Zong-Han Yao1, Wei-Yu Liao2, Chao-Chi Ho3, Kuan-Yu Chen4, Jin-Yuan Shih5, Jin-Shing Chen6, Zhong-Zhe Lin7, Chia-Chi Lin8, James Chih-Hsin Yang9, Chong-Jen Yu10. 1. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: med92leoyau@gmail.com. 2. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: wyliao33@ntu.edu.tw. 3. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: ccho1203@ntu.edu.tw. 4. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: tuff.chen@msa.hinet.net. 5. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: jyshih@ntu.edu.tw. 6. Department of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: chenjs@ntu.edu.tw. 7. Department of Oncology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: zzlin7460@ntu.edu.tw. 8. Department of Oncology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: cclin1@ntu.edu.tw. 9. Department of Oncology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: chihyang@ntu.edu.tw. 10. Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan, ROC. Electronic address: jefferycjyu@ntu.edu.tw.
Abstract
BACKGROUND: Reactivation of hepatitis B virus (HBV) is a documented risk during cytotoxic chemotherapy in patients with lung cancer. Cases of HBV reactivation in non-small-cell lung cancer (NSCLC) patients receiving epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment have been reported; however, the incidence of HBV reactivation in patients treated with EGFR TKIs has not yet been reported. MATERIALS AND METHODS: We enrolled 171 patients who were diagnosed as having NSCLC from 2011 through 2017 and who also had positive hepatitis B surface antigen (HBsAg). All patients had received EGFR TKIs as anticancer treatment for at least 2 weeks during their treatment course. Reactivation of HBV is defined as one of the following: an increase in HBV DNA by at least 10-fold compared to baseline or an absolute increase to >10ˆ5 IU/mL with abnormal liver function. RESULTS: The median duration of EGFR TKI treatment was 10.5 months (95% confidence interval: 8.2-12.8). Sixteen (9.36%) patients met the criteria of HBV reactivation during EGFR TKI treatment, with an annual incidence of 7.86%. HBV reactivation occurred during erlotinib treatment in 6 patients, followed by 5 patients with gefitinib treatments, 3 patients with osimertinib treatment and 2 with afatinib treatment. No independent risk factor for HBV reactivation was identified. CONCLUSION: NSCLC patients receiving EGFR TKI treatment may have a clinically meaningful risk of HBV reactivation during the treatment period. Thus, monitoring liver function, HBV viral load and serology of HBV (i.e., HBeAg and anti-HBc) during EGFR TKI therapy is recommended for NSCLC patients with positive HBsAg.
BACKGROUND: Reactivation of hepatitis B virus (HBV) is a documented risk during cytotoxic chemotherapy in patients with lung cancer. Cases of HBV reactivation in non-small-cell lung cancer (NSCLC) patients receiving epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment have been reported; however, the incidence of HBV reactivation in patients treated with EGFR TKIs has not yet been reported. MATERIALS AND METHODS: We enrolled 171 patients who were diagnosed as having NSCLC from 2011 through 2017 and who also had positive hepatitis B surface antigen (HBsAg). All patients had received EGFR TKIs as anticancer treatment for at least 2 weeks during their treatment course. Reactivation of HBV is defined as one of the following: an increase in HBV DNA by at least 10-fold compared to baseline or an absolute increase to >10ˆ5 IU/mL with abnormal liver function. RESULTS: The median duration of EGFR TKI treatment was 10.5 months (95% confidence interval: 8.2-12.8). Sixteen (9.36%) patients met the criteria of HBV reactivation during EGFR TKI treatment, with an annual incidence of 7.86%. HBV reactivation occurred during erlotinib treatment in 6 patients, followed by 5 patients with gefitinib treatments, 3 patients with osimertinib treatment and 2 with afatinib treatment. No independent risk factor for HBV reactivation was identified. CONCLUSION:NSCLCpatients receiving EGFR TKI treatment may have a clinically meaningful risk of HBV reactivation during the treatment period. Thus, monitoring liver function, HBV viral load and serology of HBV (i.e., HBeAg and anti-HBc) during EGFR TKI therapy is recommended for NSCLCpatients with positive HBsAg.
Authors: Ke Wang; Juan Li; Jianguo Sun; Li Li; Xi Zhang; Jianyong Zhang; Min Yu; Xianwei Ye; Ming Zhang; Yu Zhang; Wenxiu Yao; Meijuan Huang Journal: Zhongguo Fei Ai Za Zhi Date: 2021-10-21
Authors: Ahmed Abdul-Abbas Bayram; Hussein O M Al-Dahmoshi; Noor S K Al-Khafaji; Raheem Tuama Obayes Al Mammori; Ali Husain Shilib Al-Shimmery; Morteza Saki Journal: Biomedicine (Taipei) Date: 2021-12-01