studies

1230A AASLD ABSTRACTS HEPATOLOGY, October, 2015
cirrhosis (M/F: 12/5, age: median 59.2 years (49-65), etiology
of liver disease: HBV±HDV: 23.5%, HCV: 17.7%, alcohol:
41.2%, other: 17.6%, Child-Pugh score: median 7.5 (5-12),
MELD: median 10.5 (7-21), ascites (%): 3 (17.7) attending
the outpatient clinics were included. None had hepatocellular
carcinoma. Indications for PPIs administration were esophagitis
(35%), peptic ulcer (59%) and others (6%). Bacterial DNA
in serum and the levels of endotoxin, LBP, TGF-β, IL-1β, IL-6,
IL-8, IL-12, IL-10, TNF-α and NOx were assessed before (time
1) and at the end of treatment with PPIs (time 2). Bacterial
DNA was amplified by PCR using universal 16SrRNA primers,
endotoxin, LBP and TGF-β were measured by ELISA, the other
cytokines by a Cytometric Bead Array method, and NO levels
determined with a nitric oxide quantitation kit. Wilcoxon
Signed Rank Test was used to evaluate significant differences
in the parameters assayed before and after PPIs administration.
Results: None of the patients developed an infection during the
study period. Spearman’s correlation analysis demonstrated
a correlation between baseline LBP and MELD score (r=0.63,
p=0.02). Bacterial DNA was not detected before or after the
treatment. Time 1: Median endotoxin: 3.19 (1.03-4.33), LBP:
4.08 (3.23-12.99) μg/ml, NOx: 9.04 (2.44-15.72) μΜ,
TGF-β: 4.85 (2.43-16.64) ng/ml, TNF-α: 3.05 (0-8.26), IL-1:
4.7 (0-11.95), IL-6: 4.37 (0-16.09), IL-12: 7.69 (0-25.88),
IL-10: 6.56 (0-27.87), IL-8: 103.4 (0-281.4) pg/ml. Time 2:
Median endotoxin: 2.76 (1.49-86.55), LBP: 4.65 (0-17.53),
NOx: 7.36 (0.56-23.08), TGF-β: 3.49 (1.54-15.94), TNFα:
5.4 (0-60.98), IL-1: 8.57 (0-184.8), IL-6: 10.29 (0-31.5),
IL-12: 15.96 (0-159), IL-10: 5.16 (0-34.8), IL-8: 64.45 (18.99-
2892.4). No significant differences were observed between
the concentrations of all measured indices between times 1 and
2 (p>0.05). Subgroup analysis according to Child-Pugh stage
yielded similar results. Conclusions: Short-term PPIs administration
had no effect on serum bacterial DNA, bacterial products
or cytokine concentrations in patients with liver cirrhosis.
Disclosures:
Christos K. Triantos - Speaking and Teaching: Bristol, Gilead
The following authors have nothing to disclose: Maria Kalafateli, Panagiota Spadidea,
Dimitrios Goukos, Efstratios Koutroumpakis, Stelios F. Assimakopoulos,
Konstatinos Thomopoulos, Charalambos Gogos, Chrisoula Labropoulou-Karatza
C, Athanasia Mouzaki, George Daikos, Vasiliki Nikolopoulou
2096
A prognostic model evaluating neutrophil-to-leucocyte
ratio, organ failure and MELD scores as predictors of
long-term survival in acute-on-chronic liver failure
Danai Agiasotelli, Alexandra Alexopoulou, Larisa E. Vasilieva,
Georgia Kalpakou, Spyros P. Dourakis; 2nd Dept of Medicine,
Medical School University of Athens, Athens, Greece
Purpose/Background: Acute-on chronic liver failure (ACLF) is
defined as an acute deterioration of liver disease with high
mortality in patients with cirrhosis. The time needed to reverse
this condition and the factors affecting mortality after the early
28-day-period have been evaluated. Methods: One-hundredninety-seven
consecutive patients with cirrhosis were included.
Patients were prospectively followed-up for 180 days. Results:
ACLF was diagnosed in the 54.8% of patients. Infection was
the most common precipitating event in patients with ACLF.
Patients with ACLF had the worst prognosis compared to those
without (log-rank P30 days & ≤75 days) and
to 1.26 [(95% CI 0.53-3.00), P=0.609] during the third period
of observation (>75 and