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Biomedical subjects

J Slusarczyk

Publications and source records attributed to J Slusarczyk.

At least 91 records · Page 5Linked to original sources
PubMed1984

[Delta infection in HBsAg carriers].

Anti-delta as an indicator of chronic delta infection was found in 7/180 HBsAg carriers. This indicates a low incidence of delta infection in Germany. The following risk factors to acquire delta infection were established: Mediterranean origin (3 cases) and transfusion of blood products (4 hemophiliacs). All anti-delta positive individuals had a biopsy proven chronic active hepatitis and the serological pattern: HBsAg, anti-HBc and anti-HBe positive without indicators of Dane particle synthesis (negative tests for HBeAg and DNA polymerase activity).

Adolescent↗
PubMed1984

Detection of liver-kidney microsomal autoantibodies by radioimmunoassay and their relation to anti-mitochondrial antibodies in inflammatory liver diseases.

A radioimmunoassay (RIA) was developed for the detection of liver-kidney microsomal (LKM) autoantibodies. These were detected in four of 62 patients with HBsAg negative chronic active hepatitis (CAH) and in one patient with mixed connective tissue disease (MCTD). LKM antibodies were not detected in other hepatic and non-hepatic diseases. Other autoantibodies, especially anti-mitochondrial ones, do not react in this assay system. Sera positive for LKM antibodies by RIA showed a cytoplasmic staining of hepatocytes and proximal renal tubules by immunofluorescence. The LKM antigen was detected by RIA in microsomes prepared from rat liver, kidney, stomach, heart, lung, and skeletal muscle. It was destroyed after treatment with trypsin and chymotrypsin, but preserved after treatment with RNAase, DNAase and neuraminidase. Upon centrifugation of purified rat liver microsomes in CsCl gradient, LKM reactivity was detected at a density of 1.20 g/ml. In addition, the M2 antigen of the inner mitochondrial membrane specific for primary biliary cirrhosis (PBC) was localized at 1.28 g/ml in these density gradient fractions. The LKM antigen could not be solubilized. The presence of LKM antibodies characterizes a distinct subgroup of HBsAg negative CAH; they do not occur in PBC.

Adolescent↗
PubMed1981

Follow-up studies of healthy blood donors. Anti-HBs antibody carriers.

10 healthy blood donors persistently seropositive for anti-HBs and without a history of clinically overt viral hepatitis were observed for periods of time ranging from 46 to 57 months. Physical examinations and biochemical liver function tests were normal in all cases. Immunologic studies of their immune response to hepatitis B virus antigens are suggestive for a late period of convalescence from clinically inapparent hepatitis B.

Adult↗
PubMed1980

Membranous glomerulopathy associated with hepatitis B core antigen immune complexes in children.

Direct immunofluorescence, immunoelectron microscopy, and special immunohistochemical procedures including guinea pig complement fixation, differential elution, and in situ antigen binding were employed in an immunomorphologic analysis of kidney biopsy specimens from 98 children with clinically diagnosed nephrotic syndrome and/or glomerulonephritis (GN). Glomerular deposits of hepatitis B virus (HBV) antigens, immunoglobulins, and complement were detected in specimens from 24 children, all seropositive for hepatitis B surface antigen (HBsAg) and antibody to hepatitis B core antigen (HBcAg). Of these, 21 cases were diagnosed as membranous glomerulopathy (MGN), 1 as membranoproliferative GN, and 2 as diffuse mesangial proliferative GN. HBaAg was identified as the only HBV antigen in about a third of the cases of MGN, whereas in another third it was accompanied by HBsAg. HBsAg was the only HBV antigenic component detected in the glomerular deposits in the remaining third of the cases of this GN form. The results of this study indicate that apart from, or in addition to, HBsAg immune complexes, HBcAg immune complexes may also participate in the pathogenesis of a significant number of MGN cases in children subclinically infected with HBV. A possibility that these complexes include nonparticulate, presumably low-molecular-weight HBaAg components and that they are found in an environment of antibody-excess is discussed.

Adolescent↗
PubMed1979

Kidney glomerular pathology in various forms of acute and chronic hepatitis.

Kidney tissue from 99 unselected necropsy cases of various forms of hepatitis and liver cirrhosis was examined by histology and direct immunofluorescence. Glomerular deposits of hepatitis B surface antigen (HBsAg), IgG, IgM, and complement were found in nine of 59 cases (15%) of acute and subacute hepatitis and in seven of 40 cases (17%) of chronic aggressive hepatitis and liver cirrhosis. Different amounts of granular hepatitis B surface antigen immune deposits were distributed along glomerular capillary walls and/or in mesangial areas. Glomerular lesions found in these cases consisted of thickening of glomerular capillary walls, a slight increase in glomerular cellularity, and an increase of mesangial matrix. These glomerular lesions are considered to result from the humoral immune elimination of circulating viral surface antigen immune complexes.

Complement C3↗
PubMed1979

Immunoglobulin content of experimentally induced amyloid in hamsters.

Experimental amyloidosis in hamsters induced by Di-Te-Per vaccine was studied for periods of 14 to 126 days. Immunohistochemical analysis showed that after the 4th week of immunization amyloid deposits containing immunoglobulins accumulated in the liver, spleen and renal glomeruli. The amount of immunoglobulin in the amyloid deposits increased in the final stage in the kidneys, spleen and portal spaces of liver. In the spaces of Disse the amount of immunoglobulin after 4 and 18 weeks of immunization was similar.

Amyloidosis↗
PubMed1977

Cellular localization of hepatitis B virus antigens in patients with hepatocellular carcinoma coexisting with liver cirrhosis.

Specimens of liver tissue obtained by biopsy from five patients and at necropsy from seven patients with postnecrotic liver cirrhosis and hepatocellular carcinoma were examined for the presence of hepatitis B surface antigen (HBs Ag) and hepatitis B core antigen (HBc Ag) by direct immunofluorescence. In all cases, samples of serum were tested for HBs Ag and antibody to HBs Ag (anti-HBs) by immunoelectroosmophoresis and for antibody to HBc Ag (anti-HBc) by indirect immunofluorescence. Of these 12 representative cases of the main histological types of hepatocellular carcinoma, six were found to be seropositive for anti-HBc, and three of them were negative for HBs Ag. HBs Ag was detected in the cytoplasm of hepatocytes in the cirrhotic nodules in one seronegative patient and in three of the seropositive cases. In the latter cases, HBs Ag was identified in the cytoplasm of cells in well-differentiated hepatocellular carcinoma. HBc Ag was not found in any of the specimens examined.

Adolescent↗
PubMed1977

Clinical and immunological studies on healthy blood donors hepatitis B antibody carriers.

Ten healthy blood donors persistently seropositive for anti-HBs and without a history of clinically overt viral hepatitis were studied. While physical examination and biochemical liver function tests exhibited normal values in all cases, immunologic studies revealed coexistence of a long-term anti-HBs carrier state with the presence of cell-mediated immunity to HBV antigens and autoantibodies in some. These results suggest a complex immunologic phenomenon underlying the development of the anti-HBs carrier state.

Adult↗