Patients & Methods: 399 patients, including 159 HCV-seronegative and 240 HCV-seropositive patients with quantifiable HCV RNA, were included. The HCV genotype distribution was the following: 62.6%, 6.5%, 12.1%, 17.3%, 0.5% and 1.0% for genotypes 1, 2, 3, 4, 5 and 6, respectively. HCV RNA levels were determined by means of real-time PCR assays including m2000 (Abbott Diagnostics) and Cobas AmpliPrep/Cobas TaqMan HCV test, version 2.0 (CAP/CTM v2.0, Roche Molecular Systems). The HCV core antigen levels were assessed
with the Architect HCV Ag assay (Abbott Diagnostics). The results in this assay are expressed in fmol/L and its dynamic range of quantification is 3.0 – 20, 000 fmol/L. Results: Specificity was 100% (95%CI: 98.1%-100.0%). A positive significant correlation was found between HCV core antigen levels measured Z-VAD-FMK molecular weight with the Architect assay and HCV RNA levels, regardless of the real-time PCR assay used (r = 0.90 and 0.92, p < 0.0001 for m2000 and CAP/CTM v2.0, respectively) and of the HCV genotype. HCV core antigen
was detectable only if the HCV RNA level was higher than 3 Log10 IU/mL. Conclusion: The Architect HCV antigen assay, which detects and quantify HCV core antigen, is highly specific and easy to perform. It thus represents a valuable screening tool for active HCV infection. However, due to its lack of sensitivity, this assay cannot be used for response-guided antiviral therapy according to current clinical practice guidelines. Disclosures: Jean-Michel Pawlotsky – Consulting: Abbott, Achillion, Boehringer-Ingelheim, Bristol-Myers PFT�� Squibb, Idenix, Gilead, Janssen, Madaus-Rottapharm, Merck, Novartis, Roche; Grant/Research Support: Gilead; Speaking and Teaching: BoehringerIngelheim, Bristol-Myers Squibb, Gilead, Madaus-Rottapharm, Merck, JanssenCilag, Novartis, Abbott The following
people have nothing to disclose: Urocanase Stephane Chevaliez, Alexandre Soulier, Lila Poiteau Background: Long term follow up studies that describe clinical outcomes of chronic hepatitis C (CHC) patients with none, mild or severe liver fibrosis are required to determine cost benefits of anti-viral therapies. This study evaluated long term adverse clinical outcomes for CHC patients stratified by all Metavir fibrosis stages. Methods: Clinical outcomes were determined using population based data linkage methodology for 984 CHC compensated patients who had a liver biopsy performed from to 2012. This included 833 with ongoing infection and 151 with a sustained virological response (SVR). Results: 198 (20.1%) of patients had F0,458 (46.5%) had F1,145 (14.7%) had F2,98 (10%) had F3 and 85 (8.6%) had f4 fibrosis. During 11,226 person-years of follow-up, 31(3.2%) patients developed hepatocellular carcinoma (HCC), 61 (6.2%) developed liver decompensation and 49 (5.0%) had liver transplantation or liver related death (LRD).