Therefore we aimed to analyze a potential usefulness of serum CK-

Therefore we aimed to analyze a potential usefulness of serum CK-18 measurement in a large cohort of patients with chronic HBV-infection not receiving anti-HBV therapy. Patients and methods. Studied cohort consisted of 195 HBeAg(-) patients (116 male, median age 33) with persistent HBV-infection, including 122 with normal and 73 with elevated ALT activity, among them 8 with HBV-related HCC. Liver biopsy results were available in 71 patients. Serum CK-18 levels were measured by ELISA (Peviva, Sweden). Results. Serum CK-18 levels were significantly higher in CHB patients with elevated ALT activity (413±50 vs 253±24 U/L, P=0.002) as well as in those with liver

cirrhosis (679±222 vs 297±23, P=0.005). CK-18 showed a correlation with liver injury ALT (r=0.33, P<0.001), but also with platelets count (r=-0.26, P=0.002) GSK1120212 purchase and with APRI score (r=0.35, P<0.001), reflecting liver fibrosis. On the other hand, no associations with liver function or HBV viral load were noted. Most importantly, serum CK-18 was highly associated with histological advancement of liver fibrosis (ANOVA P=0.0003) and degree of inflammation (ANOVA

P=0.01). Interestingly serum CK-18 was more than trifold lower in patients with mild (S1) vs moderate/severe (S2-S4) fibrosis (Scheuer S1: 177±34, S2: 613±161, S3: 956±360, S4: 676±222 PI3K inhibitor IU/mL, P<0.001). ROC showed good discrimination ratio for patients with mild vs moderate/severe fibrosis (AUC 0.84, P<0.001), with 81% sensitivity and 80% specificity for CK-18 M30 value of 200 IU/mL. Conclusion. Based on a large cohort of CHB patients

CK-1 8 serum levels reflect both biochemical and histological activity of disease, suggesting its potential usefulness as simple biomarker predicting the need for anti HBV-therapy in patients with replication of HBV. Serum CK-18 >200 IU/mL has good sensitivity and specificity in discriminating mild vs moderate/severe fibrosis in CHB, stressing its value in its non-invasive assessment. Disclosures: Jerzy Jaroszewicz – Speaking and Teaching: Roche, Gilead, Abbott, MSD, BMS Robert Flisiak – Advisory Committees or Review Panels: Gilead, Merck, Roche, Bristol Myers Squibb, Janssen, Novartis, Achillion, Abbvie; Grant/Research Support: Roche, Bristol Myers Squibb, Janssen, Novartis, Gilead, Vertex, Merck; Speaking and Teaching: Janssen, Merck, PFKL Roche, Bristol Myers Squibb, Gilead The following people have nothing to disclose: Magdalena widerska, Anna Parfieniuk-Kowerda, Magdalena Rogalska-Plonska, Anatol Panasiuk BACKGROUND&AIM: Human beta2-glycoprotein I(beta2-GPI) binds to recombinant hepatitis B surface antigen(rHBsAg).The affinity of beta2-GPI and HBsAg is strong in plasma and gly-cosylation of beta2-GPI has no effect on this conjugation.The aim of this study was to investigate that binding of beta2-GPI to HBsAg played a role in the earliest steps of hepatitis B virus(HBV) infection.

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