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HEPATOLOGY, VOLUME 62, NUMBER 1 (SUPPL) AASLD ABSTRACTS 947A<br />

progressive decrease in ammonia concentration was observed<br />

in both groups, being higher in OP group at each time point,<br />

without significant differences. Decrease in ammonia in the first<br />

24h in the OP group [-20.40 μmol/L (-39.20, -2.80); median<br />

(IQR)] was twice that of the placebo group [-11.88 μmol/L<br />

(-36.75, 26.35)], without statistical significance. The subanalysis<br />

by Child-Pugh score showed a statistically significant<br />

ammonia decrease in Child-Pugh C treated patients at 36 h, as<br />

well as in the time normalized area under the curve (TN-AUC)<br />

0-120h in the OP group [40.16 μmol/L (37.7, 42.6 )] vs placebo<br />

group [ 65.5 μmol/L (54, 126); p=0.036]. A progressive<br />

decrease in plasma glycine and glutamine were observed in<br />

the treated group as compared to the placebo group. These<br />

differences reached statistical significance after 24 h of treatment<br />

and were maintained thereafter. Glutamine decrease<br />

associated with the appearance of phenylacetylglutamine in<br />

urine: u-PAG accumulated TN-AUC 12-120h placebo [5768<br />

μmol (1769,8808)] vs TN-AUC 12-120h OP [106851μmol<br />

(78802, 146666); p50 mmol/L). Ammonemia was higher in patients<br />

with HE than in those without (108 (95%CI: 86-123) vs 57<br />

(95%CI: 50-81), p=0.0004). In patients with HE, ammonemia<br />

was significantly correlated to severity of HE assessed by GCS<br />

(p=0.001). Overall, 34 HE patients experienced worsening of<br />

their neurological status during hospitalisation. Ammonemia<br />

at admission was significantly higher in those patients (128<br />

(95%CI: 108-147) vs 87 (95%CI: 64-110), p=0.007). In multivariate<br />

analysis, parameters independently associated with<br />

worsening of neurological status were MELD score and ammonia<br />

levels at admission (p=0.01 and 0.02, respectively). Conclusion:<br />

Ammonia levels at admission are correlated with the<br />

severity of HE and with outcome in cirrhotic patients with HE.<br />

Disclosures:<br />

Marika Rudler - Speaking and Teaching: Gilead, Mayoly<br />

Thierry Poynard - Grant/Research Support: Gilead; Stock Shareholder: BioPredictive<br />

Nicolas Weiss - Speaking and Teaching: Norgine, Alpha Wasserman<br />

The following authors have nothing to disclose: Simona Tripon, Maxime Mallet,<br />

Denis Monneret, Francoise Imbert-Bismut, Dominique Thabut<br />

1511<br />

Use of betablockers, previous hepatic encephalopathy<br />

and low albumin levels as risk factors of portal vein<br />

thrombosis in a cohort of cirrhotic patients<br />

Marta Lopez Gomez 1 , Elba Llop 1 , Angela Puente 2 , Juan de la<br />

Revilla 1 , Carlos Fernández-Carrillo 1 , Fernando Pons 1 , Jose Luis<br />

Martinez 1 , Natalia Fernández 1 , Maria Trapero 1 , Javier Crespo 2 ,<br />

José Luís Calleja 1 ; 1 Gastroenterology and Hepatology, Hospital<br />

Universitario Puerta de Hierro (MADRID. SPAIN), Pozuelo de<br />

Alarcon, Spain; 2 Hospital Universitario Marqués de Valdecilla,<br />

Santander, Spain<br />

Portal vein thrombosis(PVT) is a complication of liver cirrosis(LC).<br />

The aim of our study was to evaluate anual incidence<br />

of PVT and related risk factors.Methods: We retrospectively<br />

reviewed clinical and radiological data collected prospectively<br />

of consecutive cirrhotic patients included in the database<br />

of two Universitary Hospitals. Patients out of Milan criteria<br />

HCC, known PVT, TIPS and pregnancy were excluded. All<br />

patients with ultrasound diagnosis of PVT underwent MR or<br />

CTangiography.Results: From September 2013 to September<br />

2014, 747 cirrhotic patients were reviewed, 179 had exclusion<br />

criteria. Baseline characteristics are described in Table<br />

1. 23(4%) patients presented PVT during the inclusion period.<br />

Significant differences between patients with/without PVT<br />

were observed in: albumin (3.4SD0.8vs4.0SD0.5;p

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