Showing papers on "Hepatitis published in 1972"
TL;DR: A prospective, controlled, double blind, randomized trial of treatments for severe chronic active liver disease, involving 63 consecutive patients chosen by predefined criteria, showed that 20 mg of prednisone daily or a combination of 10 mg of Prednisone and 50 mg of azathioprine daily was superior to 100 mg of Azathiopine daily or placebo.
675 citations
TL;DR: It is suggested that the competence of the cell-mediated (T-lymphocyte-dependent) immune system would decide whether the infection is self-limited or persists with varying degrees of liver damage.
443 citations
TL;DR: In a prospective study the exclusion of commercial blood donors and donors positive for hepatitis-B antigen (HBAg) resulted in a hepatitis frequency of only 3.7 cases/1000 units transfused in patients receiving routine blood transfusions.
Abstract: In a prospective study the exclusion of commercial blood donors and donors positive for hepatitis-B antigen (HBAg) resulted in a hepatitis frequency of only 3.7 cases/1000 units transfused...
321 citations
TL;DR: A micromethod is described for determination of the cytochrome P-450 content, demethylation rate of aminopyrine and p-nitroanisole, the activities of NADPH-cytochrome-c-reductase, pseudocholinesterase and glucose-6-phosphatase in homogenates of the small amount of human liver obtained by needle biopsy.
Abstract: A micromethod is described for determination of the cytochrome P-450 content, demethylation rate of aminopyrine and p-nitroanisole, the activities of NADPH-cytochrome-c-reductase, pseudocholinesterase and glucose-6-phosphatase in homogenates of the small amount of human liver (about 20 mg) obtained by needle biopsy. 1 g of human liver contains 32–38 mg microsomal protein, much less than that present in rat liver (50–60 mg/g liver). The cytochrome P-450 content in normals was 10.8±2.6 nmoles/g liver wet weight (mean±1 S.D.). In severe hepatitis and cirrhosis the cytochrome P-450 content fell to 50% of the control value, whereas mild and moderate hepatitis did not produce any change. Similarly, only in seriously damaged livers were the demethylationrates of both substrates lowered. The activity of the NADPH-cytochrome-c-reductase was 1.88±0.51 micromoles/g liver × min and was not impaired even by severe liver damage. The activities of glucose-6-phosphatase and pseudocholinesterase also fell only in severe liver disease.
315 citations
TL;DR: A hypothetical influence of genes expressing HL-A1,8 on the proliferative or tolerance response of immunocytes could account for the linkage disequilibrium between these antigens, and also help in the interpretation of the inherited component in autoimmune disease.
263 citations
TL;DR: The hypothesis that the diseased liver fails to sequester some antigens absorbed from the gut, and that they then become available for antibody formation elsewhere and hence contribute to the hyperglobulinaemia observed in liver disease is supported.
206 citations
198 citations
TL;DR: Mitochondrial antibody was detected in the serum in 84% of 188 patients with primary biliary cirrhosis, 11% of 77 with chronic active hepatitis, 6% of 33 with cryptogenic cirrhotic disease, and 0....
Abstract: Mitochondrial antibody was detected in the serum in 84% of 188 patients with primary biliary cirrhosis, 11% of 77 with chronic active hepatitis, 6% of 33 with cryptogenic cirrhosis, and 0....
182 citations
TL;DR: Serial biopsies in a prospective, controlled, double blind, randomized trial of treatment involving 63 patients with predefined clinical and biochemical criteria of severe chronic active liver disease revealed five different histologic patterns of hepatic injury, concluding that the evolution of any lesion is influenced by at least two factors: the original histologic pattern and the therapy applied.
163 citations
TL;DR: It is suggested that, in certain kindreds, Au antigen or an Au antigenrelated infective agent is transmitted from mother to child, and is also responsible for the development of the carrier state, chronic hepatitis, cirrhosis of the liver, and eventual primary liver cancer.
148 citations
TL;DR: A clinical and pathological study of 59 patients with hepatitis-associated antigen (H.A.A.)-positive chronic liver disease is reported, finding that corticosteroids had often been used during the attack of acute hepatitis, and this seemed to predispose to relapses and chronicity.
TL;DR: Observations indicate that there is altered cell-mediated immunity in alcoholic hepatitis which may contribute to development and/or perpetuation of chronic liver injury.
TL;DR: The incidence of clinical hepatitis among 482 hemophiliacs treated here in the last ten years is reviewed, finding that in older patients, hepatitis frequently followed the first exposure to concentrate if prior blood and plasma infusions were few.
Abstract: To the Editor.— Recent reports 1-3 have aroused alarm about the danger of hepatitis after infusion of clottingfactor concentrates prepared from the pooled plasma of many donors. We have, therefore, reviewed the incidence of clinical hepatitis among 482 hemophiliacs treated here in the last ten years (Table 1). The peak incidence occurred in 1968 in hemophilia A and in 1971 in hemophilia B. Concentrate became the predominant mode of therapy in hemophilia A in late 1967 and in hemophilia B in mid1969. A total of 343 patients with hemophilia have been observed here during the six months following their first infusion of concentrate. The incidence of hepatitis in that period is listed in Table 2. Clinical hepatitis was rare in babies. In older patients, hepatitis frequently followed the firstexposure to concentrate if prior blood and plasma infusions were few. In patients with many previous transfusions, the incidence of hepatitis
TL;DR: By assuming an analogous relationship of incubation time of serum hepatitis and HAA to dose of virus inoculated, it was possible to estimate the relative infectious virus content of other materials used in the same studies, including treated fractions of the plasma pool, derivatives of the Plasma Pool, and serum from hepatitis carriers and an icterogenic lot of thrombin which were unrelated to the plasma Pool.
TL;DR: Findings add further support to the view that a wide variety of antigenic stimuli contribute to the hyperglobulinaemia in this disease.
TL;DR: The hypothesis that the cellular immune response plays an important part in the clearance of the infective agent from H.A.A.-positive patients and in the pathogenesis of the associated liver cell injury is supported.
Abstract: Cell-mediated immunity to antigens prepared from both serum and liver of patients positive for hepatitis-associated antigen (H.A.A.) was measured by using the leucocyte migration test. Altogether, 43 patients with H.A.A.-positive acute and chronic liver disease, eight with serum antibody to H.A.A., and 13 controls were studied. The cell-mediated immunity detected was specific for H.A.A. or other antigenic determinants of the associated infective agent and could be found only in patients with evidence of previous contact with H.A.A. Cell-mediated immunity to the H.A.A.-positive test antigens was found in all but one of the patients with acute hepatitis, in about half of the patients with chronic aggressive hepatitis or cirrhosis, rarely in those with chronic persistent hepatitis, and in none of the apparently healthy carriers. Our results support the hypothesis that the cellular immune response plays an important part in the clearance of the infective agent from H.A.A.-positive patients and in the pathogenesis of the associated liver cell injury.
TL;DR: Estimates of the relation of Au to the overall problem of posttransfusion hepatitis suggest that Au accounts for approximately 25% of icteric cases.
Abstract: Transfusion of blood containing Australia antigen (Au) was followed by development of hepatitis, Au antigenemia, or both in 52% of recipients. Another 23% of Au recipients exhibited an immune response. However, transfusion of Au- negative blood was associated with anticteric hepatitis in 16% and icteric hepatitis in 2% of the recipients. The typical Au recipient with hepatitis was Au positive during the acute phase and had a severe clinical illness. In the recipient of Au-negative blood, hepatitis was characterized by Au-negative tests in the acute phase and a mild illness. On the basis of these data, estimates of the relation of Au to the overall problem of posttransfusion hepatitis suggest that Au accounts for approximately 25% of icteric cases. Twenty percent of patients who developed Au antigenemia following transfusion became carriers of the antigen. Patients who became Au carriers tended to have mild or anicteric hepatitis, while those with severe, icteric attacks reverted to the Aunegative state. The frequency of Au antigen in commercial donor blood was 13-fold greater than in volunteer blood.
TL;DR: Systematic screening of 13,300 consecutively registered Danish voluntary blood donors revealed 24 donors with persistent Au-antigenemia, and a retrospective study gave no evidence of past or present acute hepatitis in any of these recipients.
Abstract: Systematic screening of 13,300 consecutively registered Danish voluntary blood donors revealed 24 donors with persistent Au-antigenemia. None of these had any clinical signs of disease. Liver biopsies were performed on all the Au-antigenemic donors. In only one of the 24 biopsies was cirrhosis demonstrated. None of the remaining 23 biopsies, of which six showed a completely normal histologic picture, exhibited the changes seen in viral hepatitis. Before detection of the antigenemia 10 of the Au-antigenemic donors had given blood to 22 recipients. A retrospective study gave no evidence of past or present acute hepatitis in any of these recipients. No Au-antigen or Au-antibody was found in any of the surviving recipients. The apparent absence of post-transfusion hepatitis in the recipients may be related to the absence of acute and chronic hepatitis in the blood donors.
TL;DR: Hepatitis and the hepatitis-associated antigen (HAA) were studied in 56 mothers who had acute viral hepatitis during pregnancy or within six months of delivery and their infants who were tested for HAA at least once.
Abstract: Hepatitis and the hepatitis-associated antigen (HAA) were studied in 56 mothers who had acute viral hepatitis during pregnancy or within six months of delivery and their infants who were tested for HAA at least once. Twenty-six mothers were HAA-positive during the acute illness, and HAA was found in the infants of ten. In 17 of these women HAA-positive hepatitis occurred within two months of delivery, and eight of their babies were found to be HAA-positive. Hepatitis-associated antigen was found in two of 19 cord bloods tested. The antigen appeared to cross the placental barrier in three cases, and neonatal contamination at birth seemed to occur in one. Persistent antigenemia and protracted subclinical hepatitis were found in all HAA-positive babies.
TL;DR: It is suggested that the association of neonatal hepatitis with α1-antitrypsin deficiency may be commoner than previously realized and that Australia antigen acts as a trigger factor in these cases.
Abstract: Five out of 28 infants investigated in a regional survey of neonatal hepatitis were found to have genetically-determined deficiency of α1-antitrypsin (ZZ phenotype). The clinical course and pathological changes varied considerably. All five infants had an acute hepatitis-like illness, and although this subsided cirrhosis later developed in three cases. The remaining two infants had minimal abnormalities of the liver function tests at 12 and 18 months of age, and one had increased hepatic fibrosis. Australia antigen was found in the serum of three infants, and Australia antigen or antibody in one or both parents of these and of one further case whose serum was negative. It is suggested that the association of neonatal hepatitis with α1-antitrypsin deficiency may be commoner than previously realized and that Australia antigen acts as a trigger factor in these cases.
Journal Article•
TL;DR: In liver cirrhosis and chronic persistent hepatitis there was a positive correlation between the amount of the Au HAA immune complexes found in the liver and the degree of hepatocellular damage.
Abstract: In a significant percentage of examined cases of fulminant hepatitis, subacute hepatitis, chronic aggressive hepatitis, liver cirrhosis and chronic persistent hepatitis, Australia (hepatitis-associated) antigen (Au HAA) was identified in the liver and in extrahepatic locations. The several immunofluorescent patterns of Au HAA localization in hepatocytes strongly suggested various stages of Au HAA accumulation and release. Deposits of a mixture of immunoglobulins G and M and occasionally β1C-globulin were found in the cytoplasm of Au HAA containing hepatocytes, on their plasma membranes, on or in the nuclei, in the cytoplasm of Kupffer cells and, rarely, in the sinusoids. The accompanying tissue changes were hepatocellular degeneration and necrosis. These intra- and extracellular complexes of Au HAA and immunoglobulins displayed strong affinity for guinea pig complement in the immunohistochemical complement fixation reaction. When tested by immunodiffusion in agar, IgG dissociated from these complexes by potassium thiocyanate (KSCN) treatment showed anti-Au HAA specificity. In fulminant hepatitis neither Au HAA nor immunoglobulins and complement were found in the liver. In chronic aggressive hepatitis and subacute hepatitis the amount of the Au HAA immune complexes identified in the liver was approximately inversely proportional to the extent and severity of the parenchymal lesions. In liver cirrhosis and chronic persistent hepatitis there was a positive correlation between the amount of the Au HAA immune complexes found in the liver and the degree of hepatocellular damage. The deposits of Au HAA, identified in extrahepatic locations including germinal centers of lymph nodes and spleen, kidney glomeruli and blood vessel walls, were as a rule accompanied by deposits of IgG, IgM, β1C-globulin and fibrin. All these deposits showed strong affinity for guinea pig complement in the immunohistochemical reaction of complement fixation. Germinal center activation, chronic membraneous glomerulonephritis, panarteritis and simple arteriolar hyalinosis were found at sites of localization of these deposits.
Journal Article•
TL;DR: It was deduced that although not a prerequisite, the liver-specific lipoprotein plays an important supportive role in the development of immune hepatitis.
Abstract: Two liver-specific antigens are known: a water soluble protein (LP-2) and a water insoluble macromolecular low density lipoprotein (LP-1).
In this paper the relative role of the two antigens in the development of experimental immune hepatitis has been investigated. Immunization of rabbits with a human preparation containing both antigens, led in all animals to lesions characteristic of an immune hepatitis. Immunization of the animals with a purified water soluble liver protein proved less efficient: only two out of six animals developed characteristic lesions which were less severe than those in the first group. It was deduced that although not a prerequisite, the liver-specific lipoprotein plays an important supportive role in the development of immune hepatitis.
TL;DR: It is hypothesized that these determinants, d and y, reflect the activity of two distinct genotypes of hepatitis-B virus (HBV), provisionally designated HBV-D and HBV -Y, which are beginning to be studied.
Abstract: Infection with type-B-hepatitis virus causes Australia antigen (HB Ag) to appear in the serum. This antigen possesses the "group" specificity, a , common to all HB Ag-positive sera; and one or other of two mutually exclusive subspecificities, d or y , which distinguish the two antigenic subtypes, D and Y. We hypothesize that these determinants, d and y , reflect the activity of two distinct genotypes of hepatitis-B virus (HBV), provisionally designated HBV-D and HBV-Y. Transmission experiments have shown that these viral subtypes "breed true." Their separate identity is further attested by the usual finding of only one subtype in localized outbreaks of hepatitis B. The clinical expressions of HBV-D and HBV-Y infection are beginning to be studied. Early results suggest significant differences in subtype distribution, such as the marked preponderance of Y in drug-abusers' hepatitis.
TL;DR: The availability of a new and more sensitive assay for HAA provided more convincing evidence that injection of gamma globulin with a hemagglutination-inhibition method decreased the incidence of both Haa-positive and HAA-negative endemic icteric hepatitis.
Abstract: A simple radioimmune assay method was used to detect Australia (HAA) antigen in serum specimens from normal military blood donors and soldiers with endemic icteric hepatitis. This method detected more than twice the number of HAA-positive specimens among both groups of subjects than by other available methods. Furthermore, it detected all positive specimens found by the agar-gel diffusion, immunoelectro-osmophoresis, complement-fixation and passive hemagglutination-inhibition methods. The radioimmune assay method showed that about 1 per cent of screened military blood donors and 25 per cent of soldiers with icteric endemic hepatitis had HAA in their serum. In these patients with hepatitis we had previously shown that the prophylactic administration of human serum gamma globulin decreased the incidence of both HAA-positive and HAA-negative endemic icteric hepatitis. The availability of a new and more sensitive assay for HAA provided more convincing evidence that injection of gamma globulin with a ...
TL;DR: It is suggested that the urine and throat should be repeatedly cultured to detect infection with CMV and to diagnose disseminated CMV infections in acute childhood leukemia, it may be necessary to repeatedly determine levels of antibody to CMV.
Abstract: Cytomegalovirus (CMV) infections were studied longitudinally in 88 leukemic children; 24 patients had cultural evidence of CMV infection at some point. There appeared to be a good correlation between excretion of virus (in urine and/or throat) and presence of complement-fixing (CF) and indirect-hemagglutination (IHA) antibody; however, a few patients had detectable antibody without excretion of virus and vice versa. Compared with patients not excreting virus, patients shedding CMV had significantly more episodes of pneumonitis and fever with rash but did not have more episodes of hepatitis, fever of unknown origin, or upper respiratory-tract infections. Clinical syndromes attributed to CMV correlated with fourfold rises in CMV antibody titer only during hematologic remission. However, dissemination of CMV occurred during hematologic relapse as well as during remission. Three patients who died after fourfold rises in CMV antibody had postmortem evidence of dissemination. Excretion of virus did not correlate with hematologic relapse, appearance of symptoms, antibody levels, or lymphocyte transformation against CMV. These data suggest that the urine and throat should be repeatedly cultured to detect infection with CMV. Moreover, to diagnose disseminated CMV infections in acute childhood leukemia, it may be necessary to repeatedly determine levels of antibody to CMV.
TL;DR: The findings suggest that the virus of hepatitis B is endemic in low socioeconomic populations and that it is probably spread, in part, by non-parenteral (or inapparent parenteral) means.
TL;DR: The ability of therapeutic doses of corticosteroids to suppress T-lymphocyte function and in combination with the other findings implies that such therapy during acute hepatitis could result in persistence of both H.H.A. and the associated infective agent.
TL;DR: HEPATITIS B antigen occurs in three general clinical groups: in acute B-type viral hepatitis in which HBAg is present in the early phase of illness and disappears in 95 per cent of patients concomitant with clinical recovery, in association with certain diseases such as Down's syndrome, uremia treated with hemodialysis, renal-transplant recipients, leukemia and lepromatous leprosy, and in asymptomatic carriers.
Abstract: HEPATITIS B antigen (HBAg) occurs in three general clinical groups: in acute B-type viral hepatitis in which HBAg is present in the early phase of illness and disappears in 95 per cent of patients concomitant with clinical recovery; in association with certain diseases such as Down's syndrome, uremia treated with hemodialysis, renal-transplant recipients, leukemia and lepromatous leprosy, in which persistence of HBAg is common; and in asymptomatic carriers who report neither exposure to blood products nor contact with patients with hepatitis.1 2 3 Persistence of HBAg in the first two groups has been postulated to be due to individual host variation in . . .
TL;DR: Empirical investigation revealed that an infected group of children in the neighborhood, an imperfect drinking water supply, a warm August day, a football team in training, and a local fire were links in the chain which resulted in this most unusual outbreak of infectious hepatitis.
Abstract: During a 15-day period in September and October 1969, an outbreak of infectious hepatitis affected the members of a college football team. Of 97 persons exposed, 90 were infected, 32 experienced typical icteric disease, 22 were anicteric but symptomatic, and 36 asymptomatic players were recognized as having significantly elevated serum glutamic pyruvic transaminase values (> 100 units). Other athletes, using the same facilities but arriving six days after the established date of exposure, were unaffected. The decision to obtain blood samples from the entire team, as soon as the initial cases were recognized, resulted in the demonstration of an unexpectedly high attack rate of 93%. Epidemiologic investigation revealed that an infected group of children in the neighborhood, an imperfect drinking water supply, a warm August day, a football team in training, and a local fire were links in the chain which resulted in this most unusual outbreak of infectious hepatitis.
TL;DR: A possible role for blood-sucking arthropods in transmission of hepatitis-B infections in the tropics and in other areas is suggested, as well as a high frequency of exposure in the early years of life when the risk of developing chronic hepatitis- B-virus infections is greatest.