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Biomedical subjects

K H Wiedmann

Publications and source records attributed to K H Wiedmann.

42 records · Page 3Linked to original sources
PubMedDate not supplied

Liver membrane antibodies detected by immunoradiometric assay in acute and chronic virus-induced and autoimmune liver disease.

In this study, we describe a radioimmunoassay to detect liver membrane binding antibodies. The assay was designed to exclude binding of aggregated IgG or immune complexes to Fc gamma receptors of hepatocytes. When this assay was applied to sera from 142 patients, antibodies were found in highest titer in patients with autoimmune chronic active hepatitis, rarely in patients with hepatitis B virus-induced chronic active liver disease, and in 32% of patients with primary biliary cirrhosis. IgM antibodies were found in 100% of patients with acute Type A but not B or non-A, non-B hepatitis. IgA class antibodies were found in the sera of 57% of patients with alcohol-induced hepatitis. All patient groups showing significant titers of liver membrane antibodies display the lesion of piecemeal necrosis except those with alcohol-induced hepatitis. Further studies are needed to determine whether this antibody is the cause of the lesion.

Adolescent↗
PubMedDate not supplied

(+)-Cyanidanol-3 in the treatment of acute viral hepatitis: a randomized controlled trial.

One-hundred sixty patients (81 cyanidanol, 79 placebo) were included in a double-blind placebo-controlled clinical trial to evaluate the effect of 3 gm (+)-cyanidanol-3 per day for 8 weeks on the clinical course of acute viral hepatitis and HBsAg elimination. Quantitative determination of HBsAg was performed at frequent intervals. The mean time for serum bilirubin to decrease to 1.3 mg per dl was 30.8 +/- 3.5 days in the treated group and 52.2 +/- 9.8 days in the control group, (p less than 0.025). The time for SGOT to decrease to 100 IU per liter was 17.98 +/- 1.82 in the treated group and 26.53 +/- 3.7 in the control group (p less than 0.025). No significant difference in the evolution of other laboratory values or symptoms was found. The elimination rate of HBsAg was identical in both groups. Treatment did not alter the incidence of chronicity.

Acute Disease↗
PubMedDate not supplied

Human hepatocellular carcinoma: cross-reactive and idiotypic antigens associated with malignant transformation of epithelial cells.

Monoclonal antibodies were isolated following immunization with the HBsAg and alpha-fetoprotein-secreting human hepatoma PLC/PRF/5 ("Alexander") cell line. Three antibodies (K-PLC1, K-PLC2 and K-PLC3) showed evidence of carcinoma-associated reactivity by indirect immunofluorescence. Antibodies K-PLC2 and K-PLC3 reacted only with PLC/PRF/5 cells, but not with any other normal or malignant cell type tested, including the Hep/G2 hepatoma cell line. The reactivity of these antibodies was not removed by absorption with homogenates of either normal liver or a primary hepatocellular carcinoma. These results suggest that K-PLC2 and K-PLC3 identify PLC/PRF/5 idiospecific determinants. Following surface iodination of PLC/PRF/5 cells, immunoprecipitation and analysis on polyacrylamide gels, these specific determinants were found to be of 200,000 and 76,000 daltons, respectively. On the other hand, antibody K-PLC1, although unreactive by immunofluorescence on the majority of normal cell types, including those of lymphoid organs and bone marrow liver cells and most epithelia, was weakly positive on some normal ductal secretory epithelia and was positive on vascular endothelium. However, K-PLC1 reacted strongly with all carcinoma specimens tested, and with most carcinoma-derived cell lines, indicating a large increase in K-PLC1 antigen expression by epithelial cells after malignant transformation. Absorption of K-PLC1 with normal liver homogenate had no affect, but absorption with a hepatocarcinoma homogenate abolished its activity. The K-PLC1 antigen could not be immunoblotted or immunoprecipitated and resolved on polyacrylamide gels; yet it showed the properties of a phospholipid, namely resistance to proteases, extractability with organic solvents and sensitivity to phospholipase C.

Antibodies, Monoclonal↗
PubMedDate not supplied

Serological classification of chronic cholestatic liver disease by the use of two different types of antimitochondrial antibodies.

Clinical and morphological features in fifteen patients with chronic cholestatic liver disease (mixed form) who had two different types of complement-fixing antimitochondrial antibodies were compared with those found in twenty-five patients with classic primary biliary cirrhosis (PBC). PBC-specific antimitochondrial antibody (M2) directed against an antigen of the inner mitochondrial membrane was always present in both groups. However, mixed-form cases had a second antimitochondrial antibody (M4) which fixed complement with a trypsin insensitive antigen probably located on the outer membrane. Histological lesions typical of chronic active hepatitis, often associated with granulomata formation and bileduct proliferation, and simultaneous increases in IgM and IgG were predominant features, indicating that these mixed-form cases may represent a separate clinical entity.

Antibody Specificity↗
PubMedDate not supplied

Parameters predicting response to alpha-interferon treatment in chronic hepatitis C.

BACKGROUND/AIMS: Sustained response to alpha-interferon treatment for chronic hepatitis C is seen in only 25% of cases. Therefore, it is desirable to define pretreatment factors predicting responders. MATERIALS AND METHODS: Forty-nine patients with chronic hepatitis C were treated with a standard alpha-interferon regimen (3 x 3 MU s.c./week). Demographic, biochemical and immunological parameters, and HCV genotypes were obtained prior to initiation of treatment and evaluated for their value in predicting response to alpha-interferon therapy. RESULTS: Response, as defined by normalization of ALT, was 71% during interferon therapy and sustained response after discontinuation of interferon 24.5%. Patients infected with HCV-genotype 1b had significantly more often "community-acquired" disease. Their outcome was worse with a response rate of 44% during therapy and a sustained response of 12.5%, as compared to 87% and 27% respectively in patients infected with genotypes other than 1b. On multivariate analysis, absence of cirrhosis, HCV-genotype other than 1b, higher ALT levels and higher numbers of CD8 positive liver infiltrates were found to be predictors of response during alpha-interferon therapy. CONCLUSION: Response to alpha-interferon therapy seems to be influenced both by viral virulence factors and by the intensity of the host immune response to HCV.

Adult↗