A controlled trial of interferon with or without prednisone priming for chronic hepatitis B

Lok, Anna S.; Wu, P. C.; Lai, Ching–Lung; Lau, Johnson Y.N.; Leung, Elsie K.Y.; Wong, Loretta S.K.; C.K., Oliver; Lauder, I.; Ng, Charmaine; Chung, Hau Tim

doi:10.1016/0016-5085(92)90337-x

Cited by 232 publications

(159 citation statements)

References 27 publications

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“…Eight patients (patients 8, 10, 12, 38, 34, 35, 36, and 44) were infected with HBV genotype C; all but 1 (patient 44) had C1858. Twenty-three (51%) patients, 14 in group I and 9 in group II, received interferon alfa treatment for 3 to 6 months in two previously reported interferon trials, 26,27 while the remaining 22 patients (49%) never received interferon or other antiviral treatment.…”

Section: Methodsmentioning

confidence: 99%

“…HBV DNA was determined by a semiquantitative dot-blot hybridization assay. 27 PCR Amplification and Direct Sequencing. DNA was extracted by incubating 100 µL serum with 50 µL buffer containing (final concentration) 0.5 mg/mL proteinase K, 10 mmol/L Tris-HCl (pH 8.0), 20 mmol/L ethylenediaminetetraacetic acid, and 0.5% sodium dodecyl sulfate at 50°C for 2 hours.…”

Section: Methodsmentioning

confidence: 99%

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Different hepatitis b virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion

1999

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Mutations in the core promoter and precore regions are frequently found in hepatitis B e antigen (HBeAg)-negative patients, but precore stop codon mutation is restricted to hepatitis B virus (HBV) genotypes that have T at nucleotide 1858. The aims of this study were to determine the role of core promoter and/or precore mutations in HBeAg seroconversion and their impact on the subsequent course of liver disease, and to determine if core promoter mutations are more frequently selected in patients with HBV genotypes that preclude the development of precore stop codon mutation. Serial sera from 45 patients with chronic HBV infection were polymerase chain reaction (PCR)-amplified, and the HBV core promoter and precore regions were sequenced. Ninety-two percent of patients had core promoter or precore mutations after HBeAg seroconversion: 42% had core promoter changes only, 38% had precore stop codon mutations only, and 12% had changes in both regions. Seventy-three percent of the patients had persistently normal aminotransferases, and only 8% had multiple flares in aminotransferases after HBeAg seroconversion. Core promoter changes were significantly more common in patients infected with HBV who have C at nucleotide 1858 (91% vs. 27%; P F .01), while precore stop codon changes were exclusively found in patients infected with HBV who have T at nucleotide 1858 (87% vs. 0; P F .01). The vast majority of our patients had core promoter and/or precore mutations after HBeAg seroconversion. Nevertheless, most patients had sustained remission of liver disease. Our data suggest that core promoter changes are preferentially selected in patients infected with HBV genotypes that preclude the development of precore stop codon mutation. (HEPATOLOGY 1999;29:976-984.)

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Different hepatitis b virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion

1999

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“…Immunoreactivity is represented by high levels of ALT, low levels of HBV-DNA and high necroinflammatory activity at histological analysis. High pretreatment ALT levels and low HBV-DNA levels are associated with higher rates of seroconversion with interferon treatment 45,46,48,49 and also associated with responses to PEG-IFN alpha-2a in HBeAg-negative patients; ALT > 5 -fold the upper limit of normality (ULN) was the most important predictor of combined response (ALT normalization, HBV-DNA suppression) in week 24 postreatment. 50 Quantitative HBsAg has recently become an important area of scientific interest.…”

Section: Pretreatment Predictors Of Response To Peg-ifnmentioning

confidence: 99%

Response predictors to treatment with pegylated interferon in chronic hepatitis B

Ferreira

Tenore

2010

Braz J Infect Dis

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The clinical and epidemiological importance of chronic B hepatitis is currently unquestionable as a cause of end-stage liver disease and hepatocellular carcinoma. Recently, predictors of treatment response of this disease have been studied, both before and during the course of medication. Therapy stopping rules have been proposed, which may be useful in patients presenting poor treatment tolerance. This review discusses the treatment response predictors usefulness, with emphasis on ALT, quantitative HBsAg and HBeAg, quantitative HBV-DNA and HBV genotyp

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“…The application of corticosteroid therapy, as a prechemotherapy antiemetic agent, recently has been implicated as a significant factor contributing to HBV reactivation. 35 In our regimen, the dexamethasone, administered on the day of gemcitabine infusion, may have been involved. We would advise routine screening for hepatitis B status before initiation of chemotherapy, particularly in high incidence areas, and the 36 gemcitabine plus docetaxel, 37 and gemcitabine plus vinorelbine 38 reported response rate of 30.4%, 36.5%, and 41%, respectively.…”

Section: Discussionmentioning

confidence: 99%

A phase II study of gemcitabine plus oral etoposide in the treatment of patients with advanced nonsmall cell lung carcinoma

Mok

Zee

Chan

et al. 2000

Cancer

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A controlled trial of interferon with or without prednisone priming for chronic hepatitis B

Cited by 232 publications

References 27 publications

Different hepatitis b virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion

Different hepatitis b virus genotypes are associated with different mutations in the core promoter and precore regions during hepatitis B e antigen seroconversion

Response predictors to treatment with pegylated interferon in chronic hepatitis B

A phase II study of gemcitabine plus oral etoposide in the treatment of patients with advanced nonsmall cell lung carcinoma

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