Evaluation of hepatitis b surface antigen (hbsag) as a surrogate marker for hepatitis b viral load estimation.

Abstract

Background: A Hepatitis B Virus (HBV) viral load measurement is recommended for diagnosis and monitoring of patients on treatment for Chronic Hepatitis B (CHB). However, these diagnostic techniques are molecular-based and expensive and unavailable to majority of the Ugandan population. Quantitation of hepatitis B surface antigen (HBsAg) by automated chemiluminescent micro-particle immunoassay has been proposed as a surrogate marker. Objectives: This study showed the correlation between HBsAg and HBV DNA levels among patients with CHB attending a referral Laboratory in Kampala, Uganda. Methods:A two-step sampling technique was employed where One hundred and seventythree (173) patients were enrolled while excluding Hepatitis C Virus (HCV) and Hepatitis D Virus (HDV) positive patients, these were then stratified into two strata notably core for chronic HBV and envelope for Acute HBV until a sample size of 52 respondents with equal proportions of core and envelope for both strata. Results: The mean age of the study patients was 37.2 years, 34 (64.7%) were male, and 66 (82.1%) were hepatitis B e antigen (HBeAg) negative while 31/52 (17.9%) were HBeAg positive. Samples above were divided into two strata; 1) HBcAb positive (n=102) and, 2) HBeAg positive (n=73). Twenty-six samples were then selected from each of the strata to yield a sample size of 52 for subsequent experimentation. Out of these 52 participants, 34 (64.7%) were male while 15 (35.3%) were female with their mean age being 37.17 years. Generally, concentrations of HBsAg ranged from 170,000,000 IU/ml/141,100,000 ng/ml to 3,600 IU/ml/2,988.0 ng/ml with a mean of13,385,986.67/11,110,368.9 respectively. We observed a positive correlation (r=0.776) between viral load and HBsAg. The correlation was strongest among acutely infected versus chronically infected.Overall, a strong and sufficient correlation was found between serum quantitative HBsAg and HBV DNA (r = 0.776; P = 0.024). Quantitative HBsAg was a weak but significant correlated with HBV-DNA among the HBeAg positive patients (r = 0.672; P = 0.093). Similarly, there was significant correlation found among the HBcAg negative patients (r = 0.741; P = 0.443). Conclusions:Given these limitations of this study that provided an insight on to differences in HBV DNA and HBsAg levels between HBeAg-positive and -negative patients, which appear to be affected by HBeAg and HBcAg status. Therefore, serum quantitation of HBsAg may replace serum HBV DNA levels among HBV patients in Uganda only if a similar study

is conducted that takes care of controls and all the confounders including HIV Status of the respondents and the above recommendation can be implemented.