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Titolo:
Promoter polymorphism of the CD14 endotoxin receptor gene as a risk factorfor alcoholic liver disease
Autore:
Jarvelainen, HA; Orpana, A; Perola, M; Savolainen, VT; Karhunen, PJ; Lindros, KO;
Indirizzi:
Natl Publ Hlth Inst, Alcohol Res Ctr, Helsinki 00101, Finland Natl Publ Hlth Inst Helsinki Finland 00101 Ctr, Helsinki 00101, Finland Univ Helsinki, Dept Clin Chem, SF-00100 Helsinki, Finland Univ Helsinki Helsinki Finland SF-00100 Chem, SF-00100 Helsinki, Finland Univ Helsinki, Dept Med Genet, SF-00100 Helsinki, Finland Univ Helsinki Helsinki Finland SF-00100 enet, SF-00100 Helsinki, Finland HUCH Lab Diagnost, Helsinki, Finland HUCH Lab Diagnost Helsinki FinlandHUCH Lab Diagnost, Helsinki, Finland Univ Calif Los Angeles, Dept Human Genet, Gonda Neurosci & Genet Res Ctr, Los Angeles, CA USA Univ Calif Los Angeles Los Angeles CA USA t Res Ctr, Los Angeles, CA USA Tampere Univ Hosp, Sch Med, Res Unit, Ctr Lab Med, Tampere, Finland Tampere Univ Hosp Tampere Finland s Unit, Ctr Lab Med, Tampere, Finland Univ Kuopio, Dept Clin Pathol & Forens Med, FIN-70211 Kuopio, Finland UnivKuopio Kuopio Finland FIN-70211 rens Med, FIN-70211 Kuopio, Finland
Titolo Testata:
HEPATOLOGY
fascicolo: 5, volume: 33, anno: 2001,
pagine: 1148 - 1153
SICI:
0270-9139(200105)33:5<1148:PPOTCE>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
FRAGMENT-LENGTH-POLYMORPHISM; RAT KUPFFER CELLS; ANTIINFLAMMATORY CYTOKINES; MYOCARDIAL-INFARCTION; END-POINTS; CIRRHOSIS; INJURY; LIPOPOLYSACCHARIDE; SUSCEPTIBILITY; PREDISPOSITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Lindros, KO Natl Publ Hlth Inst, Alcohol Res Ctr, POB 719, Helsinki 00101,Finland Natl Publ Hlth Inst POB 719 Helsinki Finland 00101 1, Finland
Citazione:
H.A. Jarvelainen et al., "Promoter polymorphism of the CD14 endotoxin receptor gene as a risk factorfor alcoholic liver disease", HEPATOLOGY, 33(5), 2001, pp. 1148-1153

Abstract

Twin concordance studies indicate that genetic factors influence the individual susceptibility for alcoholic liver disease (ALD). Both clinical and experimental data suggest that Kupffer cell activation by gut-derived endotoxins and other bacterial products is an important pathogenic factor. Activated Kupffer cells release proinflammatory cytokines, a process that is regulated by the CD14 endotoxin receptor (CD14). Recently, a C -->T (-159) polymorphism in the promoter region of the CD14 gene was detected and found to confer increased CD14 expression. In the present study, the association of CD14 promoter polymorphism with different forms of ALD was examined in 3 separate autopsy series. Among 442 men with valid alcohol-consumption data, 381 men had been moderate or heavy alcohol consumers. The allele frequency of the CD14 promoter genotype, determined by a modified cycle minisequencingtechnique, was 0.34 (CC), 0.51 (CT), and 0.16 (TT). The T allele was foundto be associated with advanced ALD, i.e., with alcoholic hepatitis (odds ratio [OR]: 2.48; P = .018), and especially with cirrhosis (OR: 3.45; P = .004), but not with fatty liver, periportal fibrosis, or bridging fibrosis. The overall age-adjusted risk for cirrhosis was 3.08 (P = .01) for the carriers of the CT genotype, and 4.17 (P = .005) for the homozygous TT genotype. These results suggest that in the relatively isolated Finnish population, the T allele confers increased risk of alcoholic liver damage. In particular, TT homozygotes are at a high risk to develop cirrhosis.

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Documento generato il 03/04/20 alle ore 11:08:35