Case: A 68 years old man diagnosed with chronic hepatitis C regularly visited our hospital. In April of 2005, ultrasonography revealed a tumor 20mm in diameter in S2 of the liver and another tumor 15mm in diameter in S6/7 of the liver. The patient was hospitalized for further examination. Computer tomography (CT) revealed that the tumor localized in S6/7 presented a pattern of hypervascular hepatocellular carcinoma (HCC). For the tumor localized in S2, the following were revealed. 1) Contrast-enhanced ultrasound findings: A tumor vessel passed from outside the tumor to the center of the tumor in the early vascular phase, then radiated in a wheel-like shape at the center of the tumor; parenchymal phase perfused imaging in the area produced a similar imaging obtained from the area surrounding the liver. 2) CT: No tumor was detected. 3) SPIO-MRI (T2 weighted imaging): Iso-low intensity images were obtained. Although these imaging findings indicated FNH, the patient was HCV positive. In order to disprove the possibility of HCC, a biopsy was performed on the tumor at S2 in the liver. The resulting diagnosis was well-differentiated HCC. Discussion: Until now, a characteristic finding of FNH has been spoke-like vasculariation, which is considered diagnostically quite important. However, some recent cases of HCC have been reported to present FNH-like vascularization. From now on, when evaluating a tumor that presents spoke-like vascularization underlining chronic hepatitis, the possibility of HCC should be considered and a close examination may be needed. Chronic infection with HCV is problem .Clinical management of chronic HCV depend on extent liver fibrosis .Liver biopsy gold stander an invasive procedure responsible for severe complications and sample variability interpretation. Serum biomarkers for inflammation/fibrosis investigated to wave liver biopsy. Diagnostic accuracy panel of Non-invasive serum biomarkers for hepatic fibrosis (Fibrosure , APRI score, Forn's score) versus liver biopsy. 20 HCV patients subjected for: APRI, Forn's , Fibrosure scores PCR quantitative HCV-RNALiver functions .Lipid Profile CBC . Ultrasound guided liver biopsy. FORNS score; AUROC (0.917) with 95% CI(0.791-1.042) for(fof1) vs. (f2f3f4) while(0.688)with 95% CI(0.464-0.91)for(fof1f2) vs.(f3f4). Cutoff(>6.9)sensitivity for significant fibrosis(f2f3f4)and extensive fibrosis (f 3f4)were (100%) and with low specificity ,with accuracy(40%) and (20%)respectively.-APRI score; AUROC(0.792)with 95% CI( 0.568 -1.015)comparing(f0f1) vs.(f2f3f4)while was(0.875)with 95% CI(0.703 -1.047)for( f0f1f2)vs.(f3f4).Cutoff(<0.5) had low sensitivity and specificity(100%)with accuracy(60%)for significant fibrosis and(80%)for extensive fibrosis.-Fibrosure(fibro-acti test); showed best AUROC(1.00)in different fibrotic stages with 95 % CI (1.00-1.00).Cutoff(>0.59) sensitivity(50%)for significant fibrosis and(100%)for extensive fibrosis while specificity(100%)in all fibrotic stages. The PPV (100%)for significant and extensive fibrosis .NPV and accuracy(75%, 80%)respectively for significant fibroses,while it was (100%) for extensive fibrosis respectively.Significant correlation between liver biopsy and Fibro-test(P0.002)and Acti-test(P0.000).Significant correlation between liver biopsy hepatitis activity score and APRI (P 0.047)and FORNS score (P0.000). Conclusion: FORNS score wasn't considered since does not discriminate between significant and extensive fibrosis. Low sensitivity of APRI prohibtes detection of minmal fibrosis and allow undetermined results. Fibrosure classified all cases of chronic HCV sufficient to wave liver biopsy PE215 Introduction: HCC is the 6 th common cancer. Global increase of hepatitis B and C infection, the incidence of HCC steadily increasing. Egypt seroprevalence of HCV in Nile delta 20 -35%. AFP had limited sensitivity 60% and specificity 90% for small HCC. GPC-3 oncofetal protein over expressed in HCC. Evaluating validity of Glypican-3 as early detector of HCC.:10 healthy controls and 40 HCV positive patients:10 patients chronic hepatitis C virus infection.10 patients compensated cirrhosis [child-Pugh class A and B].10 patients decompensated cirrhosis [child-Pugh class C]. 10 patients HCC. liver functions: ALT, AST, Bilirubin(T), Albumin, GT.Tumor markers: AFP and GPC-3.Viral markers: HCV antibodies, HBs Ag and HBc Ab. The median value of GPC-3 in HCC, DC, CC significantly higher than chronic hepatitis and control groups. No significant correlation between AFP and GPC-3. AUROC of AFP 0.85 & AUROC of GPC-3 0.84. The diagnostic Sensitivity of AFP (20 ng/ml) 70% with PPV 53.8%. The specificity85% with NPV 91.9%. While the diagnostic Sensitivity of GPC-3 (2 ng/ml) 100% with PPV 27%. The specificity 42.2% with NPV 100%. Combined serial approach of AFP and GPC-3 improved specificity to 87.5%. Conclusion:GPC-3 although a serological test for early detection of HCC, showed limited specificity, where detected in different stages of chronic liver disease,it is oncofetal protein produced by regenerating liver cells. The diagnostic signature approach for simultaneous determination of AFP and GPC-3 improve prediction accuracy of HCC patients in those showing seronegativity to AFP. Results: Patients with HCV infection (n=388) were significantly older (mean age, 69 years) than patients with dual virus (n=75, 65 years) and HBV infection (n=752; 60 years) (p< 0.0001). The male-to-female ratio for HBV, dual virus and HCV group was 5.2, 3.4 and 1.3, respectively (p< 0.0001). Patients in the HBV group more often had higher total tumor volume (mean, 409 cm 3 ) than the dual virus group (244 cm 3 ) and HCV (168 cm 3 ) group (p< 0.0001). No significant differences of the severity of liver cirrhosis, performance status, cancer staging and tumor cell differentiation were noted among the three groups. Patients in the HCV group had a significantly poor survival in comparison to the HBV group only in the subset of patients with small tumor volume (< 50 cm 3 ) in the Cox proportional hazards model (relative risk: 1.44, p=0.041). Conclusions: Dual HBV and HCV virus infection does not accelerate the speed of HCC formation in patients with chronic hepatitis B, and appears to have a modified course of carcinogenesis pathway diverted away from the biological behavior of HBV and HCV infection. Background: Patients presenting with HCC is not infrequent in our clinical practice. The aetiology vary ranging from HBV, HCV, NASH and alcohol. The aim of this study was to see the aetiology of HCC in Bangladeshi patients.