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Biomedical subjects

A J Zuckerman

Publications and source records attributed to A J Zuckerman.

At least 235 records · Page 13Linked to original sources
PubMed1976

Enhanced HBsAb production in pathogenesis of fulminant viral hepatitis type B.

The possible importance of humoral immunity in the pathogenesis of fulminant hepatitis was investigated by comparing 17 patients with fulminant hepatitis type B with 20 patients with severe but non-fulminant disease. Hepatitis B surface antigen (HBsAg) was cleared from the serum significantly faster (P less than 0-001) in those with fulminant hepatitis, and in 41% anti-HBsAg (HBsAb) was detectable by radioimmunoassay (RIA) at presentation. In all 11 sera from patients with fulminant hepatitis that were examined by electron microscopy aggregates of HBsAg and HBsAb were seen. In contrast, HBsAb was never detected by RIA in those with non-fulminant hepatitis, and in only one serum specimen (5%) were aggregates seen on electron microscopy. A significant sex difference between fulminant and non-fulminant hepatitis was observed, 65% of patients with fulminant hepatitis but only 15% of patients with non-fulminant hepatitis being women (P less than 0-01). An enhanced production of HBsAb in fulminant hepatitis, by leading to free HBsAb in portal blood, may cause an Arthus reaction in the sinusoids of the liver with ensuing ischaemic necrosis of hepatocytes.

Acute Disease↗
PubMed1976

Hepatitis B virus infection in dental surgical practice.

Sixty-one dental surgeons at King's College Hospital were interviewed to establish the incidence of attacks of viral hepatitis and to relate this to environmental risk factors. Six (10%) had a history of hepatitis, in one case due to infection with the hepatitis B virus. Screening blood for HBsAg by radioimmunoassay showed no carriers of the antigen, but transient antigenaemia was observed in one dentist. Antibody to HBsAg, tested by radioimmunoassay, was detected in four dentists (7%), only one of whom had had clinical hepatitis. Dental surgeons may be more at risk from infection with the hepatitis B virus than the general population, although this should be minimised in hospital practice, where the most infected patients will already have been identified and appropriate precautions can be taken. The risk of transmission from an antigen-positive dentist to his patients is probably much smaller, and there is no evidence to restrict his clinical activities.

Adult↗
PubMed1976

Detection of HBSAG in fixed liver tissue - use of a modified immunofluorescent technique and comparison with histochemical methods.

A modified immunofluorescent technique was used for the detection of HBSAg in formalin-fixed liver tissue, thereby allowing retrospective examination of paraffin sections and avoiding the need to split the sample at the time of biopsy. Comparison with two other methods, involving either orcein staining or standard haematoxylin and eosin (H and E) preparation for ground glass hepatocytes, showed slightly fewer positive hepatocytes in individual biopsies with the latter stain, but the specificity of both methods was high. In a series of 146 seropositive and 74 seronegative patients with a variety of liver disorders, hepatocytes positive for HBSAg were found in only one of 55 patients with acute hepatitis type B, whereas large numbers of positive cells were seen in all 22 healthy carriers of the surface antigen. In the 69 patients with chronic persistent or chronic aggressive hepatitis, the frequency of positive biopsies was 86% and 85% respectively. The positive cells in these cases were, in comparison with healthy carriers of HBSAg, much fewer in number and were scattered in random fashion throughout the lobule rather than occurring in discrete clumps or sheets. This variation in the intrahepatic expression of HBSAg may reflect differences in the immune response to hepatitis B viral antigens.

Acute Disease↗
PubMed1976

Acute and protracted changes in the liver of Syrian hamsters induced by a single dose of aflatoxin B1. Observations on pathological effects of the solvent (dimethylformamide).

Male Syrian hamsters, 8-10 weeks of age, were treated with a single intraperitoneal injection of crystalline aflatoxin B1 in solution of N -N -Dimethylformamide (DMF). The concentrations of aflatoxin were adjusted to the smallest controllable amount of solvent in relation to the size of the animal (0-5 or 1-0 ml/kg). Treatment with, respectively, 5-0 or 2-5 mg/kg aflatoxin in 1-0 ml/kg DMF was lethal to most animals within one week. However, reduction of the solvent to 0-5 ml/kg, while not eliminating the mortality entirely during the first week, made possible observation of the survivors up to 28 days. Hamsters appear to be more susceptible to DMF poisoning than other species, like rat, guinea-pig and rabbit in which this solvent was used by investigators on the biological effects of aflatoxin. Either dose given of DMF alone was lethal for several animals during the first week of observation and sufficient to produce histological lesions in the liver which were characteristic and clearly different from those induced by aflatoxin during the same period. DMF alone caused centrilobular necrosis which was accompanied by haemosiderosis of liver structures. With a aflatoxin, in addition, periportal and midzonal necrosis of the liver was present. Aflatoxin B1 and B1 and DMF both induce haemorrhagic tendency probably involvement in the coagulation process of the blood. It cannot be decided, however, at present whether this is the result of an indentical mechanism.

Aflatoxins↗
PubMed1975

Fulminant hepatic failure in leukaemia and choriocarcinoma related to withdrawal of cytotoxic drug therapy.

In three patients with malignant disease HBsAg was detected in the serum at least 6 months before the development of acute hepatitis type B, which in each case followed a fulminant course to death. It is suggested that suppression of the normal immunological responses to hepatitis-B viral antigens by cytotoxic drug therapy permitted widespread infection of hepatocytes. Subsequently, upon withdrawal of these drugs, recovery of immunocompetence resulted in rapid destruction of all infected hepatocytes and massive liver damage. Screening for HBsAg before cytotoxic drug therapy, careful monitoring of liver function during its withdrawal, and prompt treatment with corticosteroids should abnormalities occur may prevent this unfortunate sequence of events.

Adult↗
PubMed1975

Hepatitis-B antibody in polymyalgia Rheumatica.

Thirteen patients with polymyalgia rheumatica (P.M.R.) were examined for evidence of viral infection. Hepatitis-B surface antibody (HBsAb) was detected in nine out of twelve patients tested prior to therapy. The antibody persisted up to six months in four patients but reverted to negative in the other five. HBsAb was found in only one of twelve age-matched controls. Hepatitis-B surface antigen was not detected in any patient or control. No significant elevation of antibody titre was detected to a panel of twelve other organisms. Immunoglobulin levels were elevated prior to treatment in several patients. With steroid therapy the IgG and IgA levels fell serially but the IgM levels increased in six patients. These results suggest that hepatitis B is an important trigger for P.M.R. In view of the association with giant-cell arteritis, P.M.R. may represent an abnormal immunological response to infection in elderly patients.

Antibodies, Viral↗
PubMed1975

Cellular and humoral immunity to hepatitis-B surface antigen in active chronic hepatitis.

The hepatitis-B surface antigen (HBsAG) may be persistently present in the serum in a few cases of active chronic hepatitis but the cause of the disease in most patients is unknown. In a study of 39 HBsAg-negative cases cell-mediated immunity to HBsAg was observed in 24 (62%), suggesting a high frequency of previous infection with the hepatitis-B virus. Hepatitis-B surface antibody was detectable by radioimmunoassay in six patients, in all of whom complexes of HBsAg were present in the serum on electron microscopy. Out of 12 patients with HBsAg-positive active chronic hepatitis who were also studied eight, including all those untreated at the time, showed a cellular response to the antigen. Evidence of sensitization to a liver-specific cell surface lipoprotein was found with similar frequency in the two groups. These results are consistent with the hypothesis that hepatitis-B virus infection is important in initiating the disease in many cases of active chronic hepatitis and that sensitization to the liver cell membrane antigen is the autoimmune process responsible for the perpetuation of the liver injury.

Antibodies, Viral↗
PubMed1975

Immunogenetic factors in thalassemia and hepatitis B infection. A multicentre study.

Geographical variations in the prevalence of hepatitis B infection were found in association with an increased opportunity of exposure to this virus in patients with homozygous beta-thalassemia in Cyprus, Greece, Sardinia and the United Kingdom. No association was found between the Gm phenotype of the individuals investigated and susceptibility to hepatitis B virus using HBsAg as a marker, or the ability to make antibody to it. Variation in the distribution of Gm haplotypes does not appear to be a feasible explanation for variation in anti-HBs and HBsAg frequencies in a series of highly transfused populations.

Adolescent↗
PubMed1975

Virus-like particles in hepatitis A.

Distinctive 27 nm virus-like particles have been found by immune electron microscopy in faecal extracts obtained during the late incubation of naturally occurring hepatitis A infection. A variety of particles measuring 22 nm and 30 nm have also been observed. However, the predominance of the 27 nm particles suggests that these small cubic virus-like structures are closely associated with hepatitis A.

Antigens, Viral↗