Modulation of Serum Interleukin-18 Concentrations and Hepatitis B Virus DNA Levels During Interferon Therapy in Patients with Hepatitis B e-Antigen-Positive Chronic Hepatitis B
2010 (English)In: Journal of Interferon and Cytokine Research, ISSN 1079-9907, E-ISSN 1557-7465, Vol. 30, no 12, 901-908 p.Article in journal (Refereed) Published
The aim of this study was (1) to determine plasma values of interleukin-18 (IL-18) in patients with different clinical manifestations of hepatitis B (HB) and (2) to analyze the correlation between presence of circulatory levels of IL-18 and levels of HB virus (HBV) DNA during interferon-alpha (IFN-alpha)-induced HBe seroconversion in patients with chronic HB (CHB). The IL-18 levels in serum did not significantly differ between healthy control subjects (99+/-25 pg/mL), HB-immune patients (85+/-33), and asymptomatic carriers of HB surface antigen (144+/-44 pg/mL). In contrast, anti-HBe (HBV DNA <10(4) copies/mL, 555+/-248, P<0.05), anti-HBe (HBV DNA >10(4) copies/mL, 280+/-85, P<0.05), and HBe-antigen-reactive (373+/-108, P<0.0001) patients with symptomatic CHB had significantly elevated levels in circulation compared with healthy control subjects (99+/-25 pg/mL). An inverse correlation was found between serum HBV DNA copies and IL-18 levels during therapy (r--0.54, P<0.001). We consistently observed an IFN-alpha-induced suppression of viral replication, which was followed by the alanine aminotransferase (ALT) flare. There was a significant increase in IL-18 production after the ALT flare, where the peak of IL-18 preceded or coincided with the time of HBe seroconversion in patients who cleared the virus. These results suggest that IL-18 is involved in the pathogenesis of CHB and that IFN-alpha therapy can augment the production of IL-18 in patients with CHB.
Place, publisher, year, edition, pages
2010. Vol. 30, no 12, 901-908 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-139396DOI: 10.1089/jir.2010.0042ISI: 000284837700005PubMedID: 20973680OAI: oai:DiVA.org:uu-139396DiVA: diva2:381301