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1206A AASLD ABSTRACTS HEPATOLOGY, October, 2015<br />

rienced HBs loss within 3 years after treatment cessation. This<br />

observation demonstrates for the first time that baseline HBsAg<br />

titer might allows identifying patients that could or could not<br />

benefit from PegIFN therapy.<br />

Disclosures:<br />

Nathalie Boyer - Board Membership: MSD, JANSSEN, Gilead, Abbvie; Speaking<br />

and Teaching: BMS<br />

Tarik Asselah - Advisory Committees or Review Panels: AbbVie, Merck, Gilead,<br />

BMS, Roche, Janssen<br />

Patrick Marcellin - Consulting: Roche, Gilead, BMS, Vertex, Novartis, Janssen,<br />

MSD, Abbvie, Alios BioPharma, Idenix, Akron; Grant/Research Support: Roche,<br />

Gilead, BMS, Novartis, Janssen, MSD, Alios BioPharma; Speaking and Teaching:<br />

Roche, Gilead, BMS, Vertex, Novartis, Janssen, MSD, Boehringer, Pfizer,<br />

Abbvie<br />

The following authors have nothing to disclose: Michelle Martinot-Peignoux,<br />

Corinne Castelnau, Nathalie Giuily, Michele Pouteau, Martine Lapalus, Rami<br />

Moucari<br />

2046<br />

Intrahepatic IP-10 expression correlates with plasma<br />

IP-10 levels and is a response marker for HBeAg-positive,<br />

but not HBeAg-negative chronic hepatitis B patients<br />

treated with peginterferon and adefovir<br />

Sophie Willemse 2 , Louis Jansen 2 , Annikki de Niet 2 , Marjan J. Sinnige<br />

1 , Bart Takkenberg 2 , Joanne Verheij 3 ; 1 Experimental Immunology,<br />

Academic Medical Center, Amsterdam, Netherlands;<br />

2 Gastroenterology and Hepatology, Academic Medical Center,<br />

Amsterdam, Netherlands; 3 Pathology, Academic Medical Center,<br />

Amsterdam, Netherlands<br />

Background and aims Interferon-y–inducible protein-10 (IP-10)<br />

is an interferon-stimulated gene that is produced by different<br />

types of cells such as monocytes, neutrophils and hepatocytes.<br />

After binding to its receptor CXCR3, IP-10 functions as a chemotactic<br />

cytokine for T-lymphocytes, monocytes and NK-cells<br />

and induces adhesion of activated memory/effector T-cells.<br />

We aimed to establish if IP-10 expression in liver tissue and<br />

IP-10 levels in plasma of chronic hepatitis B (CHB) patients<br />

correlated with each other and further to investigate if IP-10<br />

levels could predict treatment outcome in CHB patients treated<br />

with peginterferon and adefovir. Methods A total of 86 CHB<br />

patients (41 HBeAg-positive and 45 HBeAg-negative) received<br />

combination therapy of peginterferon and adefovir for 48<br />

weeks. Combined Response (CR) (HBeAg-negativity, HBV-DNA<br />

≤2,000 IU/mL, and ALT normalization) and non-response (NR)<br />

were assessed at Week 72. Plasma IP-10 levels were measured<br />

at baseline and during treatment at Day 3 (D3) and<br />

Week 1 (W1). Pre-treatment liver biopsies were obtained in<br />

69 of 86 patients, of which 41 were stored in liquid nitrogen,<br />

enabling the analysis of intrahepatic IP-10 expression by<br />

RT-qPCR. Results CR was achieved in 14/41 HBeAg-positive<br />

and 17/45 HBeAg-negative patients. Mean baseline plasma<br />

IP-10 levels were significantly higher in HBeAg-positive patients<br />

with CR than NR (3.20 vs 3.00 log pg/mL p=0.023). This<br />

difference was not observed in HBeAg-negative patients. Baseline<br />

IP-10 levels correlated with ALT-levels in HBeAg-positive<br />

(r0.66 p

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