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Biomedical subjects

M Rizzetto

Publications and source records attributed to M Rizzetto.

At least 289 records · Page 16Linked to original sources
PubMed1984

Cell-mediated cytotoxicity to autologous hepatocytes in HBsAg positive liver disease: an analysis of the killing specificity and of the clinical use of the test.

The specificity of a system measuring cell-mediated cytotoxicity as effector-induced target cell detachment from plastic recently adopted to study autologous hepatocyte killing in liver disease, was examined in 17 HBsAg positive liver patients whose hepatocytes (after biopsy digestion with collagenase) were incubated in Terasaki plates with the corresponding blood lymphocytes over two days. The hepatocyte viability and the specificity of the effectors were evaluated as determinants of the clinical value of the test. We found that: (a) hepatocytes in all experiments showed membrane damage owing to the lytic action of collagenase on the small liver core; (b) patients' lymphocytes detached diseased autologous hepatocytes more efficiently than did normal lymphocytes with healthy hepatocytes; (c) in eight patients cytotoxicity appeared equally distributed between a population enriched in T cells and one enriched in non-T cells; yet the mean cytotoxic index of the latter subset was higher than that of the former; (d) cytotoxicity was not blocked by the addition of either aggregated IgG or purified HBsAg; (e) protein synthesis seemed required to promote hepatocyte detachment, for lymphocytes treated with Actinomycin D were no longer active. Poor target viability detracts from the specificity and the clinical value of the test, that therefore turns out to be a major problem of liver cell culture.

Adolescent↗
PubMed1983

Epidemiologic patterns of infection with the hepatitis B virus-associated delta agent in Italy.

To assess the epidemiology of infection with the delta agent associated with hepatitis B virus, sera from 1314 carriers of the hepatitis B surface antigen (HBsAg) and 687 patients with hepatitis B collected in 1978-1981 from different regions of Italy were tested for delta antigen and antibody to the antigen (anti-delta), and the characteristics of delta-positive patients were analyzed. Anti-delta was found in each center participating in the study, indicating that delta infection has spread throughout Italy. Its prevalence was higher in carriers in southern Italy and in those with chronic hepatitis. In northern Italy, delta infection predominated among southern emigrants in industrial towns but also among parenteral drug addicts with hepatitis B virus infection. The prevalence of delta markers was variable and generally low in acute hepatitis B, suggesting that in Italy self-limited forms of delta infection occur sporadically or by limited outbreaks. Delta infection appears to be endemic in southern Italy but a new epidemiologic event in northern Italy, where it was probably introduced by southern emigrants and is presently exceeding its ethnic confinement to spread selectively in communities of drug addicts. Presumably, the endemicity of delta is maintained by transmission of this agent from carrier to carrier of the HBsAg.

Adolescent↗
PubMed1983

Endemic HBV infection, tissue autoantibodies and HLA. Analysis of a Sardinian population.

Serum samples of 405 HLA-typed individuals from four Sardinian villages were analyzed for HB virus markers and for tissue autoantibodies. Of the 59% individuals who had been exposed to HBV, 10% were healthy carriers; they showed a weak association with the HLA-B40 specificity compared with the immune or non-exposed groups, and a negative association of DR4, limited to females. Tissue autoantibodies were significantly associated with DR1 and more weakly with B14, probably through linkage disequilibrium.

Adolescent↗
PubMed1983

Hepatitis B virus replication and clinical outcome in carriers of HBsAg. Perspectives of treatment with DNA inhibitors.

HBV-DNA was measured by the spot hybridization technique in serial serum samples obtained from 47 HBsAg carriers followed up for a mean of 4 years. The levels of HBV-DNA were compared to the conventional HBV serology and immunopathology to determine the relation of active HBV replication to the outcome of hepatitis and the suitability of Italian HBsAg carriers for treatment with DNA inhibitors. HBV-DNA was found in 26 carriers (53%) and persisted with comparable serum levels in 24 of them throughout the follow up. The occurrence rate of an unfavorable outcome as determined by histological evidence of cirrhosis was 6% versus 44% (p less than 0.01) in carriers with active viral infection (greater than 1 ng/ml of HBV-DNA) and in patients with absent or low levels of viral DNA (less than 1 pg/ml), respectively. Progression of the liver disease could not be predicted on the basis of active HBV replication and was presumably related to factors other than synthesis of HBV. In many patients with inactive viral infection a primary pathogenic factor was the HBV-associated delta, an agent with a putative RNA genome against which DNA inhibitors have no rationale and possibly no effects. The majority of Italian carriers do not appear suitable for treatment with DNA inhibitors and they should be considered for a different therapy.

Adolescent↗
PubMed1983

Complexes of hepatitis B surface antigen and immunoglobulin M in the sera of patients with hepatitis B virus infection.

Hepatitis B surface antigen (HBsAg) bound to immunoglobulin M (IgM) was detected in sera of HBsAg carriers by a radioimmunoassay based on selective absorption of the immunoglobulin on a solid phase coated with antiserum to human IgM. Isopycnic banding and rate-zonal sedimentation have shown that the reaction is related to particulate forms of the HBsAg complexed with IgM. The binding of IgM possibly occurred because of a selective affinity of these molecules to the surface of HBsAg particles. HBsAg/IgM was found transiently in 24 of 25 (96%) patients with acute self-limited hepatitis B and persistently in 6 of 25 patients whose acute hepatitis B progressed to chronicity. It was also found in 20 of 39 (51%) chronic HBsAg carriers with inactive and asymptomatic infection. The HBsAg/IgM phenomenon is not dependent on replication of hepatitis B virions; its persistence in patients with acute hepatitis B may provide complementary evidence of transition of the infection to chronicity.

Animals↗
PubMed1983

Chronic hepatitis in carriers of hepatitis B surface antigen, with intrahepatic expression of the delta antigen. An active and progressive disease unresponsive to immunosuppressive treatment.

To assess the characteristics of chronic hepatitis in hepatitis B surface antigen (HBsAg) carriers with intrahepatic delta antigen, the hepatic histologic findings of 137 patients were reviewed; 101 patients were followed for 2 to 6 years. The predominant liver disease was chronic active hepatitis in 93 patients or cirrhosis in 32; minor forms of chronic persistent or lobular hepatitis were seen in 12 patients. Eight of the 26 patients with an initial diagnosis of cirrhosis died during the follow-up period. Cirrhosis developed in 31 of 75 patients (41%) without nodular regeneration seen in the first biopsy specimen; 5 of these patients died. Treatment with prednisone or azathioprine did not induce histologic amelioration of delta hepatitis or prevent cirrhosis. Chronic HBsAg hepatitis with intrahepatic expression of the delta antigen is an active, progressive disease unresponsive to conventional immunosuppressive treatment.

Adolescent↗
PubMed1983

Microsomal autoantibodies in chronic infection with the HBsAg associated delta (delta) agent.

A cytoplasmic autoantibody is described which gives a distinct immunofluorescence pattern in tissues of man and of varied animal species. Fluorescence is maximal in human substrates; it is strong in human hepatocytes and nephron cells and weak in thyroid adrenal and pancreatic cells. Complement fixation and fluorescence absorption studies have shown that the homologous antigen is localized in the microsomal membranes of human liver. The autoantibody was found in 13% of 81 carriers of HBsAg with chronic delta infection. It was not detected in patients with acute delta infection or in HBsAg positive and HBsAg negative patients without delta infection. The apparently exclusive occurrence of this antibody in chronic delta infection suggests that its expression is induced by persistence of the viral event.

Adult↗
PubMed1983

Delta hepatitis in inapparent carriers of hepatitis B surface antigen. A disease simulating acute hepatitis B progressive to chronicity.

Infection with the hepatitis B surface antigen (HBsAg)-associated delta agent (delta) was determined in a series of Italian patients with a diagnosis of acute hepatitis B (HBsAg-positive) progressive to chronicity. Twenty-two of 27 (81%) and 12 of 18 (67%) patients collected, respectively, in Naples and Cagliari, where delta is highly endemic, developed immunoglobulin M antibody to delta and/or rising titers of immunoglobulin G anti-delta during the initial acute phase of the disease. In each of them, anti-delta increased to a high-titered plateau indicative of chronic delta infection. Delta markers were found in none of the 13 patients collected in Siena, where the prevalence of delta infection is low. The great majority of the patients with anti-delta and a progressive form of HBsAg-positive hepatitis lacked the IgM antibody to hepatitis B core antigen. They were presumably unrecognized carriers of HBsAg who became infected by delta and developed hepatitis induced by this agent. In areas where delta is endemic, it may represent the true cause of seemingly type B hepatitis progressing to chronic HBsAg-positive liver disease.

Carrier State↗
PubMed1982

Influence of delta infection on severity of hepatitis B.

The prevalence of serum markers of primary delta infection was determined in 532 patients with acute benign hepatitis B seen in Italy, and in 111 patients with fulminant hepatitis B seen in Italy, France and England. Patients with fulminant hepatitis had significantly higher prevalence of delta markers (43/111, 39%) than did those with benign hepatitis (101/532, 19%). In 25 of the 43 patients with delta-positive fulminant hepatitis, serum markers indicated a primary hepatitis B infection while in the remaining 18, IgM antibody to hepatitis B core antigen was absent, indicating that hepatitis B preceded superinfection with the delta agent. The increased morbidity of HBsAg hepatitis with delta infection may result from the cumulative simultaneous exposure to hepatitis B virus and delta, or from superinfection of HBsAg carriers with delta.

Acute Disease↗
PubMed1982

Multicentre study of prevalence of HBV-associated delta infection and liver disease in drug-addicts.

To assess the epidemiological and pathogenic effects of infection with the hepatitis-B-virus (HBV)-associated delta agent in addicts who take drugs parenterally, 225 symptomless addicts from Italy and 261 addicts with HBsAg-positive hepatitis from Italy, Denmark, Switzerland, and Ireland were tested for delta antigen (delta-Ag) and its antibody (anti-delta) by radioimmunoassay. 79 liver biopsy specimens from HBsAg-positive addicts were also tested for intrahepatic delta-Ag by immunofluorescence. Anti-delta was found in 9 (27%) of 33 of the symptomless HBsAg-positive addicts, in 13 (8%) of 156 of those without HBsAg but with anti-HBs, and in none of those negative for HBV markers. The prevalence of serum delta-Ag or anti-delta among addicts with HBsAg-positive hepatitis was 64% (104/161) in Italy, 44% (8/18) in Denmark, 33% (11/33) in Switzerland, and 31% (15/49) in Ireland. 32 of the 79 (40%)liver biopsy specimens from HBsAg-positive addicts showed positive delta-Ag immunofluorescence. Delta infection occurring simultaneously with HBV infection is common and possibly a major cause of liver disease in drug addicts who receive drug parenterally. The spread of delta infection in drug-using communities is not confined to one country, and the drug habit may represent the major means by which delta agent spreads in areas of the Western world where this infection is not endemic.

Adult↗
PubMed1982

Radioimmunoassay detection of IgM antibodies to the HBV-associated delta (delta) antigen:" clinical significance in delta infection.

A sensitive radioimmunoassay was developed for specific detection of IgM antibodies to the hepatitis b virus-associated delta antigen. The test is based on the selective absorption of IgM by anti-IgM fixed on a solid phase. Transient primary IgM anti-delta responses with no conversion to a secondary IgG response were observed in acute self-limited delta infection. IgM anti-delta was invariably found in hepatitis B surface antigen (HBsAg) carriers with active delta infection and liver disease, while it was absent in HBsAg-positive or negative individuals with anti-delta of IgG class but without liver damage or intrahepatic delta antigen. IgM anti-delta appears useful in defining the epidemiology of acute delta infection and in the serological diagnosis of active delta disease from nonpathogenic or past delta infection.

Antibodies, Viral↗
PubMed1982

Perinatal transmission of the hepatitis B virus and of the HBV-associated delta agent from mothers to offspring in northern Italy.

We report a prospective study on infants born to hepatitis B surface antigen (HBsAg) carrier mothers to estimate the incidence of perinatal transmission of HBV and HBV-associated delta agent in Northern Italy. The risk of infection to the infant was related to the presence of the HBe antigen-antibody system, HBV-specific DNA polymerase activity and antibody to delta in maternal sera, and to the titer of anti-HBe in babies at birth. The data of this study indicate: 1. Babies born to HBsAg carrier mothers with HBeAg in serum are at extremely high risk of acquiring HBV infection and of developing a chronic carrier state, whereas those born to anti-HBe-positive mothers are at a lower (P less than .01) yet consistent risk of infection. 2. HBs antigenemia is usually prolonged and symptomatic in babies born to HBeAg-positive mothers while being self-limited and asymptomatic in babies born to anti-HBe-positive mothers. 3. DNA polymerase activity in maternal serum appears to be the most sensitive marker predicting HBV transmission to the infant since it was detected in all the HBeAg-positive mothers and also in two anti-HBe-positive mothers and in one HBeAg/anti-HBe-negative mother who transmitted infection to their babies. 4. High titers of anti-HBe (up to 1:103) do not prevent HBV infection. 5. Vertical transmission of delta infection seems to occur only in circumstances that permit perinatal transmission of HBV infection.

Antibodies, Viral↗
PubMed1982

Delta infection and liver disease in hemophilic carriers of hepatitis B surface antigen.

The prevalence of infection with hepatitis B virus (HBV)-associated delta (delta) agent was assessed in 277 treated hemophiliacs (primarily adolescents and adults) and 24 treated hemophilic children. Hemophiliacs who carry hepatitis B surface antigen (HBsAg) are at high risk of delta infection. Antibody to delta (anti-delta) was found in 14 (49%) of 29 HBsAg-positive adult or adolescent hemophiliacs and four (25%) of 16 HBsAg-positive hemophilic children; it was identified in none of the patients without serologic evidence of exposure to HBV and only occasionally and in low titers in hemophiliacs convalescent from HBV infection. Either histologic or biochemical evidence of chronic hepatitis was found in 10 (56%) of 18 HBsAg-positive hemophiliacs with anti-delta. In two patients with anti-delta a potentially pathogenic role for delta was suggested by the intrahepatic expression of delta antigen, detected by immunofluorescence. It appears that delta infection is a major cause of chronic liver disease in hemophiliacs.

Adolescent↗
PubMed1982

Nonprogressive course of non-A, non-B chronic hepatitis in multitransfused hemophiliacs.

Eleven hemophiliacs with chronic liver disease were studied prospectively for 6 yr, with liver function tests and liver biopsies carried out at intervals of 3 yr. The second series of biopsies, compared with the first series, showed continuation of chronic persistent hepatitis in four patients, change to chronic lobular hepatitis in two, and spontaneous improvement of the disease in the four cases who had had chronic active hepatitis characterized by moderate piecemeal necrosis. One patient with active cirrhosis died of liver failure during the follow-up period. Study of the serum and intrahepatic markers for hepatitis B and delta viruses suggests that chronic liver disease is nonprogressive in hemophiliacs who have no intrahepatic viral marker.

Adolescent↗