Salvatore Vernace

Periarteritis Nodosa, Australia Antigen and Lymphatic Leukemia

Abstract A patient who had both lymphatic leukemia and periarteritis nodosa also had persistent Australia antigenemia. Various morphologic forms of Australia antigen were observed in the patients serum on electron microscopy, but circulating immune complexes were not demonstrable. At autopsy, there was no evidence of persistent hepatitis. Examination of tissues by fluorescent-antibody technic revealed Australia antigen and IgG in the liver-cell nuclei, most probably in the form of immune complexes. Australia antigen was detected in the subacute lesions of periarteritis nodosa in the absence of immunoglobulins or complement.

Immune Complexes in Hepatocytic Nuclei of Hb Ag-Positive Chronic Hepatitis

To localize immune complexes in viral hepatitis Type B and to assess their pathogenic role, we examined by the direct fluorescent-antibody technic 21 liver specimens with hepatitis B core antigen (HBc Ag) in hepatocytic nuclei from 10 patients with HBs Ag-seropositive acute viral hepatitis and from 11 patients with HBs Ag-seropositive chronic active hepatitis. IgG with in vitro fixation of complement was demonstrated in HBc Ag-containing hepatocytic nuclei of all patients with chronic active, but not in those with acute viral hepatitis. All patients except for one had antibody to HBc Ag in the serum as determined by indirect immunofluorescence. The evidence suggests that intranuclear IgG in chronic active hepatitis has anti-HBc specificity and forms immune complexes with HBc Ag. The binding of IgG to intranuclear HBc Ag might have pathogenic importance in chronic active hepatitis.

Chronic septal hepatitis.

A type of chronic hepatitis designated as chronic septal hepatitis was distinguished morphologically from chronic aggressive and chronic persistent hepatitis: 18 cases were separated from chronic aggressive hepatitis by the absence of destruction and inflammatory infiltration of the limiting plate and from chronic persistent hepatitis by the presence of connective tissue septa. Clinically, many patients were asymptomatic despite hepatomegaly and elevated serum transaminase activities while immune markers were usually absent from the serum. Chronic septal hepatitis was often seen after corticosteroid therapy of chronic aggressive hepatitis, but it also occurred de novo. Transition to cirrhosis was not observed during follow-up for 5 years to 2 months except in one case with high serum gamma-globulin. Until a classification based on etiology becomes available chronic septal hepatitis might be separated from other types of chronic hepatitis.

Immunologic Studies in Patients with Chronic Active Hepatitis and Primary Biliary Cirrhosis I. Cytotoxic Activity and Binding of Sera to Human Liver Cells Grown in Tissue Culture

Summary Sera from patients with chronic active hepatitis and primary biliary cirrhosis containing a variety of antibodies (smooth muscle, mitochondria, nuclei) as well as hepatitis B antigen failed to show a cytotoxic activity against autologous liver cells, heterologous liver cells, Chang liver cells or other cell lines of nonhepatic sources. Cytotoxicity was measured by the microassay technique using morphologic evaluation and counting of surviving cells, and by 51Cr release from labeled cells. Lack of cytotoxicity was observed in spite of reactivity of antibodies with cultured liver cells. Mitochondrial antibodies stained the cells diffusely; smooth muscle antibodies bound to the cells in a filamentous pattern.

Migration of Peripheral Leukocytes in the Presence of Carcinoembryonic Antigen. Studies in Patients with Chronic Inflammatory Diseases of the Intestine and Carcinoma of the Colon and Pancreas

Summary The leukocyte migration technique was employed to study in vitro cell-mediated immune responses to purified CEA in patients with Crohns disease and active ulcerative colitis and in those with colonic and pancreatic carcinoma. No significant inhibition of leukocyte migration was demonstrated by CEA, with the exception of one patient with pancreatic carcinoma. Thus, with the leukocyte migration technique, no consistent in vitro cell-mediated immunity to CEA was demonstrated supporting the hypothesis that CEA is not the antigen toward which cell-mediated host response phenomena are directed. The authors wish to thank Jacques Vandevoorde, of the Hoffmann-La Roche Research Division, Nutley, NJ, for performing the radioimmunoassays for CEA and Carlos Pereira for skillful technical assistance. These studies were supported under U.S.P.H.S. Grant No. Al 09857, a N.I.H. Training Grant (AM-05126), and Mount Sinai Clinical Genetics Center Grant No. GM 19-443.