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HEPATOLOGY, VOLUME 62, NUMBER 1 (SUPPL) AASLD ABSTRACTS 1217A<br />

2069<br />

Impact of genetic variation of the AVP1a receptor on<br />

the presence of circulatory failure in patients with acute<br />

decompensation of liver cirrhosis or acute-on-chronic<br />

liver failure<br />

Annarein J. Kerbert 1 , Jelte Schaapman 1 , Johan van der Reijden 1 ,<br />

Amorós Àlex 2 , Aiden McCormick 3 , Bart van Hoek 1 , Vicente<br />

Arroyo 4 , Pere Gines 4 , Rajiv Jalan 5 , Victor Vargas 6 , Rudolf E.<br />

Stauber 7 , Hein W. Verspaget 1 , Minneke Coenraad 1 ; 1 Gastroenterology-Hepatology,<br />

Leiden University Medical Center, Leiden,<br />

Netherlands; 2 Data Management Center, CLIF consortium, Barcelona,<br />

Spain; 3 Gastroenterology-Hepatology, St Vincent’s University<br />

Hospital, Dublin, Ireland; 4 Liver Unit, Hospital Clinic, University<br />

of Barcelona, Barcelona, Spain; 5 Gastroenterology-Hepatology,<br />

University College London, London, United Kingdom; 6 Liver Unit,<br />

Hospital Vall d’Hebron, CIBERehd, Barcelona, Spain; 7 Internal<br />

Medicine, Medical University of Graz, Graz, Austria<br />

Background & aims: Acute-on-chronic liver failure (ACLF)<br />

is defined as an acute decompensation of former stable<br />

chronic liver disease (AD) accompanied by the presence of<br />

organ failure and a high risk of short-term mortality. Systemic<br />

hemodynamic derangement and activation of endogenous<br />

vasoconstrictor systems are thought to contribute to the pathogenesis.<br />

Arginine vasopressin is a key-regulator in hemodynamic<br />

homeostasis and mediates splanchnic vasoconstriction<br />

through the arginine vasopressin 1a receptor (AVP1aR). Aim<br />

of the present study was to assess whether genetic variation of<br />

AVP1aR is associated with the presence of circulatory failure<br />

in patients with AD or ACLF. Methods: Eight single nucleotide<br />

polymorphisms (SNPs) of AVP1aR with possible clinical relevance<br />

were identified. From 824 cirrhotic patients admitted for<br />

AD, clinical, laboratory and survival data were retrieved from<br />

the CANONIC database. Presence of circulatory failure was<br />

defined as a mean arterial blood pressure (MAP) < 70 mmHg<br />

or the use of vasopressors. ACLF was defined according to<br />

the CLIF Consortium Organ Failure score. All patients were<br />

genotyped for all eight SNPs using polymerase chain reaction<br />

(PCR) followed by restriction fragment length polymorphism<br />

or PCR allele-specific amplification primers. Fisher’s exact test<br />

and linear regression analysis were used to test for association<br />

between allele frequencies and dichotomous and continuous<br />

variables respectively. Results are shown as mean ± SD. P<<br />

0.05 was considered statistically significant. Results: Patients<br />

with ACLF (n=184) had a significantly lower MAP as compared<br />

to patients without ACLF (80 ± 13 vs. 84 ± 12 mmHg,<br />

p< 0.001). The use of vasopressors was also significantly more<br />

frequent in patients with ACLF as compared to those without<br />

ACLF (19.0% vs. 2.9%, p< 0.001). Circulatory failure was<br />

present in 61 out of 824 patients, of whom 44 fulfilled the<br />

criteria of ACLF. A C>T mutation in SNP rs7308855 showed<br />

a significant association with the presence of circulatory failure<br />

in patients with AD (p= 0.025) and a clear trend towards the<br />

presence of circulatory failure in patients with ACLF (p= 0.085).<br />

A trend was also found for a T>A mutation in SNP rs7298346<br />

to be associated with the presence of circulatory failure in<br />

patients with AD (p= 0.062). In addition, this mutation showed<br />

a significant association with the presence of circulatory failure<br />

in the subgroup of patients with ACLF (p= 0.046). Conclusions:<br />

Single nucleotide polymorphisms in the AVP1a receptor are<br />

associated with the presence of circulatory failure in patients<br />

with acute decompensation of liver disease and ACLF.<br />

Disclosures:<br />

Bart van Hoek - Advisory Committees or Review Panels: Janssen-Cilag, Bristol<br />

Meyers Squib, Gilead, Merck, Abbvie<br />

Vicente Arroyo - Speaking and Teaching: GRIFOLS<br />

Pere Gines - Advisory Committees or Review Panels: Ferring, Ikaria; Grant/<br />

Research Support: Sequana Medical, Grifols<br />

Rajiv Jalan - Consulting: Ocera Therapeutics, Conatus; Grant/Research Support:<br />

Grifols, Gambro; Patent Held/Filed: Yaqrit, Cyberliver<br />

Rudolf E. Stauber - Advisory Committees or Review Panels: Gilead, BMS; Grant/<br />

Research Support: Abbvie, MSD; Speaking and Teaching: Merz<br />

The following authors have nothing to disclose: Annarein J. Kerbert, Jelte Schaapman,<br />

Johan van der Reijden, Amorós Àlex, Aiden McCormick, Victor Vargas,<br />

Hein W. Verspaget, Minneke Coenraad<br />

2070<br />

Prevalence, risk factors and outcome of infections by<br />

multidrug resistant bacteria (MDR) in a liver intensive<br />

care unit (ICU): a prospective study<br />

Amrish Sahney 1 , Cyriac A. Philips 1 , Rakhi Maiwall 1 , Ashok<br />

Choudhary 1 , Lalita G. Mitra 2 , Ankur Jindal 1 , Manoj Kumar 1 , Kapil<br />

D. Jamwal 1 , Vikram Bhatia 1 , Vikas Khillan 3 , Shiv K. Sarin 1 ; 1 Hepatology,<br />

ILBS, New Delhi, India; 2 Critical care, ILBS, New Delhi,<br />

India; 3 Microbiology, ILBS, New Delhi, India<br />

Background & Aim:There is limited data on prevalence, predictors<br />

and impact on extra hepatic organ failure and mortality<br />

due to MDR bacterial infections in critically ill cirrhotic<br />

patients. Methodology: We prospectively studied 522 cirrhoticpatients<br />

admittedto dedicated liver ICU during March<br />

to October 2014. Organ failure was defined as: Kidney failure:<br />

SCr ≥2mg% or need for dialysis, cerebral failure: Grade<br />

3 or 4 hepatic encephalopathy, Circulation failure: shock, &<br />

Lung failure: PaO2/FiO2

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