Original Article
Association of hepatitis B e antigen and DNA viral load with severity of liver dysfunction and in-hospital outcomes in hepatitis B-related liver cirrhosis
Abstract
Background: Hepatitis B virus (HBV) infection is a common cause of liver cirrhosis. Our study aimed to evaluate the clinical relevance of hepatitis B e antigen (HBeAg) and HBV DNA viral load in HBV-related liver cirrhosis.
Methods: All HBV-related cirrhosis patients consecutively admitted to our hospital between January 2012 and June 2014 were retrospectively reviewed. Clinical profiles were collected. HBV DNA viral load would be detectable, if HBV DNA viral load was >200 IU/mL.
Results: Overall, 428 patients were included. The prevalence of positive HBeAg was 11.9% (40/335). HBeAg-positive patients had significantly higher proportions of moderate-large ascites and Child-Pugh class B/C than HBeAg-negative patients. The in-hospital mortality was not significantly different between them. The prevalence of detectable HBV DNA viral load was 38.25% (109/285). Patients with detectable HBV DNA viral load had a significantly higher proportion of moderate-large ascites and higher Child-Pugh and model for end-stage liver disease (MELD) scores than patients with undetectable HBV DNA viral load. The in-hospital mortality was not significantly different between them. The prevalence of HBV DNA viral load >2,000 IU/mL was 31.9% (91/285). Patients with HBV DNA viral load >2,000 IU/mL had significantly higher proportions of moderate-large ascites and in-hospital death and higher Child-Pugh and MELD scores than patients with HBV DNA viral load <2,000 IU/mL. After adjusting Child-Pugh score, HBV DNA viral load >2,000 IU/mL was not significantly associated with in-hospital death (odds ratio =2.154, P=0.272).
Conclusions: In HBV-related cirrhosis, HBeAg and HBV DNA viral load were significantly associated with the severity of liver dysfunction, but not independently associated with in-hospital death.
Methods: All HBV-related cirrhosis patients consecutively admitted to our hospital between January 2012 and June 2014 were retrospectively reviewed. Clinical profiles were collected. HBV DNA viral load would be detectable, if HBV DNA viral load was >200 IU/mL.
Results: Overall, 428 patients were included. The prevalence of positive HBeAg was 11.9% (40/335). HBeAg-positive patients had significantly higher proportions of moderate-large ascites and Child-Pugh class B/C than HBeAg-negative patients. The in-hospital mortality was not significantly different between them. The prevalence of detectable HBV DNA viral load was 38.25% (109/285). Patients with detectable HBV DNA viral load had a significantly higher proportion of moderate-large ascites and higher Child-Pugh and model for end-stage liver disease (MELD) scores than patients with undetectable HBV DNA viral load. The in-hospital mortality was not significantly different between them. The prevalence of HBV DNA viral load >2,000 IU/mL was 31.9% (91/285). Patients with HBV DNA viral load >2,000 IU/mL had significantly higher proportions of moderate-large ascites and in-hospital death and higher Child-Pugh and MELD scores than patients with HBV DNA viral load <2,000 IU/mL. After adjusting Child-Pugh score, HBV DNA viral load >2,000 IU/mL was not significantly associated with in-hospital death (odds ratio =2.154, P=0.272).
Conclusions: In HBV-related cirrhosis, HBeAg and HBV DNA viral load were significantly associated with the severity of liver dysfunction, but not independently associated with in-hospital death.
