1876
The role of hepatitis B surface antigen quantification predict HBV reactivation after discontinuation of nucleos(t)ide analogs treatment in chronic hepatitis B patients with cirrhosis
Chien-Hung Chen, Chuan-Mo Lee, Tsung-Hui Hu, Chao-Hung Hung, JIng-Houng Wang, Sheng-Nan Lu;
Chang Gung Memorial Hospital-Kaohsiung Medical Center, Kaohsiung, Taiwan
Background and Aims:This study investigated the incidence of hepatitis B virus (HBV) reactivation and role of quantification of HBsAg (qHBsAg) levels in HBV reactivation after stopping nucleos(t)ide analogs (NA) treatment in chronic hepatitis B (CHB) patients with cirrhosis.
Patients and Methods: From 2004 to 2012, a total of 85 CHB patients with cirrhosis (20 HBeAg-positive, 65 HBeAg-negative at baseline) received NAs treatment (50 lamivudine, 30 entecavir, 5 telbivudine) (treatment duration: mean ± SD: 128±60.1 weeks, range: 78-409 weeks) and have stopped the treatment at least 12 months were recruited. The criteria of stopping NAs therapy met the recommendations of APASL 2012. HBV reactivation is defined as serum HBV DNA level > 2000 IU/mL after stopping NAs treatment. Serum qHBsAg levels were determined at baseline, month 12 of treatment and at the end of treatment. Results: Of the 85 CHB patients with cirrhosis, the cumulative rates of HBV reactivation at months 12, 24 and 36 were 48.2%, 57%, and 65.8% respectively after stopping NAs treatment. Cox regression analysis showed that only qHBsAg at the end of treatment [increased per one year; hazard ratio (HR):2.15, 95% confidence interval (CI): 1.50-3.09] was an independent predict for HBV reactivation. Time-dependent receiver-operating characteristic (ROC) curve analysis showed that the best cut-off value for predicting HBV reactivation within 3 years after cessation of NAs treatment was 388.6 IU/mL (area under the ROC curve: 0.804). We used HBsAg of 350 IU/mL as a marker to predict HBV reactivation (p < 0.001). Of the patients who had qHBsAg levels of ≤ 350 and > 350 IU/mL at the end of treatment, the cumulative rates of HBV reactivation at month 36 were 28.9% and 90.2% respectively. Fourteen of 85 cirrhotic patients experienced HBsAg loss during follow-up period. Of the 54 patients who experienced HBV reactivation, 45 had clinical relapse (ALT>80 IU/L) during follow-up. Of them, 9 experienced hepatic decompensation (total bilirubin >3 mg/dL). Of the 9 patients with hepatic decompensation, 1 expired although antiviral agent was used. Of the 14 patients who experienced HBsAg loss, 4 developed hepatocellular carcinoma (HCC) after HBsAg loss.
Conclusions: Serum qHBsAg level was a useful predictor for HBV activation after stopping NAs treatment in CHB patients with cirrhosis. Hepatitis relapse with hepatic decompensation was still an important issue after cessation of NAs therapy in cirrhotic patients. HBsAg loss after cessation of NAs treatment did not completely eliminate the risk of HCC in cirrhotic patient, and such patients should be continuously monitored for HCC.
Disclosures:
The following people have nothing to disclose: Chien-Hung Chen, Chuan-Mo Lee, Tsung-Hui Hu, Chao-Hung Hung, JIng-Houng Wang, Sheng-Nan Lu