosis. The patients with anti-delta manifested certain characteristic features. There prevailed children from epidemiologically unfavourable regions as regards virus hepatitis B. There also prevailed boys. In one-third of the patients with chronic liver diseases and anti-delta, acute hepatitis ran a biphasic course. According to the data obtained, super-addition of delta-infection aggravates the disease; the process becomes chronic more rapidly, exacerbations are more pronounced. 16 out of 23 children showed delta-antigen in liver biopsy specimens; in patients with active disease, the antigen was detected in the nucleus and cytoplasm at a time. As the activity decreases, the antigen becomes mostly detectable in the cytoplasm.
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PMID:[Characteristics of the course of chronic liver diseases of hepatitis B etiology with delta infection in children]. 178 97

Four hundred and four patients (273 men, 131 women) aged 3 to 85 years with chronic Hepatitis B virus (HBV) infection seen during a five year period were analysed. At presentation, 177 patients (44%) were Hepatitis B e Antigen (HBeAg) positive (mean age 32 years) and 217 patients (54%) were anti-HBe-positive (mean age 40 years). Ten patients (2%) were negative for HBeAg and anti-HBe. Serum HBV-DNA was detected in 169 patients (42%). 85% of the HBeAg-positive patients had detectable serum HBV-DNA and 9% of the HBeAg-negative patients were positive for serum HBV-DNA. The mean serum Alanine amino-transferase (ALT) and Aspartate amino-transferase (AST) levels were higher in HBeAg-positive patients (75 and 52 iu/l) than in HBeAg negative patients (46 and 37 iu/l) (P less than 0.001). Liver biopsies were performed in 135 patients. Fifty-three (39%) had minimal changes, 61 (45%) chronic hepatitis (CPH, CLH & CAH) and 21 (16%) cirrhosis. There was no significant difference in the histologic distribution between HBeAg-positive and HBeAg-negative groups. Two hundred and fifty eight patients were followed up for a mean duration of 2 years (range 3 to 108 months). The cumulative probability of clearing HBeAg at the end of the first, second and third year were 14%, 16% and 18% respectively. Of these, the cumulative probability of developing anti-HBe over one, two and three years were 8%, 9% and 11% respectively. Reversion to HBeAg occurred in 1.5% of patients who were HBeAg-negative at presentation and 11% of HBeAg-positive patients who cleared HBeAg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic hepatitis B infection in Singapore. 179 64

To complement investigations of hepatitis B virus infection in hepatocellular carcinoma associated with cirrhosis, we studied hepatitis B virus infection in 137 hepatoma patients without cirrhosis. Ninety-five were from the U.K. (where the prevalence of hepatitis B virus markers is very low) and 42 were from overseas. Of these 137 patients, seven (5%) were hepatitis B surface antigen seropositive. None of the hepatitis B surface antigen positive patients had any recognisable risk factors other than birth in an area of high hepatitis B virus prevalence in four of the patients. Of the 95 U.K. patients three (3%) were hepatitis B surface antigen positive as compared to a carriage rate of less than 0.1% in the normal population. The frequency of antibodies to hepatitis B surface and core antigens alone (both 7.5%) was also higher than that seen in the normal U.K. population (2.4%). Histological examination of the non-tumorous liver showed fine fibrous septa in three patients, more extensive subcapsular scars in one, chronic persistent hepatitis in two and non-specific inflammation in one. On immunohistochemical examination five patients had hepatitis B surface antigen (but not core antigen) detectable in the non-tumorous liver tissue. Hepatitis B virus infection appears to be a small, but significant, risk factor for the development of hepatoma in the non-cirrhotic group.
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PMID:Hepatitis B virus related hepatocellular carcinoma in the non-cirrhotic liver. 184 73

The presence of pre-S polypeptides in paraffin wax embedded liver sections from the biopsy specimens of 15 hepatitis B surface antigen (HBsAg) seropositive patients (five with chronic persistent hepatitis (CPH), four with chronic active hepatitis (CAH), four with cirrhosis and two "healthy" HBsAg carriers) was investigated using monoclonal antibodies directed to distinct epitopes on pre-S1 (18/7 and TO 606) and pre-S2 (5535 and Q 19/10). Pre-S1 was found in 13 cases when MA 18/7 was used but in only one specimen when TO 606 was used. Pre-S2 was detected in all the biopsy specimens with 5535 and in eight samples with Q 19/10. Mild enzymatic digestion annulled the staining of all monoclonal antibodies but Q 19/10. No association was observed between pre-S polypeptide expression and hepatitis B virus (HBV) replication or disease severity. Pre-S polypeptides can be detected readily in paraffin wax embedded material but the results obtained largely depend on the monoclonal antibodies used.
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PMID:Detection of hepatitis B virus pre-S1 and pre-S2 determinants in paraffin wax embedded liver tissue: importance of reagents used. 185 86

Pre-S2 protein and its antibody were detected in 130 children with hepatitis B virus (HBV) infection and 30 with T6 hepatitis B (HB) vaccination. The results showed that pre-S2 was positive in most chronic persistent hepatitis (CPH) and chronic active hepatitis(CAH) patients, while anti-pre-S2 was positive in only 8% (2/92 cases) and 11.5% (3/26 cases) respectively. The positive rate of anti-pre-S2 was 78.9% (15/19 cases) in cases at the convalescent stage of acute hepatitis B, 91.7% (55/60 cases) in cases with T6 HB vaccination and 83.3% (25.30 cases) in naturally acquired anti-HBs children, while pre-S2 was not noted. Anti-pre-S2 was negatively related to ALT and positively to anti-HBs (P less than 0.01). The positive relation of pre-S2 to HBsAg was observed. These results suggest that pre-S2 could be a marker for HBV infection, and anti-pre-S2 may indicate a favourable prognosis of HBV infection. There was no correlation between anti-pre-S2 and pathogenic damages induced by HBV.
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PMID:Significance of pre-S2 protein and its antibody in children with HBV infections. 187 11

This paper reviews the main necro-inflammatory liver lesions observed in chronic viral hepatitis B and their apparent immunological mechanisms. Focal necrosis seems to represent the mechanism for clearance of virus replicating hepatocytes by cytotoxic T lymphocytes under HLA class I restriction and with hepatitis B virus nucleocapsid antigens as target antigen. Piecemeal necrosis involves CD8+ lymphocytes, possibly with hepatocellular membrane autoantigens as target antigen. Confluent lytic necrosis (bridging hepatic necrosis) presumably results from humoral immune mechanisms. Focal necrosis, piecemeal necrosis and confluent lytic necrosis determine the extent of necro-inflammatory activity in liver biopsy specimens, classified as chronic persistent hepatitis (low activity) or chronic active hepatitis (high activity). The extent of necro-inflammatory activity fluctuates during the natural course of chronic viral hepatitis B: from low activity during the viral replicative phase, through high activity in the viral elimination phase, into low activity again in the ensuing viral integration phase. The role of HLA antigens, intercellular adhesion molecules, cytokines and accessory antigen presenting cells is emphasized.
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PMID:Immunopathology of chronic viral hepatitis. 190 15

The effect of human immunodeficiency virus (HIV) infection on type and severity of liver disease was studied in 61 HIV-positive patients who did not have AIDS and in 45 AIDS patients. Liver biopsies revealed viral hepatitis in 12 of 18 non-AIDS patients but in only 4 of 34 AIDS patients (P less than .0005, Fisher's exact test). Acute, non-A non-B, and chronic active hepatitis B were seen exclusively in the non-AIDS group; however, chronic persistent hepatitis B was seen in both groups. In 9 of 18 AIDS patients intra vitam liver histopathology established diagnoses of opportunistic infections or tumors. Tissue reaction to certain pathogens, such as hepatitis B virus, mycobacteria, and cryptococci, seems to be milder in AIDS patients than in others who are HIV positive or the expected reaction of the normal host. This is likely because of impaired cell-mediated immunity in patients with advanced HIV disease.
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PMID:Hepatic involvement in patients with human immunodeficiency virus infection: discrepancies between AIDS patients and those with earlier stages of infection. 201 Jun 40

One hundred and five hepatitis B surface antigen (HBsAg) positive patients presenting with chronic persistent hepatitis (n = 46) or chronic active hepatitis without cirrhosis (n = 59) were followed longitudinally for one to 16 years (mean 5.5 years) and underwent follow up biopsy. During a mean histological follow up of 3.7 years, active cirrhosis developed in 21 (20%) patients one to 13 years after entry to the study with a calculated annual incidence of 5.9%. The probability of evolution to cirrhosis was significantly higher in patients with chronic active hepatitis and bridging hepatic necrosis than in those with moderate chronic active hepatitis or chronic persistent hepatitis (p less than 0.0001). Cox multiple regression analysis showed that the following three variables independently implied poor prognosis: older age, presence of bridging hepatic necrosis, and persistence of hepatitis B virus DNA in serum (p less than 0.0001). These findings indicate that patients with severe chronic active hepatitis and persistent hepatitis B virus replication are at very high risk of rapid progression to cirrhosis.
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PMID:Natural history and prognostic factors for chronic hepatitis type B. 201 23

The efficacy of interferon treatment for Australian patients with chronic active hepatitis B (CAH-B) was assessed by a three-centre randomised controlled trial in Sydney and Brisbane. Thirty patients (29 with histologically-proven CAH-B with and without cirrhosis and one with chronic persistent hepatitis) were allocated to receive either thrice weekly intramuscular injections of recombinant human leucocyte interferon -alpha A (either 2.5, 5.0 or 10.0 million units/m2) for six months followed by 12 months of observation, or to be observed for 18 months without active treatment. Three of 23 treated patients but none of seven controls underwent clinical, biochemical and histological resolution of their disease with loss of HBsAg, HBeAg and HBV-DNA from serum. An additional six treated and two control patients underwent a sustained partial remission of their disease. This was characterised by resolution of symptoms and serum aminotransferase abnormalities in association with seroconversion from HBeAg positive to negative, loss of HBV-DNA from serum but persistent hepatitis B surface antigenaemia. In such patients, there was significant improvement in histological appearances but some necroinflammatory activity remained and fibrosis was unchanged. Although total response rates were similar in treated and control subjects, they appeared to occur earlier after interferon treatment. Treatment with interferon was associated with predictable but minor side effects that usually did not necessitate dose reduction and rarely compromised the patient's life style. Interferon is thus a feasible treatment for CAH-B. Complete responses occurred only in treated patients and partial responses appeared to occur earlier in treated than in untreated patients. However, differences in the partial response rate at 18 months were not significant and seroconversion from HBeAg positive to negative was not associated with complete histological resolution of disease activity. Hence, while interferon is a promising agent for treatment of CAH-B, efforts must continue to define more optimal treatment regimes and to identify those patients most likely to respond to this agent.
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PMID:Randomised controlled trial of recombinant human interferon -alpha A for chronic active hepatitis B. 218 91


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