19 / 22
Volume 7, Issue 6 (Suppl)
J Gastrointest Dig Syst, an open access journal
ISSN: 2161-069X
Page 70
December 07-08, 2017 Madrid, Spain
&
13
th
International Conference on Clinical Gastroenterology & Hepatology
2
nd
International Conference on Digestive Diseases
CO-ORGANIZED EVENT
Associationof 4874A/G(rs4969170) polymorphisminSOCS3genepromoterregionandRNAexpression
with liver fibrosis progression in patients with chronic hepatitis C
Jadid Fatima Zahra
1,2
, Chihab Hajar
1
, Elfihry Raouia
1
, Zaidane Imane
1
, Salih Alj Hanane
2
, Saile Rachid
2
, Alaoui Rhimou
3
, Badre Wafaa
3
, Tazi Sanaa
1
,
Pascal Pineau
1
, Ezzikouri Sayeh
1
and
Benjelloun Soumaya
1
1
Institut Pasteur du Maroc, Morocco
2
Université Hassan II, Morocco
3
Institut Pasteur, France
4
Service de Medecine B, Morocco
Context:
Chronic hepatitis C virus infection (CHC) is one of the most important risk factor of hepatocellular carcinoma
(HCC). However, the pathogenesis of Insulin Resistance (IR) in hepatitis C infection is a very intriguing problem. In fact, the
HCV is now recognized responsible for direct interference with the insulin signaling pathway. In addition, HCV-related IR has
been shown to have a remarkable clinical impact on the progression of hepatic fibrosis and development of HCC.
Objective:
The present study aims to evaluate the association of 4874 A/G (rs4969170) polymorphism in SOCS3 gene promoter
region and RNA expression with liver fibrosis progression in chronic hepatitis C infected patients.
Materiel & Methods:
In this study 226 Moroccan patients chronically infected with HCV (95 patients with mild fibrosis
and 131 patients with advanced fibrosis) were genotyped for 4874 A/G (rs4969170) variant using the real time PCR. SOCS3
mRNA expression analysis was performed by using Sybr Green. Logistic regression was used to assess the association between
polymorphism and progression of HCV infection.
Results:
A significant difference in genotypes distribution of rs4969170 was detected betweenmild and advanced fibrosis group.
The AA genotype was significantly overrepresented in Ad-LD patients compared to m-LD, the AA genotype was associated
with a 5-fold increase of AdLD risk when compared to mild chronic hepatitis C (OR = 5.14; 95% CI, 2.29 - 11.54; P=0.00004).
A similar situation was observed with the dominance model (OR = 4.18; 95% CI, 2.19 - 7.97; P=6.374e-06). The relative
expression of SOCS3 to GAPDH mRNA was increased by 2 fold in Ad-LD as compared to m-LD group with AA genotype.
Conclusion:
Our results suggest that polymorphism in SOCS3 gene promoter modulates the progression of chronic hepatitis
C infection toward advanced liver disease by affecting its mRNA expression.
jadid.fz@gmail.comJ Gastrointest Dig Syst 2017, 7:6(Suppl)
DOI: 10.4172/2161-069X-C1-059