NRH-4 is caused by primary outflow obstruction

(congestive heart failure or HV thrombosis). Conclusions: 1) 4 distinct patterns of NRH were identified, forming the basis of a novel classification Selleck FK228 of NRH subtypes. 2) NRH results when there is congestion or atrophy with or without arterialization. Varying severity and distribution of these parameters yield the 4 subtypes. 3) The pathogenesis of NRH can be summarized as the result of increased arterial flow and limited outflow capacity of the tissue. 4) The subtypes correlate with etiology and location of initial vascular insult. 5) NRH should be considered a group of similar diseases with differing pathogenesis, rather than a single entity. Disclosures: The following people have nothing to disclose: Ian R. Wanless, Ashley E. Stueck Background: Liver fibrosis develops as a consequence of liver injury such as HCV infection. Fibrosis is characterized

by structural changes and altered remodeling of extracellular Nivolumab concentration matrix (ECM) proteins. Protein fragments of the fibrotic tissue are generated consequent to disease pathogenesis and released into the circulation where that may be used as biomarkers, so-called protein fingerprints. There is clinical need for early diagnosis of patients as well as separating mild and moderate stages of liver fibrosis. Aim: In this study we evaluated the diagnostic value of an algorithm combining novel protein fingerprint markers of ECM formation and matrix metalloproteinase (MMP)-mediated ECM degradation for the detection of

mild and moderate liver fibrosis. Methods: The Protein Fingerprint Cobimetinib cell line markers Pro-C3, P4NP, P5CP (type III, IV, and V collagen formation, respectively), C3M, C4M, C6M (type III, IV, and VI degradation, respectively) and CRPM (C-reactive protein degradation) were measured in plasma from 194 HCV patients from a prior phase II antifibrotic study (CTgov reg. NCT00244751) and 22 healthy controls. Patients were stratified into Ishak stages F2 (n=78), F3 (n=88), or F4 (n=28). Liver biopsy from each patient was stained for total collagen and α-SMA and evaluated by a single pathologist. Results: A multiple regression analysis combining C4M, C6M, Pro-C3 and P4NP showed a strong correlation to Ishak stages (Multiple correlation coefficient = 0.4544, R2=0.1904, p<0.001). Plasma levels were significantly higher in HCV patients than in healthy controls (p<0.001). The diagnostic value of the algorithm was significant when separating controls from HCV patients (AUC=0.824, p<0.0001), mild fibrosis (Ishak F2/3) from moderate fibrosis (Ishak F4) (AUC=0.771, p<0.0001) and individual fibrosis stages (F2 vs. F3 AUC=0.619, p=0.0062; F3 vs. F4 AUC=0.732, p=0.001). Controls and HCV patients were divided into quar-tiles according to the plasma levels calculated from the algorithm.