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Biomedical subjects

A Craxi

Publications and source records attributed to A Craxi.

51 records · Page 3Linked to original sources
PubMed1984

Tissue markers of hepatitis B virus infection in hepatocellular carcinoma and cirrhosis.

In order to assess the prevalence of tissue markers of HBV infections (HBsAg and HBcAg) in HBsAg seropositive and seronegative hepatocellular carcinoma (HCC) as compared with other advanced liver diseases (inactive cirrhosis, IC, and active cirrhosis, AC), we studied 49 patients with HCC (13 HBsAg+), 52 patients with IC (5 HBsAg+) and 53 patients with AC (14 HBsAg+). Among HBsAg seropositive patients, intrahepatic HBsAg was frequently found (26/32 cases), while HBcAg was present more rarely (5/32 cases) and correlated with serological features of high-level viral replication. HBsAg seronegative, anti-HBc +/- anti-HBs positive subjects had intrahepatic HBsAg in 8/34 cases, and HBcAg in liver cell nuclei in 14/34 cases. HBcAg was more frequent in cirrhosis than in HCC. No other differences in the intrahepatic display of HBV markers was observed, nor was a specific pattern identified for HCC. Viral components were never found in the liver in the absence of serum HBsAg or anti-HBc. Neoplastic hepatocytes did not usually support the synthesis of HBsAg or HBcAg.

Antibodies, Monoclonal↗
PubMed1984

Measles virus variants: viral replication and cytopathogenicity in human T lymphocytes and B lymphoblastoid cells.

Measles virus can replicate in circulating T cells, B cell and monocytes of man as well as in different human lymphoblastoid cell lines. In the present report we describe the effects on lymphoblastoid cells and on a defined population of human T lymphocytes of infection with three measles virus variants characterized by different cytopathogenicity in human and simian epithelial cell lines. The aim of the investigation was to establish some evidence that the evolution of the viral infection and the cellular damage in lymphocytes can be directly controlled by viral properties.

Cell Line↗
PubMed1983

Relationship between HBV-specific DNA polymerase and HBe antigen/antibody system in chronic HBV infection: factors determining selection of patients and outcome of antiviral therapy.

The sera of 23% of HBe antigen positive patients with chronic hepatitis are HBV-DNA polymerase negative. These patients are probably undergoing spontaneous seroconversion from a state of high to low viral replication and do not require antiviral therapy. In chronic HBV infection rapid changes in viral replication as a result of antiviral therapy are reflected by changes in HBV-DNA and HBV-DNA polymerase but not by changes in HBe antigen concentrations. Disappearance of HBe antigen from serum may be delayed for 180 days after permanent inhibition of HBV replication with adenine arabinoside or its monophosphate derivative.

DNA-Directed DNA Polymerase↗
PubMed1982

Genetic and sex-linked factors influencing HBs antigen clearance. I. Nonimmune clearance in inbred strains of mice.

Differences in the clearance values of polyvinylpyrrolidone (KPVP) and HBs antigen (KHBs) were seen in several strains of inbred mice. In addition, in all strains studied KHBs was greater in females than in males, while KPVP was not significantly different in the two sexes. In the strain with the lowest KHBs values, the incidence of HBs antibody formation was lower than in the other strains. These data indicate that genetic and sex-linked factors influence nonimmune clearance of HBs antigen in mice. If similar factors exist in man they may explain some of the variation in clinical manifestation of HBV infection.

Animals↗
PubMed1982

Effects of prednisolone/azathioprine in chronic hepatitis B viral infection.

Changes in markers of hepatitis B viral replication and standard liver function tests were studied in 30 patients with HBsAg positive chronic liver disease starting or stopping prednisolone/azathioprine therapy, and compared with those occurring in 15 patients who did not receive therapy. On stopping prednisolone/azathioprine, 10 out of 11 HBeAg positive patients and one out of three patients negative for HBeAg and anti-HBe, lost HBV-DNA polymerase activity (p less than 0.01), five lost HBeAg, three developed anti-HBe and HBsAg concentration decreased (p less than 0.01). Only one out of seven untreated HBeAg positive patients lost HBeAg and there were no significant changes in DNA polymerase activity. In the anti-HBe positive patients, 14 starting therapy and eight untreated, there were no significant changes in the markers of viral replication - although two patients developed DNA polymerase activity on high maintenance doses of prednisolone - but a significant decrease (p less than 0.05) in aspartate transaminase in the treated group. It is concluded that the cessation of prednisolone/azathioprine therapy in HBeAg positive patients will result in a reduction in viral replication. In anti-HBe positive patients such therapy may be beneficial.

Azathioprine↗
PubMed1982

Successful treatment of HBs and HBeAg positive chronic liver disease: prolonged inhibition of viral replication by highly soluble adenine arabinoside 5'-monophosphate (ARA-AMP).

In eight HBs and HBe antigen positive patients with chronic active liver disease, adenine arabinoside 5'-monophosphate (ARA-AMP) given, intravenously or intramuscularly, six or 12 hours, produced inhibition of viral replication. In five patients given a short course of therapy with 10 or 15 mg/kg/day this effect was transient and in two thrombocytopenia occurred. In three further consecutive cases given a longer course with 5 mg/kg/day after five days of the high dose, thrombocytopenia was not seen and inhibition of viral replication for up to 13 months occurred. These patients lost HBV-DNA polymerase activity, serum viral DNA and HBeAg, developed anti-HBe, and HBsAg concentrations decreased. A course of twice daily intramuscular ARA-AMP given for three to five weeks as an outpatient may be expected to produce a long-term reduction in infectivity.

Adult↗
PubMedDate not supplied

Close association between basal cell layer antibodies and hepatitis B virus-associated chronic delta infection.

Antibodies reacting in immunofluorescence with the basal cell layer of rat forestomach (BCLA) have been detected in 36 of 121 (30%) hepatitis B virus (HBV)-mediated chronic liver disease (CLD), in 1 of 30 (3%) HBV-negative CLD, in 3 of 36 (8%) alcoholic liver disease (with no correlation with serum HBV markers), in 1 of 25 (4%) primary biliary cirrhosis, in none of 19 HBV-related HBsAg-negative CLD and 60 healthy blood donors. Of 352 hospitalized patients with miscellaneous diseases (including immunological conditions), the antibodies were found in four (1%). In the 36 BCLA positive cases from HBV-mediated CLD, evidence of chronic delta infection was found in 34. The overall prevalence of BCLA in 68 delta cases was 50% (58% in chronic active hepatitis, 46% in cirrhosis), and in 28 delta negative cases was 4% (p less than 0.00002). BCLA of delta cases were mainly of the IgG class (38 of 41 sera), and high titers (up to 40,960) were found in the majority (66% greater than or equal to 1:640). The high titer BCLA has to be considered a marker of chronic delta infection in HBV cases.

Adolescent↗
PubMedDate not supplied

Recombinant interferon alpha-2B for acute post-transfusion hepatitis in acute myeloid leukemia.

Post-transfusion hepatitis (PTH) is a major problem in patients with acute leukemias requiring blood products during induction or consolidation therapy. In fact, PTH causes delays of chemotherapy with major violations in the timing of protocols. In order to assess the efficacy and safety of a short course of alpha-interferon (alpha-IFN) in inducing early remission of PTH, we treated seven patients who developed acute hepatitis during a post-remissional phase of AML. Patients received 3 MU of alpha-IFN i.m. three times weekly for one month. One patient stopped alpha-IFN at 2 weeks because of severe itching, after ALT normalization. Five out of 6 subjects normalized ALT within a mean time of two weeks. Minor side effects were observed in 2 cases. Three patients relapsed within eight weeks after stopping alpha-IFN. They underwent a second remission upon treatment with the same schedule. All patients continued their treatment protocol for AML without delay.

Adolescent↗