End-of-treatment HBsAg links to clinical HBV relapse rate
Click Here to Manage Email Alerts
Higher end-of-treatment hepatitis B surface antigen level correlated with nucleos(t)ide clinical relapse among patients with chronic hepatitis B virus, according to a presentation at The Liver Meeting Digital Experience.
The HBsAG level did not, however, correlate with relapse severity or earlier relapse.
“HBsAG levels has been considered as a surrogate marker of cccDNA and also as a marker of fatty hepatocytes. Lower HBsAG level at end of treatment was associated with lower relapse rate and higher rate of HBsAG lows,” Yen-Chun Liu, MD, of the Chang Gung University College of Medicine, said during the presentation. “Quantitative HBsAG at end-of-treatment is a better predictor for off-nucleos(t)ide (NUC) clinical relapse.”
To investigate clinical relapse of HBV, researchers evaluated 1,245 patients with HBeAg-negative HBV who stopped entecavir or tenofovir following undetected HBV DNA for longer than 1 year. They collected data on alanine aminotransferase levels, HBV DNA, hepatic decompensation and end-of-treatment HBsAg categorized by less than 100 IU/mL (17%), 100 IU/mL to 999 IU/mL (61%) or 1,000 IU/mL and greater (22%). They further compared relapse severity, time to relapse and decompensation and used multivariate Cox regression to determine predictors of decompensation and severe hepatitis.
Study results showed that within 2 years of discontinued treatment, 60% of patients clinically relapsed and 7% of patients developed severe hepatitis, of which 11 patients experienced hepatic decompensation. Higher end-of-treatment HBsAg within each IU/mL category correlated with an increased rate of relapse (70%, 63% and 38%, respectively; P < .01) but a later median onset (35 weeks, 33 weeks and 27 weeks; P < .01). Researchers noted comparable relapse ALT levels between groups (232 IU/mL vs. 254 IU/mL vs. 259 IU/mL) with no correlation between HBsAg level and ALT fold changes (Pearson’s correlation coefficient = –.03). Among patients who clinically relapsed, HBsAg did not predict severe hepatitis (adjusted HR = 0.769) or hepatic decompensation (aHR = 0.749).
“HBsAG level above 100 IUmL at end-of-treatment was not correlated with greater relapse severity or earlier relapse while patients with higher end-of-treatment HBsAg have higher relapse rate incidence but later onset of the relapse event,” Liu concluded. “A 2-year clinical relapse rate was reported as below 20% in patients with HBsAG at end-of-treatment below 100 IU/mL. Moreover, 5-year surface antigen low rates was as high as 33% in patients with HBsAG level below 100.”
Editors note: The lede had been updated to reflect a more concise depiction of the study.