Short-Term Corticosteroid Therapy for Chronic Active Hepatitis B

Laskus, Tomasz; Cianciara, J; Loch, T; J, Slusarczyk

doi:10.1159/000200485

Cited by 2 publications

(1 citation statement)

References 12 publications

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“…The results demonstrated that 12 patients (46%) seroconverted to anti-HBe during a 1-year period of follow-up, while 14 (54%) did not. Although the seroconversion rate after a short-term corticosteroid treatment in this study seemed to be relatively high compared with the rates described previously [Hoofnagle et al, 1986;Laskus et al, 1990;Lee et al, 1991 I, it was, in part, due to the fact that this study included several young patients with active liver inflammation, in whom the seroconversion was induced more frequently by this treatment, as reported previously "air et al, 19861. The baseline serum HBV-DNA concentration was similar between the two groups.…”

Section: Discussionsupporting

confidence: 52%

Analysis of wild‐type and e antigen‐defective hepatitis B viruses during the course of a short‐term corticosteroid therapy in chronic hepatitis B

Daikoku

Nakata

Hamasaki

et al. 1995

Journal of Medical Virology

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Hepatitis B virus (HBV), with a G-to-a point mutation at nucleotide 83 in the precore region (mutant HBV83), accounts for most cases of hepatitis B e antigen (HBeAg)-defective HBV. However, it is still not clear how mutant HBV83 is associated with HBe seroconversion. Twenty-six HBeAg-positive patients with chronic hepatitis B who received oral prednisolone (30 mg/day) for 3 weeks were studied to clarify the prevalence of mutant HBV83 during the treatment using polymerase chain reaction with a restriction fragment length polymorphism assay. Twelve (46%) patients seroconverted to anti-HBe 1 year after treatment, whereas 14 (54%) did not. The proportion of mutant HBV83 to whole HBV remained unchanged in both groups during an acute exacerbation induced by withdrawal of corticosteroids. Among 12 anti-HBe-seroconverted patients, five (56%) of nine patients with only wild-type HBV at baseline developed detectable levels of mutant HBV83 while all three patients with a mixed viral population of wild-type HBV and mutant HBV83 at baseline developed a higher proportion of mutant HBV83 one year after treatment. In contrast, these changes were observed in only one (14%) of seven who failed to seroconvert. The results indicate that a flare-up of hepatitis precedes emergence or selection of mutant HBV83, followed by HBe seroconversion in patients with chronic hepatitis B.

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Section: Discussionsupporting

confidence: 52%

Analysis of wild‐type and e antigen‐defective hepatitis B viruses during the course of a short‐term corticosteroid therapy in chronic hepatitis B

Daikoku

Nakata

Hamasaki

et al. 1995

Journal of Medical Virology

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Short report: prednisolone withdrawal followed by lymphoblastoid interferon in the therapy of adult patients with presumed childhood‐acquired chronic hepatitis B virus infection

Brook

Main

Yap

et al. 1993

Aliment Pharmacol Ther

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Eighteen patients with presumed childhood acquisition of chronic hepatitis B virus infection were initially entered into this randomized controlled trial. Twelve were treated with prednisolone for 4 weeks followed, after a 2-week gap, by thrice weekly lymphoblastoid a-interferon for 12 weeks. Two of these had previously acted as untreated controls. Three of the 12 patients (2 5 %) [who were initially hepatitis B virus (HBV) surface antigen (HBsAg), 'e' antigen (HBeAg) and HBV-DNA positive] became HBeAg and HBV-DNA negative during therapy and remained so after 12 months post-therapy follow-up. One of these also lost HBsAg. A further two patients lost HBeAg and HBV-DNA during therapy but relapsed 6 and 9 months later. Two additional patients were HBV-DNA negative but HBeAg positive at the end of follow-up. None of the eight untreated control patients seroconverted during an identical follow-up period. Two further patients were HBsAg and HBeAg positive but HBV-DNA negative at the start of therapy. These were omitted from the final analysis: both subsequently lost HBeAg. The treatment response was associated with a rise in aspartate aminotransferase, peaking 2-6 weeks after prednisolone withdrawal, loss of HBV-DNA 0-8 weeks later and subsequent normalization of liver function tests. Treatment was well tolerated.

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Short-Term Corticosteroid Therapy for Chronic Active Hepatitis B

Cited by 2 publications

References 12 publications

Analysis of wild‐type and e antigen‐defective hepatitis B viruses during the course of a short‐term corticosteroid therapy in chronic hepatitis B

Analysis of wild‐type and e antigen‐defective hepatitis B viruses during the course of a short‐term corticosteroid therapy in chronic hepatitis B

Short report: prednisolone withdrawal followed by lymphoblastoid interferon in the therapy of adult patients with presumed childhood‐acquired chronic hepatitis B virus infection

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