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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course of 10 liver transplant recipients who had hepatitis B virus (HBV) and five recipients with HBV and D (delta) infection before transplantation is described. Six patients who underwent eight transplants died. The estimated one and two year survival rates in patients with HBV only before transplantation were 74% and 67% respectively. The estimated one and two year survival in patients with HBV and HDV infection beforehand was 100%. Graft infection by HBV occurred in 8 of 10 patients infected with HBV only; and in 4 of 5 patients with previous HBV and HDV infection. There was a widely variable time from transplantation to the appearance of HBV markers in liver or serum, ranging from 6-331 days. Hepatitis D antigen (HDAg) appeared in three grafts very rapidly after transplantation at 4, 8, and 37 days respectively. Graft infection by HBV was accompanied by significant liver injury in six allografts in five recipients. In particular, there was a striking morphological appearance in five infected livers in which the hepatocytes became progressively enlarged and distorted as they accumulated huge amounts of hepatitis B surface and core antigens (HBsAg, HBcAg). These features were accompanied by pericellular fibrosis and cholestasis but little associated inflammation. This syndrome carried a poor prognosis. A gradual progression to cirrhosis occurred in one additional liver. Finally, recurrent HBV infection was a principal or a contributing factor in all deaths. The presence of HBcAg and inflammation in he native liver increased the risk of HBV induced tissue damaged in the graft whereas HDV infection in the host liver seemed to reduce the risk of significant HBV induced tissue damage in the allograft. These data suggest that post transplant HBV infection is accompanied by a variety of changes in the liver allograft, some of which are unique to the transplanted liver and may result in impaired allograft function.
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PMID:Recurrence of hepatitis B and delta hepatitis after orthotopic liver transplantation. 144 66

Hemodialyzed patients and kidney recipients are frequently multiply-transfused and infected by hepatitis B virus (HBV). Hepatitis delta virus (HDV) has a symbiotic association with HBV. The prevalence of HDV infection has, surprisingly, not been assessed in patients in hemodialysis or renal transplantation setting. We retrospectively studied the prevalence of serum delta antigen and antidelta antibodies by a microenzyme-linked immunosorbent assay in 77 of the 80 HBsAg-positive patients who underwent a kidney transplantation over a 10-year period. Of these patients, 73% had active HBV replication as assessed by the presence of serum HBV DNA and 65% had a biopsy-proved chronic active hepatitis, including cirrhosis. None of our patients had any marker of HDV infection at the end of the hemodialysis period or at the end of follow-up in transplantation. These results establish that HDV superinfection has indeed been extremely rare during end-stage renal failure and kidney transplantation in France, in contrast to HBV reactivation or hepatitis C virus infection.
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PMID:Absence of hepatitis delta virus infection in chronic hemodialysis and kidney transplant patients in france. 146 75

Four patients who received an auxiliary partial liver graft for decompensated liver cirrhosis due to hepatitis B (HBV), associated in two cases with hepatitis D virus (HDV) superinfection, were studied. The sequential appearance of hepatitis B and D antigens in the grafts was investigated in serial liver biopsies by immuno-histochemical methods and compared with the viral antigenic profiles of the host livers. The histological changes in the liver grafts were studied in relation to the viral expression patterns. One week after transplantation, expression of HBsAg was already apparent in two grafts. HBcAg was found in the graft of the only patient with HBcAg in the host liver. HDAg was expressed in the grafts of both patients with HDV superinfection; in one of these cases HDAg was present without HBsAg. At 3 months, viral antigen expression was maximal. Expression of HBsAg and HBcAg in the grafts of the two HDV-positive patients was, however, less extensive than in the two HBV-positive patients. All patients developed a mild lobular hepatitis, histologically demonstrated between the 47th and 107th posttransplantation day. In the two HBV-positive, HDV-negative patients, cirrhotic transformation of the graft occurred within 1 year. In the HDV-positive patients only a mild chronic active hepatitis with slight or moderate fibrosis was observed after 1 year. We conclude that recurrence of HBV and HDV infection in auxiliary liver grafts is demonstrable within 1-3 weeks. HBV infection in liver grafts may be a rapidly progressive disease. Coinfection with HDV does not aggravate the acute hepatitis and may even suppress the progression of chronic HBV.
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PMID:Course of hepatitis B and D virus infection in auxiliary liver grafts in hepatitis B-positive patients. A light-microscopic and immunohistochemical study. 150 Jun 81

From a series of 100 patients hospitalized for chronic hepatitis B infections (HBV), 51 chronic carriers of the HBs antigen without elevated aminotransferases or circulating HBV DNA were studied retrospectively. They had no unusual epidemiological or clinical features compared to the other patients, but were distinguished by their normal liver function tests, except for 5 cases of isolated hypergammaglobulinemia. Hepatic biopsies performed on 28 patients showed minor lesions or normal tissue in 61% of the cases and persistent chronic hepatitis (PCH) in 39% of them. No clinical or biological abnormality was significantly associated with PCH, which was attributed to a delta hepatitis (HDV) superinfection in only one case. There were no cases of active chronic hepatitis or cirrhosis. The significance of the histological lesions in the absence of HBV replication or other symptoms of hepatocyte aggression was not elucidated; their longterm prognosis is not known even if no other difference, identifiable by usual methods, seems to exist between these "pseudo-healthy" carriers and real healthy carriers of HBV.
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PMID:[Healthy and pseudo-healthy carriers of hepatitis B virus. A comparative clinical, biological and pathological approach]. 152 50

Parenterally shared blood and sexual transmission are the main routes of spread of hepatitis B in the United States. Most cases resolve spontaneously without specific treatment. Passive immunization provides temporary protection in certain postexposure settings. Active immunization achieves high protection rates. Duration of protection and the need for booster doses are not well defined. Many cases of fulminant B hepatitis, severe chronic active hepatitis, and end-stage cirrhosis secondary to hepatitis B are due to hepatitis delta virus infection. The delta virus requires the presence of hepatitis B for expression of disease. Hepatitis B prophylaxis should help eliminate delta hepatitis.
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PMID:Viral hepatitis in the 1990s, Part II: Hepatitis B and delta virus. 152 72

In carriers of HBsAg (Hepatitis B virus surface antigen) the incidence of Hepatitis D virus infection was studied in 72 (61.3%) males and 45 (38.5%) females, totally in 117 cases with a mean age of 34.8 years. There were 26 (22.2%) asymptomatic carriers of HBsAg where in other chronic carriers the diagnosis were as follows; 29 (24.7%) chronic persistent hepatitis, 20 (17.0%) chronic lobular hepatitis, 23 (19.6%) chronic active hepatitis and 19 (16.2%) posthepatic cirrhosis. The incidence of HDV serologic markers were found to be positive in 19 (16.2%) out of 117 cases.
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PMID:[Incidence of hepatitis D virus infection in chronic hepatitis B virus carriers]. 152 42

The hepatitis D virus (HDV) infection plays a major role in severe liver damage caused by hepatitis. To establish the prevalence of HDV infection in haemophilic patients and patients without haemophilia, 87 patients with chronic hepatitis B virus (HBV) infection were examined for serological evidence of delta hepatitis. In addition HBV, HDV and human immunodeficiency virus type 1 (HIV) infection markers were compared to clinical and histopathological outcome of hepatitis. Out of 46 haemophiliacs 30 (65%) were anti-HD-seropositive; 10 out of 30 anti-HD-positive patients (33%) had pathological liver function tests compared to 2 out of 16 anti-HD-negative haemophiliacs (13%). The rate of HIV infection did not differ between the HDV infected and the non-HDV infected individuals with haemophilia (17/27 anti-HD-positive patients versus 12/16 anti-HD-negative patients). Two haemophilic anti-HD-positive patients underwent liver biopsy, in both cases hepatitis D antigen (HDAg) was detected in the biopsies. Only 2 out of 41 patients without haemophilia were anti-HD-positive. Both had pathological liver function tests; chronic active hepatitis and cirrhosis, respectively, were diagnosed and HDAg was found in the liver biopsies. Out of 39 anti-HD-seronegative patients without haemophilia, 26 (67%) were hepatitis B e antigen positive; in the sera of 20 patients (51%) HBV-DNA was demonstrated, but only 6 patients (15%) had pathological liver function tests. In conclusion a high seroprevalence of HDV infection was found in haemophilic patients treated with non-pasteurized commercial clotting factor concentrates. An endemic spreading of HDV infection in patients without haemophilia with chronic HBV infection could not be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation of hepatitis B virus, hepatitis D virus and human immunodeficiency virus type I infection markers in hepatitis B surface antigen positive haemophiliacs and patients without haemophilia with clinical and histopathological outcome of hepatitis. 153 69

Seven carriers of the Hepatitis B surface antigen who had acquired a form of chronic hepatitis D in the recent past were treated with lymphoblastoid alpha interferon (IFN) (10 MU three times weekly for 4 months, 6 MU three times weekly for other 8 months, with a 12 month follow-up after treatment). At the beginning of the study, these patients had a chronic active hepatitis with intrahepatic hepatitis D antigen but without signs of cirrhosis. By the end of therapy, five had normal amino-transferases and no trace of HDV-RNA in the serum. In two patients the liver enzymes and viremia relapsed during follow up; biochemical and virologic remission persisted after discontinuation of therapy in the other three patients. In the early non-cirrhotic stage of chronic hepatitis D, IFN may play a more consistent therapeutic role than in the average advanced case of the disease. Cytokine should be used as soon as a diagnosis of progressive hepatitis D is reached.
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PMID:Treatment of early chronic delta hepatitis with lymphoblastoid alpha interferon: a pilot study. 156 48

Hepatitis delta virus (HDV), a recently discovered infectious agent, participates in severe, often lethal forms of acute and chronic hepatitis and liver cirrhosis. Based on theoretical analysis of secondary structure, hydrophilicity and acrophilicity data, several regions of HDV antigen, presumably containing B-epitopes, have been revealed and the corresponding peptides have been synthesized by the solid phase method. All the peptides obtained reacted with the respective antipeptide rabbit sera. The peptides and their conjugates with BSA or KLH were used for ELISA with individual and pooled anti-HD-positive sera from patients with chronic delta hepatitis. The high antigenicity of the peptide 65-80 shows that one of the antigenically active regions of HDAg is situated between these amino acid residues and that the peptide may be used for detection of anti-HD antibodies in patients blood sera.
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PMID:[Synthesis and antigenic activity of peptides of the nucleocapsid protein of the hepatitis delta virus]. 160 2

Hepatitis viruses may cause liver cancer (HCC) through an indirect mechanism inducing inflammation and cirrhosis. Only hepatitis B virus (HBV) was shown to have a direct oncogenetic potential. Hepatitis D virus (HDV) infection, superimposed on the oncogenetic background provided by chronic HBV infection, appears to provide an additional risk for HCC. Patients with florid infections from both HBV and HDV and active liver inflammation develop HCC at a significantly younger age than those infected by HBV alone or infected by hepatitis C virus (about 10 years earlier). In patients positive for serum HBV-DNA/HDV-RNA and/or IgM anti-HBc/IgM anti-HD it is mandatory to program a more frequent (thrice a year) schedule of screenings (ultrasound scan, alpha-1-phetoprotein, etc.) for prophylaxis of HCC.
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PMID:Pathobiology of chronic hepatitis virus infection and hepatocellular carcinoma (HCC). 166 Nov 97


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