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Biomedical subjects

F Rosina

Publications and source records attributed to F Rosina.

At least 73 records · Page 4Linked to original sources
PubMed1990

Autoantibodies and response to alpha-interferon in patients with chronic viral hepatitis.

One hundred and fifteen patients with chronic type B, D and non-A, non-B hepatitis treated with recombinant alpha-interferon were tested for six different autoantibodies prior to or during therapy, and the course of treatment was compared in autoantibody-positive and -negative patients. Three out of 25 (12%) hepatitis B patients, 14 out of 30 (47%) hepatitis D patients and 19 out of 60 (32%) chronic non-A, non-B hepatitis carriers had baseline or post-therapy autoantibodies. The rate of response between patients with and without autoantibodies among B, D and non-A, non-B patients was, respectively, 67 vs. 79%, 23 vs. 25%, 70 vs. 61% (p = N.S.). No adverse reaction was observed in the 36 patients who had or developed nuclear, smooth muscle, parietal cells and thyroid autoantibodies during therapy. A patient with baseline antibodies against liver and kidney microsomes developed an icteric acute hepatitis at the fourth month of therapy, but five other patients with this reactivity responded to therapy uneventfully. The presence of autoantibodies before therapy or their induction following therapy is not a contraindication to the use of interferon in patients with chronic viral hepatitis.

Animals↗
PubMed1989

A controlled trial of human lymphoblastoid interferon in chronic hepatitis B in Italy.

Sixty-four heterosexual Italian carriers of HBsAg with chronic HBeAg and hepatitis B virus DNA-positive hepatitis were assigned randomly either to receive human lymphoblastoid interferon (injections of 5 million units per m2 three times per week for 6 months) or to serve as untreated controls. After 18 months of follow-up evaluation, 26 of the 33 treated patients (79%) had cleared hepatitis B virus DNA, 23 (70%) had lost HBeAg and 20 (61%) had seroconverted to anti-HBe. Fifteen of the 31 controls (48%) had cleared hepatitis B virus DNA (p = 0.01), 12 (39%) had lost HBeAg and nine (29%) had seroconverted to anti-HBe (p = 0.002). Eight treated patients but only one control had lost HBsAg and seroconverted to anti-HBs (24% vs. 3%, p = 0.01). Treated patients cleared hepatitis B virus markers after a mean interval of 4 months, compared with 8 months in the controls. All responders to interferon cleared intrahepatic HBcAg, and 50% showed histological improvement. The baseline hepatitis B virus DNA levels and the original histology were not predictive of a response to therapy; women appeared to respond better than men. Lymphoblastoid interferon provides an effective therapy in the heterosexual Italian patient with chronic hepatitis B.

Adolescent↗
PubMed1988

Human lymphoblastoid interferon for the treatment of chronic hepatitis B. A randomized controlled trial.

The aim of this study was to demonstrate whether interferon alone could affect the course of chronic hepatitis B. A total of 66 patients have so far been randomly assigned to receive six months of interferon therapy or no therapy; three patients in the interferon group and two in the control group have withdrawn from the study. Loss of hepatitis B virus-DNA and hepatitis B e antigen was significantly higher in the patients receiving interferon than in the control group; a significant loss of hepatitis B surface antigen was observed only in patients who received interferon. The time to alanine aminotransferase normalization was significantly shorter in patients receiving interferon than in the control group. These data encourage the use of interferon in treatment of chronic hepatitis B.

Adult↗
PubMed1988

Serologic markers with fulminant hepatitis in persons positive for hepatitis B surface antigen. A worldwide epidemiologic and clinical survey.

Of 377 cases of fulminant hepatitis in persons positive for hepatitis B surface antigen (HBsAg) in Greece, Italy, the United States, the United Kingdom, the Central African Republic, Taiwan, Egypt, and India, only 52% could be attributed to infection with hepatitis B virus, which was defined as the presence of the IgM antibody to the hepatitis B core antigen (IgM anti-HBc) and the absence of serum markers of infection by extraneous viruses. Thirty percent of cases were caused by coinfection with hepatitis B virus and hepatitis delta virus or by infection with hepatitis delta virus superimposed on carriers of chronic HBsAg. In 18.5% of the patients, the absence of IgM anti-HBc indicated that they were not known to carry HBsAg, but no obvious superimposed factor of hepatitis could be identified. The cause of fulminant hepatitis is complex, and major risk factors are a pre-existing HBsAg state and hepatitis delta virus infection. Superinfection of HBsAg carriers by non-A, non-B viruses seems to be the cause in a consistent proportion of cases.

Adult↗
PubMed1987

Rapidly progressive HBsAg-positive hepatitis in Italy. The role of hepatitis delta virus infection.

Serum or liver markers of hepatitis delta virus (HDV) infection were found in 20 of 22 (90%) Italian patients presenting with an ostensible type B hepatitis that ran an accelerated course to cirrhosis. The features of the illness conformed to a syndrome of HDV infection in young males carrying the hepatitis B surface antigen (HBsAg); a latent HBsAg state was documented in many patients by a history of prior exposure to the hepatitis B virus (HBV) or by the absence of IgM antibodies to the HB core antigen. Characteristic of the disease were the clinical overture as a severe hepatitis, the lobular involvement by an extensive necroinflammatory reaction, the exuberant expression of intrahepatic hepatitis delta antigen and an atypical HBV profile of inactive infection or accelerated seroconversion from HBeAg to anti-HBe. Superimposed upon HBV infection, HDV may create a rapidly progressive course which resembles very aggressive hepatitis B but is infrequently observed in hepatitis B alone.

Adolescent↗
PubMed1987

Natural killer response to exogenous interferon in delta hepatitis: boost or depression defined within the first week of therapy.

Six patients with hepatitis B surface antigen (HBsAg)-positive chronic active liver disease and superimposed delta virus infection were followed up for changes of natural killer (NK) cell function during a 3-month course with median doses of recombinant leukocyte alpha interferon (rIFN). Careful record of the off-therapy NK function means revealed that 3 subjects were boosted, 2 were depressed, and 1 was unchanged. The NK activity patterns showed that after the start of therapy the maximal shift from the off-therapy mean was concentrated in the first week; then the trend, although confirmed, had a gentler slope on the follow-up. This indicated that the first week reflects the availability of rIFN-sensitive NK cells and characterizes the immunological competence of the patient; whilst later in follow-up, suppressive control mechanisms or loss of receptor affinity tend to blur the response. The serum levels of delta RNA dropped in the NK-boosted patients; persistently negative RNA together with clearance of intrahepatic delta antigen was demonstrated solely in that 1 patient showing 164% NK cell function increment in the first week. This study shows that paradoxical responses to exogenous rIFN are not confined to cancer patients, as indicated so far, but may appear in other subjects as well, and reflect the peculiar response of the individual; whenever an NK-dependent clearance of virus-infected cells is required, recognition of the early pattern of reactivity would be useful.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Chronic hepatitis in HBsAg carriers with serum HBV-DNA and anti-HBe.

We compared the clinical and serologic features of 118 hepatitis B surface antigen carriers with hepatitis B e antibody (anti-HBe) followed up for 3-10 yr (mean 6.1 yr), separated according to the presence or absence of hepatitis B virus-deoxyribonucleic acid (HBV-DNA) in serum. The test was performed by molecular hybridization. There were 28 carriers with and 90 without viral DNA. Carriers with serum anti-HBe/HBV-DNA had major liver disease; cirrhosis developed during the follow-up period in 9 of the patients. All had the hepatitis B "core" antigen in the liver, localized prevalently in the cytoplasm of the hepatocytes. Among carriers of anti-HBe alone, 73 had persistently normal tests of liver function and 17 had abnormal levels of alanine transaminase and usually minor forms of liver damage at histology. In a group of 24 carriers of hepatitis B e antigen who spontaneously seroconverted to anti-HBe, hepatitis and a prevalent nuclear distribution of intrahepatic hepatitis B core antigen were found in temporal correlation with the presence of hepatitis B e antigen in serum. The replication of the hepatitis B virion terminated and liver disease remitted after seroconversion to anti-HBe. A positive HBV-DNA test in anti-HBe carriers is associated with a severe and evolutive liver disease and may provide an indication for treatment with drugs inhibiting the synthesis of HBV-DNA.

Adolescent↗
PubMed1986

Treatment of chronic delta hepatitis with alpha-2 recombinant interferon.

The Hepatitis Delta Virus (HDV), a defective ribonucleic acid virus dependent on the Hepatitis B Virus (HBV) is a cause of severe liver disease that often leads to cirrhosis and death. Since the HDV finds in the HBV infection a biological niche in which to thrive indefinitely, the major victims of its infection are the carriers of HBsAg. Spontaneous resolution of chronic HDV hepatitis has been observed rarely and therapeutic attempts with steroids or azathioprine and levamisole have been discouraging. With the advent of recombinant DNA technologies several human alpha-interferons (IFNs) have been synthesized by genetic engineering and the availability of large amounts of the drug has dramatically altered the therapeutic prospects of viral hepatitis. In view of the wide range of biological activities of IFN, including inhibition of viral nucleic acid replication, we have tested the tolerance and the efficacy of this drug in chronic HDV hepatitis. The preliminary results of this study are reported.

Adult↗
PubMed1985

Risk of post-transfusion infection with the hepatitis delta virus. A multicenter study.

Hepatitis delta virus is a defective virus that can replicate only in the presence of hepatitis B virus. To determine the prevalence, circumstances of transmission, and clinical importance of infection with hepatitis delta virus, we obtained data on 262 patients with post-transfusion hepatitis who were positive for the hepatitis B surface antigen (HBsAg) even though they had received blood screened for it. We also studied 94 HBsAg carriers who were receiving repeated blood transfusions for other diseases, and 103 HBsAg carriers with hemophilia who were receiving various forms of coagulation factors. Antibody to hepatitis delta virus was found in 9 of 262 patients (3.5 per cent) with post-transfusion hepatitis, 5 of 234 (2 per cent) with self-limited disease, and 4 of 28 (14.5 per cent) with fulminant disease (P less than 0.05). The absence of IgM antibodies to the hepatitis B core antigen indicated that three of the nine patients with both HBsAg and antibodies to hepatitis delta virus had been carriers of HBsAg at the time of transfusion, and the acute disease represented the combined effects of the two viruses. Antibody to hepatitis delta virus was found in 3 of 94 Italian carriers of HBsAg who were receiving repeated blood transfusions, in none of 24 Brazilian, East German, or Australian hemophiliac carriers infused with clotting factors prepared from single or mini-pool volunteer plasma, and in 27 to 100 per cent of 79 hemophiliac carriers from European and U.S. series who received coagulation factors manufactured from large pools of plasma. We conclude that infection with hepatitis delta virus is likely to be more severe than infection with hepatitis B virus alone and that screening for HBsAg provides a high degree of safety in preventing infection with hepatitis delta virus, but that the risk is considerably greater in patients who are already carriers of HBsAg. We recommend that HBsAg carriers be given only blood derivatives prepared from a single donor or mini-pool donors.

Acute Disease↗
PubMedDate not supplied

Interferon treatment of chronic hepatitis B surface antigen (HBsAg) carriers. A description of the activation profiles of natural killer cells obtained with different schedules of administration in three subsets of carriers.

By monitoring immunobiological parameters known to be influenced by interferon (IFN), the natural killer (NK) cell activity of 10 low replication (anti-HBe) virus B-DNA (HBV-DNA) hepatitis patients receiving rIFN alpha-A, of 5 anti-HBe/delta positive hepatitis patients treated with rIFN alpha-2, and of 6 high replication (HBeAg) HBV-DNA hepatitis patients on lymphoblastoid IFN was followed-up during therapy. Overall, strong and significant (p less than 0.01) shift to increase segregated with the low replication subset; the delta positive subset was non-significantly increased (0.30 greater than p greater than 0.2); the high replication subset was depressed in a nearly significant (0.10 greater than p greater than 0.05) manner. Kinetic studies showed the activation of the first subset to follow an early steep rise and a subsequent plateau as fitted with a quadratic curve (p = 0.02); an early rise and a depression at 2 months delineated a complex cubic model (p = 0.06) in the high replication subset. The profound NK depression was clinically witnessed by a sharp rise of the aminotransferases and following drop of viremia. The study shows that i. discrete patterns of NK response as amenable to mathematical models may associate to differential patterns of virus B replication in patients responding to IFN; ii. point(s) on the NK curve may acquire clinical meaning as they coincide with a consensual or opposite shift of a clinical index.

Adult↗
PubMedDate not supplied

The immunopathogenesis of primary biliary cirrhosis.

There have been several recent advances in our understanding of primary biliary cirrhosis. Foremost amongst these has been the cloning and identification of the mitochondrial autoantigens as members of the 2-oxo-dehydrogenase complex. These include the E2 components of PBC, BCKD and OGDC. The immunodominant autoepitopes of the autoantigens have been mapped and, in all cases, correspond to the inner lipoyl domain. Limited progress has also been made on T cells, particularly the CD4 response. However, the fundamental mechanisms and the role, if any, of CD8 cells are unknown. Finally, at least 2 groups have identified a molecule that cross-reacts with PDC-E2, i.e., a mimic, on the luminal surface of biliary epithelium in PBC but not controls. The identification of this molecule will be critical in further understanding the immune response of this disease.

Autoantibodies↗
PubMedDate not supplied

Patterns of natural killer cell function activation in response to interferon in chronic HBsAG positive hepatitis: relationship with the state of viral infection and with the early clinical response.

In an effort to define immunobiological parameters identifying "responders" vs "non-responders" to IFN among hepatitis patients, 16 patients with chronic active hepatitis were screened for changes of Natural Killer cell activity (NK). 10/16 patients replicated the hepatitis B virus (HBV-DNA positive) whereas 6/16 replicated the defective B virus associated delta virus (HDV-RNA positive). Patients received 9 MU/3x/weekly/3 months of recombinant IFN alpha A. Mean NK activity of the HBV-DNA patients rose significantly from 29.9 +/- 5.3 to 45 +/- 4.7 during therapy, whereas the 6/16 HDV-RNA positive patients did not show any significant increase of NK activity. Interestingly, individual HDV-RNA positive patients exhibiting boosted NK activity also showed improvement of disease confirmed by clearance of intrahepatic delta antigen at one year. No such a correlation was found amongst the HBV-DNA positive patients. These data indicate that in spite of widespread individual variability, IFN-mediated NK boost may herald delta clearance and help in identifying "responders" and "non-responders" in IFN trials.

Adult↗