226 LONG-TERM ANTIBIOTIC AND PROTON-PUMP INHIBITOR USE ARE STRONG PREDICTORS OF RECURRENT INFECTIONS IN CIRRHOSIS: A PROSPECTIVE MULTI-CENTER STUDY FROM NACSELD

Abstract

(type V collagen), C6M (type VI collagen), BGM (Biglycan), ELM (Elastin), and CRPM (CRP)), and ECM formation markers (P3NP (type III collagen) and P4NP7S (type IV collagen)) were measured. Results: The markers measured in hepatic venous blood correlated to the level measured in arterial blood (R=0.89–0.98; p < 0.0001). In hepatic venous blood, all markers correlated directly to Child Score and MELD, and inversely to ICG clearance and serum albumin, strongest with P3NP (R=0.46, 0.48, −0.53, and −0.46; respectively, p < 0.0001). All markers except ELM were inversely correlated to hematocrit and to hemoglobin, especially C4M and C1M showed strongest correlations (R = −0.31; −0.40; respectively, p = 0.001p < 0.0001). In both arterial and hepatic venous blood all markers except CRPM correlated to HVPG (e.g. P3NP for both sites R =0.47, p < 0.0001). A multiple regression analysis including P3NP, C6M and MELD improved the correlation (R =0.62, p < 0.0001). P3NP could clearly separate controls from HVPG levels <10mmHg (p < 0.01) and those with HVPG<10mmHg from those with HVPG levels ≥10mmHg (p < 0.0001). C4M, C5M, and ELM were all significantly higher in patients with HVPG levels ≥12mmHg compared to lower HVPG levels (p < 0.01–0.0001). Conclusion: The Protein Fingerprint markers reflect liver function and stage of disease. A strong correlation between the markers measured in hepatic venous and arterial blood was observed. A multimarker model in combination with clinical scores predicted HVPG and separated clinical relevant HVPG thresholds noninvasively. Therefore these markers and their models are suitable for non-invasive evaluation of portal hypertension in cirrhosis.