The Efficacies of Lamivudine in Chronic Hepatitis B Patients with Acute Flare and Decompensated Liver Function

Lamivudine用於慢性B型肝炎伴隨嚴重急性肝炎導致肝功能代償性機能減退患者的成效

李建瑩(Chien-Ying Lee) ； 林俊哲(Chun-Che Lin) ； 施宏哲(Hung-Che Shih) ； 張秋純(Chiu-Chun Chang)

《中山醫學雜誌》 22卷2期 (2011/06) Pp. 195-203

https://doi.org/10.30096/CSMJ.201106.0006

摘要

Background: Decompensation of liver function after acute flare of chronic hepatitis B has hazardous outcomes and requires early anti-viral therapy.
Materials and Methods: From January 2006 to January 2008, we enrolled sixty-six patients with decompensated liver function caused by acute flare up of chronic hepatitis B. Lamivudine 100 mg was administered daily for more than 12 months. We made records of age, gender, HBeAg status, HBV DNA level, and liver enzyme and function tests. Biochemical, serological, and virological responses were recorded at 12 months after therapy.
Results: After 12 months treatment with lamivudine, we found a decline in HBV DNA (mean±SD) from 3.30±4.80 log copies/ml to 2.52±8.60 log copies/ml (p＜0.05) in HBeAg positive patients. HBV DNA declined from 2.92±4.41 log copies/ml to 1.89±3.94 log copies/ml (p=0.61) in HBeAg negative patients. Thirty-nine patients (59.0%) achieved ALT normalization, 49 patients (74.2%) achieved prothrombin time normalization, 34 patients (51.5%) achieved total bilirubin normalization, 69.2% achieved undetectable HBV DNA, 45.5% achieved HBeAg seroconcevrsion. Twenty-two of the 44 HBeAg negative patients produced anti-Hbe, and nine of the positive patients produced anti-Hbe.
Conclusion: Lamivudine is an effective therapy for patients with acute decompensation cause by a flare up of chronic hepatitis B, and should be administered as early as possible.

關鍵字

Lamivudine ； 慢性B型肝炎 ； HBeAg ； HBV DNA

並列摘要

Background: Decompensation of liver function after acute flare of chronic hepatitis B has hazardous outcomes and requires early anti-viral therapy.
Materials and Methods: From January 2006 to January 2008, we enrolled sixty-six patients with decompensated liver function caused by acute flare up of chronic hepatitis B. Lamivudine 100 mg was administered daily for more than 12 months. We made records of age, gender, HBeAg status, HBV DNA level, and liver enzyme and function tests. Biochemical, serological, and virological responses were recorded at 12 months after therapy.
Results: After 12 months treatment with lamivudine, we found a decline in HBV DNA (mean±SD) from 3.30±4.80 log copies/ml to 2.52±8.60 log copies/ml (p＜0.05) in HBeAg positive patients. HBV DNA declined from 2.92±4.41 log copies/ml to 1.89±3.94 log copies/ml (p=0.61) in HBeAg negative patients. Thirty-nine patients (59.0%) achieved ALT normalization, 49 patients (74.2%) achieved prothrombin time normalization, 34 patients (51.5%) achieved total bilirubin normalization, 69.2% achieved undetectable HBV DNA, 45.5% achieved HBeAg seroconcevrsion. Twenty-two of the 44 HBeAg negative patients produced anti-Hbe, and nine of the positive patients produced anti-Hbe.
Conclusion: Lamivudine is an effective therapy for patients with acute decompensation cause by a flare up of chronic hepatitis B, and should be administered as early as possible.

並列關鍵字

lamivudine ； chronic hepatitis B ； HBeAg ； HBV DNA