4.3 Article

Lack of association between tumour necrosis factor receptor types 1 and 2 gene polymorphism and severe acute alcoholic hepatitis

Journal

EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
Volume 22, Issue 7, Pages 794-800

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MEG.0b013e32832f5bba

Keywords

36 TNFR; 676 TNFR; acute alcoholic hepatitis; genetic polymorphism; Maddrey score; TNF-alpha; TNF receptor

Funding

  1. MILDT and INSERM 2006 (Mission Interministerielle de Lutte contre le Drogue et la Toxicomanie)

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Background/aims Tumour necrosis factor-alpha (TNF-alpha) is involved in the physiopathology of severe acute alcoholic hepatitis (AAH) binding with TNF receptor types TNFR1 and TNFR2, whose serum concentrations are elevated. We studied the role of TNFR1 and TNFR2 gene polymorphism in AAH patients. Methods One hundred and ninety-two patients (58 AAH with Maddrey score >= 32, 44 non-AAH cirrhoses, 90 healthy individuals) were genotyped for A36G TNFR1 and T676G TNFR2 using polymerase chain reaction-restriction fragment length polymorphism technique. Serum sTNFR1 and sTNFR2 were assayed. Results The AAH and two control groups did not differ for genotype distribution. In three groups, A (36 TNFR1) and T (676 TNFR2) allelic frequencies were similar, at 0.47, 0.47, 0.44 and 0.78, 0.81, 0.80, respectively. The 36 TNFR1, 676 TFNR2 genotypes did not influence on prognostic scores (Maddrey, Child-Pugh), nor in response to corticosteroids or 6-month survival. sTNFR1 levels were higher in AAH than healthy group (3.07 +/- 1.14 vs. 1.17 +/- 0.27 ng/ml, P < 0.001) and sTNFR2 levels were higher in AAH than cirrhosis (3.6 +/- 1.02 vs. 3.1 +/- 1.03, P < 0.05) and healthy groups (3.6 +/- 1.02 vs. 1.91 +/- 0.54, P < 0.001). However, sTNFR1 and sTNFR2 levels did not vary significantly according to genotypes. Conclusion These results did not support an association between 36 TNFR1, 676 TNFR2 gene polymorphisms and AAH. Eur J Gastroenterol Hepatol 22:794-800 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

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