Viral genotype and baseline load predict the response to adefovir treatment in l

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Journal of Hepatology

Volume 47, Issue 3, September 2007, Pages 366-372

Viral genotype and baseline load predict the response to adefovir treatment

in lamivudine-resistant chronic hepatitis B patients

M. Buti, a, , I. Elefsiniotisa, R. Jardia, V. Vargasa, F. -Friasa,

M. Schappera, S. Bonovasa and R. Estebana

aLiver Unit and Biochemistry Department, Hospital Universitario Vall d’

Hebron and CIBER-EHD, Barcelona, Spain

Received 3 January 2007; revised 6 March 2007; accepted 3 April 2007.

Associate Editor: G.K.K. Lau. Available online 24 May 2007.

Background/Aims

To determine the factors associated with virological response (VR), HBeAg

loss or the emergence of adefovir (ADV)-related mutations in ADV-treated

chronic hepatitis B (CHB) patients with lamivudine (LAM) resistance.

Methods

Fifty-four LAM-resistant CHB patients (46% HBeAg-positive) were treated with

ADV monotherapy (n = 28) or ADV plus LAM (n = 26) for a mean of 30.4 months.

Results

Thirty-eight patients (70.4%) achieved VR defined as HBV-DNA levels <104

copies/ml within the first 12 months of treatment. Six (24%) of 25

HBeAg-positive patients exhibited HBeAg loss and 20% seroconverted to

anti-HBe. Eight patients (14.8%) developed ADV-related mutations. In the

multivariate analysis, female gender (HR = 0.20, 95% CI: 0.05–0.76, p =

0.018), HBeAg-negative (HR = 0.37, 95% CI: 0.14–0.96, p = 0.040) and low

baseline HBV-DNA levels (HR = 0.65, 95% CI: 0.45–0.95, p = 0.027) were

independent predictors of VR, whereas low HBV-DNA levels (HR = 0.36, 95% CI:

0.11–1.20, p = 0.095) and HBV-genotype D (HR = 0.06, 95% CI: 0.004–0.84, p =

0.037) independently predicted HBeAg loss.

Conclusions

ADV therapy suppresses viral replication in more than 70% of LAM-R patients.

Factors associated with virologic response are female gender, HBeAg-negative

status and low baseline serum HBV-DNA levels. Genotype D HBV infection and

low baseline HBV-DNA levels independently predict HBeAg loss.

The authors who have taken part in this study declared that they have no

relationship with the manufacturers of the drugs involved either in the past

or present and did not receive funding from the manufacturers to carry out

their research. M Buti, R Jardi, F -Frias and R Esteban received a

grant from the European Community (VIRGIL Network of Excellence, grant

LSHM-CT-2004-503359).

Corresponding author. Tel.: +34

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