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http://purl.uniprot.org/citations/16148556http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16148556http://www.w3.org/2000/01/rdf-schema#comment"

Background

Four polymorphisms have been described associated with either increased risk for alcoholic liver disease (ALD) or more serious histological lesions: tumour necrosis factor alpha (TNF-alpha) G(-238)A, interleukin-10 (IL-10) C(-627)A, promoter of CD14 endotoxin receptor gene C(-159)T and manganese superoxide dismutase (MnSOD) C(-1183)T/valine --> alanine.

Methods

We sought confirmatory evidence, through individual and simultaneous analysis of the four aforementioned polymorphisms, in 176 heavy drinkers: ALD (n = 100) if histology-compatible or clinical evidence of hepatic decompensation; and no evidence of liver disease (NLD) (n = 76) if normal liver tests on two occasions or normal liver histology (steatosis alone).

Results

Patients with ALD were older (53+/-10 vs. 48+/-10 years, P<0.05), with a similar sex distribution. TNF-alpha G(-238)A showed no difference in heterozygous GA-genotype prevalence (ALD, 9.0%/NLD, 7.9%). IL-10 C(-627)A showed no difference between groups, either homozygote AA (8.0% vs. 10.5%) or heterozygote CA (34.0% vs. 39.5%). CD14 promoter C(-159)T showed no difference between groups in T-allele frequency, either homozygote TT (27% vs. 21%) or heterozygote CT (49% vs. 50%). Alanine MnSOD allele carriers showed no difference between groups in either the heterozygote (55.0% vs. 49.3%) or homozygote (22% vs. 25%). No difference was observed in the probability of having simultaneously two, three or four of the implicated polymorphisms: respectively, 43%, 33% and 0% in ALD, and 43%, 24% and 5% in NLD (not significant).

Conclusions

No association was found between the previously implicated polymorphisms of TNF-alpha, IL-10, CD14 and MnSOD, either individually or simultaneously, and the presence of established ALD."xsd:string
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http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Machado M."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Martins A."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Marques-Vidal P."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Goncalves M.S."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"de Moura M.C."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Camilo M.E."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Cortez-Pinto H."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/author"Soren S."xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/name"Eur J Gastroenterol Hepatol"xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/pages"1099-1104"xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/title"Are genetic polymorphisms of tumour necrosis factor alpha, interleukin-10, CD14 endotoxin receptor or manganese superoxide dismutase associated with alcoholic liver disease?"xsd:string
http://purl.uniprot.org/citations/16148556http://purl.uniprot.org/core/volume"17"xsd:string
http://purl.uniprot.org/citations/16148556http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16148556
http://purl.uniprot.org/citations/16148556http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16148556
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