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Effects of lamivudine on serum albumin levels correlate with pretreatment HBV-DNA levels in cirrhotic patients

Makoto Nakamuta1 email, Kazuhiro Kotoh1 email, Munechika Enjoji1 email, Eiji Kajiwara3 email, Junya Shimono4 email, Akihide Masumoto5 email, Toshihiro Maruyama6 email, Norihiro Furusyo7 email, Hideyuki Nomura8 email, Hironori Sakai9 email, Kazuhiro Takahashi10 email, Koichi Azuma11 email, Shinji Shimoda12 email, Yuichi Tanabe2 email and Jun Hayashi7 email

1Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Japan

2Department of Medicine, Fukuoka City Hospital, Fukuoka, Japan

3Department of Internal Medicine, Nippon Steel Yawata Memorial Hospital, Kitakyushu, Japan

4Department of Medicine, Yahata Saiseikai Hospital, Kitakyushu, Japan

5Department of Clinical Research, National Hospital Organization Kokura Hospital, Kitakyushu, Japan

6Department of Medicine, Kitakyushu Municipal Medical Center, Kitakyushu, Japan

7Department of Environmental Medicine and Infectious Diseases, Graduate School of Medical Sciences, Kyushu University, Japan

8Department of Internal Medicine, Shin-Kokura Hospital, Kitakyushu, Japan

9Department of Gastroenterology, National Hospital Organization Kyushu Medical Center, Fukuoka, Japan

10Department of Medicine, Hamanomachi Hospital, Fukuoka, Japan

11Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Japan

12Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Kyushu University, Japan

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Comparative Hepatology 2007, 6:3doi:10.1186/1476-5926-6-3

Published: 1 May 2007

Abstract

Background

Lamivudine treatment has been recently demonstrated to increase the serum albumin levels in cirrhotic patients with hepatitis B virus (HBV) infection, but the precise mechanism remains unclear. We hypothesized that the improvement of hypoalbuminemia by lamivudine may be attributable to the reduction of HBV replication itself, rather than to cessation of hepatitis. In order to confirm this hypothesis, in this study we evaluated factors which correlated with the increase in serum albumin levels. Fifty-four patients (Child-Pugh A/B/C, 35/9/10) with HBV-related liver cirrhosis who had been treated with lamivudine for more than 12 months were evaluated. We analyzed the correlation between the increase in serum albumin levels at month 12 after starting treatment (Δ-albumin) and various pretreatment variables. We also analyzed the correlation between Δ-albumin and the reduction in serum levels of HBV-DNA (Δ-HBV-DNA) or alanine aminotransferase (Δ-ALT) at month 12.

Results

The average Δ-albumin was 0.38 g/dL and only serum HBV-DNA levels before treatment correlated significantly with Δ-albumin. We also analyzed the correlation in patients whose alanine aminotransferase levels were normalized after 12 months so that the possible influence of breakthrough hepatitis could be excluded. Even among this subgroup of patients, there was no significant correlation between Δ-albumin and either pretreatment alanine aminotransferase levels or Δ-ALT. In contrast, in patients whose serum HBV-DNA was undetectable at month 12, we found a significant correlation between Δ-albumin and both pretreatment serum HBV-DNA levels and Δ-HBV-DNA.

Conclusion

Our results demonstrated that albumin levels are associated with pretreatment HBV-DNA but not with alanine aminotransferase levels.


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