Quantitative HBsAg levels do not identify hepatic fibrosis in HBeAg-negative chronic hepatitis B patients
Fatima A Ahmed1, Maryam S Bajaifar2, Mohammed A Ahmed1, Abduljaleel Alalwan3, Faraaz A Sanai4, Khalid Albeladi5, Abdulrahman A Aljumah3, Faisal M Sanai6
1 College of Medicine, Ibn Sina National College for Medical Studies, Jeddah, Saudi Arabia
2 College of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia
3 Hepatology Division, Department of Hepatobiliary Sciences and Organ Transplant Center, King Abdulaziz Medical City; King Saud bin Abdulaziz University for Health Sciences and King Abdullah International Medical Research Center, Ministry of National Guard Health Affairs, Riyadh, Saudi Arabia
4 Emergency Department, King Fahd Hospital, Jeddah, Saudi Arabia
5 Gastroenterology Unit, Department of Medicine, King Abdulaziz Medical City, Jeddah, Saudi Arabia
6 Gastroenterology Unit, Department of Medicine, King Abdulaziz Medical City, Jeddah; Liver Disease Research Center, College of Medicine, King Saud University, Riyadh, Saudi Arabia
Faisal M Sanai,
Gastroenterology Unit, Dept. of Medicine, King Abdulaziz Medical City, PO Box: 9515, Jeddah 21423
Source of Support: None, Conflict of Interest: None
Background/Aims: Quantitative serum hepatitis B surface antigen (qHBsAg) has been evaluated in limited patient groups as a marker of histological fibrosis. The accurate identification of inactive chronic hepatitis B virus (HBV) carriers from those with active carriers is difficult because of wide and frequent HBV DNA fluctuations. We aimed to assess the utility of qHBsAg in distinguishing histologically significant fibrosis in untreated HBeAg-negative chronic HBV patients.
Patients and Methods: qHBsAg levels were measured at baseline as single-point quantification and correlated with virologic and biochemical profiles of consecutive carriers (median, 29; range, 12-110 months). HBeAg-negative patients (n = 75) with HBV DNA <2000 (n = 5), 2000-20,000 (n = 16) and >20,000 IU/mL (n = 54) were included and all had liver biopsy. A qHBsAg cutoff point of 1000 IU/mL was assessed to demonstrate whether it better delineated patients with non-significant histology (F0-1, inflammatory grade A0-1).
Results: Mean age of the patients was 39.4 ± 11.4 years and 58 (77.3%) were male. Patients with qHBsAg levels >1000 IU/mL were more likely to be males (84.5%, P = 0.006) or with elevated AST (68.4%, P = 0.0002) and ALT levels (72.4%, P < 0.0001), higher HBV DNA (log10 6.4 ± 1.4, P < 0.0001) and those with F2-4 fibrosis (48.3%, P = 0.028). Serum log10 qHBsAg were significantly lower in patients with HBV DNA <2000 (2.80 ± 1.47) and HBV DNA 2000-20,000 (2.71 ± 0.83) vs. >20,000 IU/mL (3.89 ± 0.61, P < 0.0001). Overall, qHBsAg were not different in patients with F0-1 (3.44 ± 0.91) and F2-4 fibrosis (3.74 ± 0.85, P = 0.161). Serum qHBsAg were higher in patients with significant (A2-3) inflammation (3.85 ± 0.72) compared to A0-1 (3.38 ± 0.95; P = 0.018). Serum qHBsAg demonstrated poor accuracy (AUROC, 0.61, P = 0.111) in identification of F2-4 fibrosis.
Conclusion: Serum qHBsAg levels do not help differentiate between those with HBV DNA <2000 or 2000 – 20,000 IU/mL or distinguish patients with significant fibrosis. Moreover, more than half of the patients with non-significant fibrosis have a qHBsAg level greater than 1000 IU/mL.