Author/Authors :
Sun Kim, Eun Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Seok Seo, Yeon Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Keum, Bora Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Hoon Kim, Ji Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , An, Hyonggin Biostatistics - Korea University College of Medicine - Seoul, Korea , Joon Yim, Hyung Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Sik Kim, Yong Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Tae Jeen, Yoon Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Sik Lee, Hong Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Jai Chun, Hoon Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Ho Um, Soon Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Duck Kim, Chang Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea , Sang Ryu, Ho Departments of Internal Medicine - Korea University College of Medicine - Seoul, Korea
Abstract :
Background: Patients with HBeAg-negative chronic hepatitis B (CHB) has a significantly
different prognosis than inactive carriers; there is however, no reliable strategy for accurately
differentiating these two disease conditions.
Objectives: To determine a strategy for discriminating patients with HBeAg-negative
CHB from inactive carriers.
Materials and Methods: Consecutive inactive carriers (i.e. HBeAg-negativity, anti-HBepositivity,
normal ALT levels, and HBV DNA < 2000 IU/mL) were enrolled. HBV reactivation
was defined as the elevation of the HBV DNA level to ≥ 2000 IU/mL. Patients were
classified into true inactive carriers when their HBV DNA levels remained at < 2000
IU/mL or false inactive carriers when their HBV DNA levels increased to ≥ 2000 IU/mL
during the first year.
Results: The Mean ± SD age of 208 inactive carriers (140 males) was 47.7 ± 12.6 years.
The Mean ± SD serum ALT and HBV DNA levels were 22.8 ± 8.6 IU/L and 360 ± 482 IU/
mL, respectively. HBV reactivation developed in 41 (19.7%) patients during the first year.
Baseline HBV DNA and ALT levels differed significantly between true inactive and false
inactive carriers. The AUROCs of the baseline ALT and HBV DNA levels for predicting a
false inactive carrier were 0.609 and 0.831, respectively. HBV reactivation developed
more often in patients with a baseline HBV DNA level of ≥ 200 IU/mL than in those
with a baseline HBV DNA level of < 200 IU/mL during a Mean ± SD follow-up of 622 ±
199 days.
Conclusions: The HBV DNA level was useful for discriminating patients with HBeAgnegative
CHB from true inactive carriers. The follow-up strategies applied to inactive
carriers need to vary with their HBV DNA levels.