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POSTER PRESENTATIONS

THU-042 Methods: In 129 patients (72% male; age:53.9 ± 11.3years) we


END-OF-LIFE HEALTHCARE COSTS AND UTILIZATION AMONG estimated the following GFRs according to: a) sCr-based MDRD-4
PATIENTS WITH END-STAGE-LIVER-DISEASE IN ONTARIO: A and the CKD-EPI-sCr equations, b) cysC-based Hoek, Larsson and
POPULATION-BASED STUDY CKD-EPI-CysC equations and c) mathematical formulae which
E.M. Kelly1, S. Murthy1, F. Wong2, T. Shaw-Stiffel1, L. Scully1, combined both sCr and cysC [i.e. CKD-EPI Cr-cysC and the equation
M. Chalifoux3, P. Tanuseputro3, P. James1. 1The Ottawa Hospital, proposed recently (Mindikoglou et al., Clin GH. 2015) (Mindi-eGFR)].
Ottawa; 2University of Toronto, Toronto; 3OHRI, Ottawa, Canada All estimated GFRs were compared with “true GFR”. Multivariable
E-mail: ekelly@toh.on.ca linear regression analysis was used for GFR predictors.
Results: The mean “true GFR” was 74.2 ± 27. The mean values of
Background and Aims: Healthcare for patients with end stage liver MDRD, CKD-EPI-sCr, eGFR-Hoek, eGFR-Larsson, CKD-EPI-cysC,
disease (ESLD) is often initiated in response to acute deterioration
CKD-EPI Cr-cysC and Mindi-eGFR were 79.4 ± 31, 76.1 ± 26, 44.6 ±
from disease progression. Despite guarded prognoses, many ESLD
19, 42.2 ± 21, 41.4 ± 20, 54.6 ± 21 and 62 ± 20 mL/min, respectively.
patients continue to receive expensive therapeutic interventions at The correlations between “true GFR” with MDRD, CKD-EPI-sCr, eGFR-
the end-of-life (EOL).
Hoek, eGFR-Larsson, CKD-EPI-cysC, CKD-EPIsCr-cysC and Mindi-
The aims of this study were to evaluate EOL costs and utilization in eGFR were good (Spearman r2:0.72, 0.71, 0.68, 0.68, 0.71, 0.75 and
patients with ESLD as compared to non-ESLD patients within the
0.76, respectively, p < 0.001). The factors independently associated
province of Ontario, Canada.
with the presence of “true” GFR < 60 mL/min were: sCr (OR: −0.56
Methods: Using the Ontario Health Administrative Database, we 95%C.I.: −0.87 to −0.41, p < 0.001) and 24 h urinary sodium excretion
performed population-based retrospective cohort study was
(UNa24h) (OR:0.21, 95%C.I.: 0.0–0.003, p = 0.04). Based on the area
conducted of all decedents within the province of Ontario, between under the ROC curves, sCr had better discriminative ability for the
April 1, 2010 and March 31, 2013. Patients with ESLD were defined
presence of “true” GFR <60 mL/min, compared to UNa24h (AUROC:
using international classification of disease codes (ICD-9) for cirrhosis
0.87 and 0.74, respectively). In multivariable linear regression
and decompensation (variceal bleeding, encephalopathy, ascites, analysis, the factors independently associated with the “true GFR”
hepatorenal syndrome and peritonitis). Patients with ESLD were
were age, cysC and sCr. These variables were included in the “new
compared to non-ESLD patients on direct health care costs in the last GFR” equation, which had very good correlation (Spearman r2: 0.76)
year of life, including hospitalizations, outpatient services and long-
with “true” GFR, it had lower bias, compared to the other eGFRs (0.89,
term care. Multivariate modelling was performed to compare the
p < 0.05 for all comparisons with the other estimated GFRs) and
total costs in the final 90 days of life, adjusting for individual
high discriminative ability to predict the presence of “true” GFR <
demographic (age and sex), co-morbidity burden.
60 mL/min (AUC: 0.90).
Results: The study cohort consisted of 264,754 decedents, of which
Conclusions: In our study, we developed a new formula based on age,
ESLD patients comprised 2.1% (n = 5,575). Direct health care
sCr and cysC. This formula had a strong correlation with “true GFR”
expenditure for patients with ESLD increased more in the last 90
and significantly lower bias, compared to the other conventional
days of life compared to non-ESLD patients. The mean cost in the last
GFRs (including Mindi-eGFR).
90 days of life was $35,008 for patients with ESLD and $21401 for
patients without ESLD ( p < 0.01), and this was predominantly THU-044
related to increased acute care utilization [ESLD = $30,667 (88% URINE ALBUMIN-TO-CREATININE RATIO IS ASSOCIATED WITH THE
of total costs) vs non-ESLD = $15,162 (71%)]. ESLD patients had SEVERITY OF LIVER DISEASE, RENAL FUNCTION AND SURVIVAL IN
higher rates of acute care utilization in the last and 90 days of life [19 PATIENTS WITH DECOMPENSATED CIRRHOSIS
days vs 6 days, p < 0.01], longer hospitalization stays [additional 4.5 E. Cholongitas1, I. Goulis1, M. Ioannidou1, S. Soulaidopoulos1,
days [95% CI 4.2–4.9 days ( p < 0.001)], and increased odds of dying in P. Chalevas1, E. Akriviadis1. 14th Department of Internal Medicine,
an institutional [OR 1.9 (95% CI 1.8–2.0; p < 0.001)]. ESLD patients Hippokratio General Hospital, Aristotle University, Thessaloniki, Greece
with peritonitis or hepatorenal syndrome incurred the highest mean E-mail: cholongitas@yahoo.gr
total costs in the last 90 days of life [$43,196 and $38,584,
respectively]. Background and Aims: Several studies have shown that urine
Conclusions: EOL care in ESLD patients is associated with albumin-to-creatinine ratio (UACR) >30 mg/g is associated with the
substantially higher costs than in the general population, presence of kidney damage. The aim of this prospective study was
predominantly from increased acute care utilization including to investigate if UACR is associated with the presence of renal
hospitalization. Whether optimizing outpatient services for dysfunction (glomerular filtration rate, GFR < 60 mL/min), severity of
patients and/or offering timely palliative services for patients liver disease and survival in patients with decompensated cirrhosis.
with ESLD can lead to more cost-effective EOL care warrants further Methods: We evaluated 220 patients (73% male; age 52.8 ± 12 years).
evaluation. In each patient, assessment of GFR was based on 51Chromium-EDTA.
Collection of 24-hour urine for calculation of urine sodium (24UNa)
THU-043 was done and random urine samples were obtained for measurement
COMPARISON OF CREATININE AND CYSTATIN C BASED of UACR.
GLOMERULAR FILTRATION RATE FORMULAE WITH 51CHROMIUM- Results: Thirty eight patients (17%, group 1) had UACR ≥ 30 mg/g and
EDTA CLEARANCE IN PATIENTS WITH DECOMPENSATED CIRRHOSIS 182 (83%, group 2) had ACR < 30 mg/g. Group 1, compared to group 2
E. Cholongitas1, I. Goulis1, M. Ioannidou1, S. Soulaidopoulos1, patients, had significantly lower levels of “true” GFR (61 vs 71 mL/
P. Chalevas1, E. Akriviadis1. 14th Department of Internal Medicine, min, p = 0.035), but higher levels of INR (1.7 vs 1.4, p = 0.05), serum
Hippokratio General Hospital, Aristotle University, Thessaloniki, Greece creatinine (1.3 vs 1.0 mg/dL, p = 0.05) and MELD score (18.2 ± 5 vs
E-mail: cholongitas@yahoo.gr 14.3 ± 6, p = 0.019). Patients with “true” GFR < 60 mL/min (n = 93),
compared to those with “true” GFR ≥ 60 mL/min (n = 127), had higher
Background and Aims: The accurate assessment of glomerular
levels of serum creatinine (1.4 vs 0.9 mg/dL, p < 0.001), cystatin-C (2.4
filtration rate (GFR) in cirrhosis has become very important. Serum vs 1.4 mg/dL, p < 0.001), plasma renin activity (23 vs 11 ng/mL*h, p <
cystatin-C (CysC) and its derived GFR formulae estimates have been 0.001), bilirubin (4.6 vs 2.8 mg/dL, p = 0.04), UACR (34 vs 19 mg/g, p =
proposed as superior predictors of renal function than those based
0.028) and MELD score (18 vs 12, p < 0.001), but lower albumin (3.1
on serum creatinine (sCr). Our aim was to compare CysC and sCr vs 3.5 g/dL, p = 0.01) and 24UNa (46 vs 74 mmol/24 h, p = 0.004).
GFR formulae with 51Chromium-EDTA (“true GFR”) in patients with
In multivariable analysis, serum creatinine and UACR were
decompensated cirrhosis and to derived a “new GFR” formula. independently associated with the presence of GFR < 60 mL/min.

Journal of Hepatology 2016 vol. 64 | S213–S424 S259


POSTER PRESENTATIONS
Based on the area under the ROC curves, the best cut off point for THU-046
UACR was >16.51 mg/g giving a sensitivity 70%, specificity 49%, PPV CLINICAL TRIAL TO EVALUATE THE EFFICACY OF PRIMARY
68% and NPV 51%. During the follow up period [17 (6–52) months], PROPHYLAXIS WITH L-ORNITHINE L-ASPARTATE TO PREVENT THE
the patients who died or underwent LT (n = 158), compared to DEVELOPMENT OF OVERT HEPATIC ENCEPHALOPATHY IN
those who remained alive (n = 62), had higher levels of UACR (41 vs PATIENTS WITH CIRRHOSIS AND ACUTE VARICEAL BLEEDING
13 mg/g, p = 0.025). Patients with UACR ≥ 30 mg/g had worse F. Higuera-de la Tijera1, A.I. Servín-Caamaño2, F. Salas-Gordillo1,
outcome, compared to those with ACR < 30 mg/g (log rank p = 0.05). J.M. Abdo-Francis1, J. Camacho-Aguilera2, J.L. Pérez-Hernández1,
UACR > 30 mg/g had specificity 92% and PPV 87.5% for mortality, F. Jiménez-Ponce3. 1Gastroenterology/Hepatology; 2Internal Medicine,
while the best cut off point for mortality was UACR > 2.49 giving Hospital General de México; 3Research Department, ISSSTE, Mexico City,
sensitivity, specificity, PPV and NPV were 97%, 29%, 78% και 79%, Mexico
respectively. E-mail: fatimahiguera@yahoo.com.mx
Conclusions: we showed for the first time that UACR ≥ 30 mg/g was
associated with more severe liver disease, lower GFR and worse LT- Background and Aims: Variceal bleeding (VB) is one of the most
important precipitating factors of overt hepatic encephalopathy
free survival in patients with decompensated cirrhosis. However,
further studies are needed to confirm these findings. (OHE). L-ornithine L-aspartate (LOLA), an anti-ammonia therapy, has
never been evaluated as primary prophylaxis to prevent the
THU-045 development of OHE in cirrhotic patients after an acute episode of
PORTAL VEIN THROMBOSIS IN PATIENTS WITH CIRRHOSIS. VB. The aim of this study was to evaluate if primary prophylaxis with
INCIDENCE AND FACTORS ASSOCIATED WITH ITS LOLA is effective to prevent the development of OHE after VB.
DEVELOPMENT Methods: A randomized, double-blind, placebo-controlled clinical
F. Turon1, A. Baiges1, A. Garcia-Criado2, I. Nuñez2, R. Gilabert2, C. Bru2, trial, approved by Ethics and Research Committees from México’s
A. Berzigotti1, J.C. Reverter3, S. Seijo1, J. Bosch1,4, V. Hernández-Gea1,4, General Hospital, it included cirrhotic patients with VB and without
J.C. Garcia-Pagan1,4. 1Hepatic Hemodynamic Laboratory. Liver Unit. OHE according to West-Haven criteria (WHC), and without minimal
IMDM. IDIBAPS.; 2Department of Radiology; 3Hemotherapy and hepatic encephalopathy (MHE) assessed by the Psychometric Hepatic
Hemostasis Unit, Hospital Clínic, Barcelona; 4Centro de Investigación Encephalopathy Score (PHES) and critical flicker fusion (CFF) at
Biomedica en Red de Enfermedades Hepáticas y Digestivas, CIBERehd, admission-time. Sample size was calculated considering a one-
Spain tailed 5% type I error, a statistic power of 80%, a difference between
E-mail: jcgarcia@clinic.ub.es groups of 26%, and considering an additional 20% of patients for
possible losses. Group 1 (22 patients) received a 24-hour intravenous
Background and Aims: Data on the incidence of portal vein infusion of 500 mL of 0.9% saline solution containing 10 mg of LOLA
thrombosis (PVT) in patients with cirrhosis and its predictive during 7 days. Group 2 (22 patients) received placebo. All patients
factors is scarce. The aim of this study is to determine the were daily evaluated searching for signs of OHE according with WHC.
prevalence and incidence of PVT in cirrhosis and to evaluate its Acute VB was treated according with recommendations from Baveno
predictive factors. V consensus.
Methods: Prospective single center study including consecutive Results: There were no differences between groups regard to
cirrhotic patients undergoing abdominal Doppler-Ultrasound (US) demographic, clinical and biochemical basal characteristics.
for systematic screening of PVT between December 2010 and April Patients in the placebo group had a greater frequency regard to the
2013 and followed until August 2015 or until death, liver development of OHE compared with LOLA group (54.5% vs. 22.7%, p =
transplantation, TIPS or evidence of tumoral thrombosis. PVT was 0.03). In those who developed OHE, the grade according to WHC was
confirmed by angio-CT. Clinical, laboratory, US and coagulation data worst in the group receiving placebo (median 3, range 2-4) than in
were collected. those receiving LOLA (median 1, range 1–2), ( p = 0.004) The time in
Results: 400 patients were included: 59% male, median age 59 ± 10 days for the development of OHE has a median of 2 days (range 1–4)
years, cirrhosis etiology: 56% HCV and 36% alcoholic, Child-Pugh A/B/ and 3 days (range 1–3) for placebo and LOLA groups respectively ( p =
C 68/24/8%. Baseline US detected PVT in 23 (5.8%) patients (21 partial 0.65). There were no adverse effects or deaths. One patient receiving
and 2 occlusive). The presence of PVT was independently associated placebo developed spontaneous bacterial peritonitis despite
with Child-Pugh score (OR 1.74; 95% CI = 1.40–2.16) and spleen antibiotic prophylaxis, however, he had a good response when
diameter (OR 1.505; 95% CI = 1.23–1.82). The 377 patients without antibiotic was adjusted according to the ascites culture result.
PVT at diagnosis were followed-up during a median of 41 months Conclusions: This is the first study that demonstrates that LOLA is
(range 0–56). 26 (6.9%) patients developed PVT (24 partial and 2 an effective therapy for primary prophylaxis in cirrhotic patients
occlusive). The incidence of PVT was 2, 4.3 and 7.6% at 1, 2 and 3 years. with VB to prevent the development of OHE; this therapy also was
Incidence of PVT stratifying by Child-Pugh A or B/C was 0.8, 2 and 4.7% well tolerated and was free of adverse effects.
and 5.8, 11.7 and 18% at 1, 2 and 3 years respectively. Child-Pugh
score (OR 1.35; 95% CI = 1.06–1.71), spleen diameter (OR 1.22; 95% THU-325
CI = 1.05–1.4) and portal flow velocity (OR 0.92; 95% CI = 0.85–0.98) INADEQUATE NUTRITION IN PATIENTS WITH CIRRHOSIS: THE
were independently associated with development of PVT, suggesting NEED OF A PERSONALIZED EDUCATIONAL PROGRAM
that the severity of portal hypertension and the degree of liver F.A. Giannone1, P. Caraceni1, M. Domenicali1, M. Baldassarre1, P. De
failure are key factors in the development of PVT. A complete Pasquale1, S. Boffelli1, M. Laggetta1, M. Biselli1, M. Bernardi1.
coagulation study was done in 316 patients (including 20 developing 1
Department of Surgical and Medical Sciences, U.O. Semeiotica Medica
PVT). In this subgroup, portal flow velocity and low levels of the and Center for Applied Biomedical Research (CRBA), Alma Mater
procoagulant factor synthesized in liver, Factor X (OR 0.91: IC 95% = Studiorum University of Bologna, Bologna, Italy
0.88–0.95) were the only two independent predictors of the E-mail: ferdinando.giannone@gmail.com
development of PVT.
Background and Aims: Malnutrition and sarcopenia occur
Conclusions: PVT in liver cirrhosis is a multifactorial event that
frequently in patients with cirrhosis, contributing to excess
occurs preferentially in patients with more advanced liver disease
morbidity and mortality. Unfortunately, the management of
and more severe portal hypertension. The hemostatic disturbances of
nutrition is often difficult, as these patients constitute a very
cirrhosis do not seem to play an essential role.
heterogeneous population in terms of needs of nutrients, due to
the various co-morbidities or complications, as well as motivation
and adherence to recommendations. This prospective observational

S260 Journal of Hepatology 2016 vol. 64 | S213–S424

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