studies

HEPATOLOGY, VOLUME 62, NUMBER 1 (SUPPL) AASLD ABSTRACTS 995A
and coagulation failures (58.3%) followed by cerebral (13.9%)
and kidney failures (11.1%). The mortality was 44.4%, 62.5%,
and 100% in patients with ACLF grade 1, ACLF grade 2 and
ACLF grade 3, respectively, which was significant higher in
comparison with patients in CANONIC study in corresponding
grade (22.1% in grade 1, 32% in grade 2 and 76.7%
in grade 3, respectively). The results indicated that the EASL-
CLIF criteria may be too strict for diagnosis HBV-related ACLF.
Of note, there were 21.4% of HBV-ACLF patients underlying
chronic HBV hepatitis had more than one organ failure (assessing
by CLIF-SOFA), and the mortality was 66.7% among them.
The results suggested that diagnosis of HBV-ACLF should not
exclude those patients without cirrhosis. Conclusions: ESAL-CLIF
diagnostic criteria may not be suitable for assessing the patients
with HBV-related ACLF in our study. A large, prospective, and
multicenter study is needed to further validate the criteria.
Disclosures:
The following authors have nothing to disclose: Zhihong Wan, Chen Li, Shaoli
You, HongLing Liu, ShaoJie Xin, Bing Zhu
1610
Anti-platelet therapy reduces the incidence of hepatocellular
carcinoma in patients with chronic hepatitis B
Minjong Lee 2 , Jeong-Hoon Lee 2 , Sohee Oh 1 , YOUNG CHANG 2 ,
Joon Yeul Nam 2 , Young Youn Cho 2 , Jeong-Ju Yoo 2 , Yuri Cho 2 ,
Donghyeon Lee 2 , Eun Ju Cho 2 , Su Jong Yu 2 , Yoon Jun Kim 2 , Jung-
Hwan Yoon 2 ; 1 Department of Biostatistics, Seoul Metropolitan
Government Seoul National University Boramae Medical Center,
Seoul, Korea (the Republic of); 2 Department of Internal Medicine
and Liver Research Institute, Seoul National University College of
Medicine, Seoul, Korea (the Republic of)
Background: Platelets contribute to liver damage by promoting
the intrahepatic accumulation of virus-specific CD8 T cells in
mouse models of viral hepatitis. A recent study showed that
the long-term use of the anti-platelet drugs in a mouse model
of chronic hepatitis B can prevent hepatocarcinogenesis. We
aimed to compare the incidence of hepatocellular carcinoma
in patients not treated with anti-platelet drugs to those treated
with anti-platelet drugs. Methods: We performed a retrospective
analysis of data from 3,479 consecutive patients with
chronic hepatitis B who had HBV DNA completely suppressed
with antiviral treatment. The population was divided into two
groups: Group 1(n=2,891) not treated with anti-platelet drugs;
Group 2 (n=588) treated with aspirin and/or clopidgrel. Data
were collected from patients analyzed by a multivariable Cox
proportional hazards model for the entire cohort. Results:
During the study period, hepatocellular carcinoma was developed
in 229 patients (7.9%) in Group 1 and 15 (2.5%) in
group 2. In multivariable analyses, Group 2 patients showed
a significantly lower risk of HCC than that in Group 1 (hazard
ratio [HR]=0.21, 95% confidence interval[CI]=0.11–0.39,
P5 ×ULN) were excluded
due to potential overestimation of fibrosis by TE. Results: Serum
M30 levels were significantly increased in significant fibrotic
patients compared with no/minor fibrosis or NC (259.9 [IQR:
122.6-501.2] vs 70.6 [IQR: 41.3 - 105.3] U/L, P