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2015SupplementFULLTEXT

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984A AASLD ABSTRACTS HEPATOLOGY, October, 2015<br />

was lower in patients with F4-F6 (n=27) compared to those<br />

with F0-F3 (7.6 vs. 8.1 log U/mL, p=0.02), and declined with<br />

increasing fibrosis stage (Figure). HBcrAg levels were independently<br />

associated with advanced fibrosis when adjusting<br />

for age and serum ALT (OR 0.5, CI-95% 0.3-0.8, p=0.003).<br />

In HBeAg-negative patients, fibrosis stage was available for<br />

all patients. The mean HBcrAg was 5.5 (SD 0.1), median HAI<br />

score 5 (IQR 3), and median Ishak fibrosis stage 3 (IQR 2).<br />

Genotypes A/B/C/D/other were present in 13/1/2/81/3%.<br />

In these patients, log HBcrAg was not correlated with Ishak<br />

fibrosis score (r s<br />

=-0.1, p=0.59), similar to fibrosis correlation<br />

to qHBsAg (r s<br />

=-0.1, p=0.19), and HBV DNA (r s<br />

=0.2, 0.07).<br />

When adjusting for age and serum ALT, HBcrAg levels were<br />

not associated with advanced fibrosis (OR 0.9, CI-95% 0.5-<br />

1.6, p=0.83) and did not change with increasing fibrosis<br />

stage (Figure). For both HBeAg-positive and HBeAg-negative<br />

patients, variation of qHBsAg levels across fibrosis stages<br />

was comparable to that of HBcrAg levels (Figure). Conclusion.<br />

In this study, serum HBcrAg levels were inversely correlated<br />

with Ishak fibrosis stage in HBeAg-positive CHB, but not in<br />

HBeAg-negative CHB.<br />

obtainable mutation analysis in 2 centers. Of 177 HBeAg(+)<br />

patients, 6(3.39%) were genotype A, 65(36.72%) genotype<br />

B, 104(58.76%) genotype C, 1(0.57%) genotype B/C, and<br />

1(0.57%) genotype C/D. Of 90 HBeAg(-) patients, 1(1.11%)<br />

were genotype A, 50(55.56%) genotype B, 37(41.11%) genotype<br />

C and 2(2.22%) genotype D. When compared to HBeAg(-)<br />

patients, HBeAg(+) patients were significantly younger in mean<br />

age (37.93 vs. 44.40; P

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