Chien-Wei Su1,2, Chun-Ying Wu2,3,4,5,6, Jaw-Town Lin7,8,9, Hsiu J Ho3, Jaw-Ching Wu3,10. 1. Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, ROC. 2. Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC. 3. Division of Translational Research, Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan, ROC. 4. Department of Public Health and Graduate Institute of Clinical Medical Sciences, China Medical University, Taichung, Taiwan, ROC. 5. National Institute of Cancer Research, National Health Research Institutes, Miaoli, Taiwan, ROC. 6. Department of Life Sciences and RongHsing Research Center for Translational Medicine, National Chung-Hsing University, Taichung, Taiwan, ROC. 7. School of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan, ROC. 8. Division of Gastroenterology and Hepatology, Fu-Jen Catholic University Hospital, New Taipei City, Taiwan, ROC. 9. Institute of Population Health Sciences, National Health Research Institutes, Miaoli, Taiwan, ROC. 10. Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
Abstract
BACKGROUND: Nucleos(t)ide analogue (NA) therapy reduces the risk of disease progression in chronic hepatitis B virus-infected patients. However, the risk of liver decompensation, hepatic failure, and mortality after discontinuation of NA therapy remains unknown. METHODS: Among 51,574 chronic hepatitis B patients who received NAs in the Taiwan National Health Insurance Research Database, we identified 8,631 patients who continued NA therapy (treatment cohort) and 8,631 propensity-score matched patients who stopped NA therapy after their initial 1.5 years treatment (off-therapy cohort) between October 1, 2003 and December 31, 2011. All study subjects were followed up from the index date, that is, the date 1.5 years after the first prescription of NA, until development of liver decompensation and hepatic failure, death or end of 18-month follow-up period. RESULTS: Treatment cohort had significantly lower risks of liver decompensation (1.05%; 95% confidence interval [CI], 0.81%-1.30% vs 2.13%; 95% CI, 1.82%-2.45%; p < 0.001), hepatic failure (0.35%; 95% CI, 0.21%-0.49% vs 0.63%; 95% CI, 0.46%-0.80%; p = 0.008) and overall mortality (1.67%; 1.37%-1.98% vs 2.44%; 95% CI, 2.10%-2.77%; p < 0.001) during the 18-month follow-up period. After adjusting for potential confounders, NA continuous therapy was associated with reduced risks of liver decompensation (hazard ratio [HR]: 0.47; 95% CI, 0.36-0.62, p < 0.001), hepatic failure (HR: 0.53; 95% CI, 0.33-0.86, p = 0.01) and overall mortality (HR: 0.67; 95% CI, 0.53-0.84, p = 0.001). The number needed to reduce one less disease progression and mortality was 47. The protective effect of NA continuous therapy was found in nearly all subgroups. CONCLUSION: NA continuous therapy is associated with reduced risks of liver decompensation, hepatic failure, and overall mortality.
BACKGROUND: Nucleos(t)ide analogue (NA) therapy reduces the risk of disease progression in chronic hepatitis B virus-infectedpatients. However, the risk of liver decompensation, hepatic failure, and mortality after discontinuation of NA therapy remains unknown. METHODS: Among 51,574 chronic hepatitis Bpatients who received NAs in the Taiwan National Health Insurance Research Database, we identified 8,631 patients who continued NA therapy (treatment cohort) and 8,631 propensity-score matched patients who stopped NA therapy after their initial 1.5 years treatment (off-therapy cohort) between October 1, 2003 and December 31, 2011. All study subjects were followed up from the index date, that is, the date 1.5 years after the first prescription of NA, until development of liver decompensation and hepatic failure, death or end of 18-month follow-up period. RESULTS: Treatment cohort had significantly lower risks of liver decompensation (1.05%; 95% confidence interval [CI], 0.81%-1.30% vs 2.13%; 95% CI, 1.82%-2.45%; p < 0.001), hepatic failure (0.35%; 95% CI, 0.21%-0.49% vs 0.63%; 95% CI, 0.46%-0.80%; p = 0.008) and overall mortality (1.67%; 1.37%-1.98% vs 2.44%; 95% CI, 2.10%-2.77%; p < 0.001) during the 18-month follow-up period. After adjusting for potential confounders, NA continuous therapy was associated with reduced risks of liver decompensation (hazard ratio [HR]: 0.47; 95% CI, 0.36-0.62, p < 0.001), hepatic failure (HR: 0.53; 95% CI, 0.33-0.86, p = 0.01) and overall mortality (HR: 0.67; 95% CI, 0.53-0.84, p = 0.001). The number needed to reduce one less disease progression and mortality was 47. The protective effect of NA continuous therapy was found in nearly all subgroups. CONCLUSION: NA continuous therapy is associated with reduced risks of liver decompensation, hepatic failure, and overall mortality.