THE EFFECTS OF PREDNISOLONE AND INTERFERONS ON SERUM MACROPHAGE-COLONY-STIMULATING FACTOR CONCENTRATIONS IN CHRONIC HEPATITIS-B

Citation
Y. Itoh et al., THE EFFECTS OF PREDNISOLONE AND INTERFERONS ON SERUM MACROPHAGE-COLONY-STIMULATING FACTOR CONCENTRATIONS IN CHRONIC HEPATITIS-B, Journal of hepatology, 26(2), 1997, pp. 244-252
Citations number
49
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
01688278
Volume
26
Issue
2
Year of publication
1997
Pages
244 - 252
Database
ISI
SICI code
0168-8278(1997)26:2<244:TEOPAI>2.0.ZU;2-N
Abstract
Backgrounds/Aims: Serum concentrations of macrophage-colony stimulatin g factor (M-CSF) are increased in parallel with hepatic inflammation. The aim of this study was to assess the immunologic significance of el evated M-CSF in patients with chronic hepatitis B virus infection. Met hods: The subjects included 20 asymptomatic HBV carriers and 45 patien ts with chronic hepatitis B, including 8 undergoing prednisolone treat ment, 10 experiencing an acute exacerbation, and 12 undergoing daily a dministration of interferons. Results: Serum concentrations of M-CSF s ignificantly decreased during prednisolone administration, but signifi cantly increased following prednisolone withdrawal, similar to the inc rease during acute exacerbation. Changes in the lipopolysaccharide-sti mulated production of interleukin-1-beta and tumor necrosis factor-alp ha by peripheral whole blood, or of interferon-gamma by peripheral blo od mononuclear cells showed similar pattern. Serum concentrations of M -CSF did not correlate with the titers of HBV-DNA or HBV-DNA polymeras e activity. However, serum M-CSF peaked preceding seroconversion to HB e antibody in three HBe antigen positive patients. Exogenous interfero n-alpha, -beta, or -gamma induced significant elevation in serum M-CSF concentrations, irrespective of changes in the serum alanine aminotra nsferase levels. Conclusions: Increased serum M-CSF is closely associa ted with increased serum interferons and/or proinflammatory cytokines produced by peripheral blood cells during hepatic inflammation in chro nic hepatitis B. This may be a consequence of the altered cytokine cas cade resulting from the host immune response against hepatitis B virus .