Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “chronic viral hepatitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMedDate not supplied

[HBs-antigenemia and the state of cellular and humoral immunity in children with chronic viral hepatitis B].

In chronic virus hepatitis B the causative virus replicates for a long time as manifested by HBsAg persistence. Examinations of 92 sick children revealed changes in cellular and humoral immunity indices. The content of T-lymphocytes (determined according to Bach et al.) was reduced to 31.5 +/- 1.4% in the exacerbation stage (the normal content 50.8 +/- 1.3%), the percentage of O-cells increased, while the number of B-cells according to Mendes et al. did not change significantly. The inhibition of adhesion of A-cells (Halliday et al.--A. F. Blyuger) and "immune" plaque formation (according to A. F. Blyuger) in the presence of HBsAg were also increased maximally in the exacerbation stage. HBs-antigenemia was found to occur most frequently in the exacerbation stage. The content of immunoglobulin G was reduced. An increase in the number of tissue lymphocytes and their blast forms (in the "skin window" sample by Rebuck) was demonstrated. The authors assume that the long-term persistence of HBs-Ag and, consequently, the maintenance of the pathologic process activity are due to a defficiency of cellular immunity factors. The prospects of enhancing cellular immunity in virus hepatitis B in children are discussed.

Adolescent↗
PubMed1978

[Circulating immune complexes in acute viral hepatitis, chronic active hepatitis, and periarteritis nodosa (author's transl)].

Circulating immune complexes were determined in patients with acute viral hepatitis, chronic active hepatitis and periarteriitis nodosa with the Raji cell technique. Circulating immune complexes were found in 11/18 HBsAg positive and HBsAg negative cases of acute viral hepatitis. In HBsAg positive chronic active hepatitis immune complexes were detectable in 42/43 cases but only in 1/27 HBsAg negative cases. Ten healthy HBsAg carriers demonstrated no detectable immune complexes. Using FITC conjugated antisera against HBs, HBc, and e antigen, immune complexes could not be found in any case of acute viral hepatitis or chronic active hepatitis. Elution of immune complexes from Raji demonstrated IgG, C'3 and a lack of HBsAg, HBc or e antigen. Immune complexes were present in 4/8 cases with periarteriitis nodosa. Viral components were detectable in one case.

Acute Disease↗
PubMed1975

[Cellular immune reaction in acute and chronic viral hepatitis (author's transl)].

The course of viral hepatitis is markedly influenced by the immunologic response to the infective agent. The immune defense of viral diseases is specially connected to an intact function of T lymphocytes. Investigation of T cell function during acute and chronic viral hepatitis showed an altered immune response, recognizable from the relative number of T lymphocytes, the affinity and ability of lymphocytes to be stimulated by phytohemagglutinin and the demonstration of in vivo activated lymphocytes. Although the interpretation of some of these findings is still difficult, the study of the various cellular immune reactions permits a better understanding of the pathogenesis and course of viral hepatitis.

Acute Disease↗
PubMed1979

[Acute and chronic viral hepatitis in childhood. A review].

The author reviews nomenclature, pathogenetic agents, immunological markers and mode of infection of hepatitis in childhood. Epidemiology, incubation period, prejaundiced phase, clinic and course in regard to different types of viral hepatitis are characterised. Especially jaundiced and nonjaundiced courses, biochemical parameters immunological diagnosis of hepatitis type A and type B respectively are emphasized together with histological and histologic-immunological criteria. Therapy and prophylaxis of A- and B-hepatitis are discussed. The author reports on the chronic, chronic-persisting and chronic-active form of the hepatitis including immunological markers, auto-antibodies and therapy.

Autoantibodies↗
PubMed1975

[Humoral immune phenomena in acute and chronic viral hepatitis (author's transl)].

During HBAg positive acute viral hepatitis transitory antibodies of a low titer against smooth muscle, vascular endothelium, nuclei, and liver cell membrane antigens (polygonal pattern of immunofluorescence) occur. In HBAg positive chronic aggressive hepatitis, sometimes antibodies against nuclei or smooth muscle are associated with HBAg. Their occurrence heralds an unfavorable prognosis. High titer antibodies against nuclei and smooth muscle - a typical serology finding in lupoid chronic aggressive hepatitis - and mitochondrial antibodies have not been observed in a HBAg positive hepatitis. Subdividing chronic hepatitis in six different groups is possible with HBAg and antibodies. The predominance of histocompatability antigen HLA 8 in lupoid hepatitis and a lack of this leukocyte antigen in HGAg positive chronic aggressive hepatitis suggests that in the various forms of hepatitis, a different susceptability and capability for immune response towards microorganism is reflected. It is postulated that for course and outcome of hepatitis, the type of immune reaction plays a decisive role.

Acute Disease↗