Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-6-12
pubmed:abstractText
Genetic factors are likely to contribute to the variable presentation of community-acquired pneumonia (CAP). The purpose of this prospective cohort study was to determine whether the LTalpha+250 (TNFbeta+250) and TNFalpha-308 gene polymorphisms are associated with different presentations of CAP. Septic shock (SS) was defined using American College of Chest Physicians/Society of Critical Care Medicine (ACCP-SCCM) criteria. Type I respiratory failure (T1RF) was defined as an O(2) saturation on room air of < 90% with a normal PCO(2). A total of 280 patients were genotyped; 31 had SS, 80 had T1RF. Genotype proportions are given in the order of AA/GA/ GG. The proportion of patients in each genotype developing SS was as follows: LTalpha+250 0.19/0.07/0.09 (p = 0.01 AA versus non-AA); TNFalpha-308 0.16/0.06/0.12 (p = NS). Carrying at least one AA (tumor necrosis factor [TNF] high secretor) genotype had an 18.0% risk of SS versus 6.8% (p = 0.006). GG homozygotes (TNF low secretors) at both loci had only a 2.9% risk of SS. Septic shock was associated with the LTalpha+250:TNFalpha-308 A:G haplotype but not the A:A haplotype, suggesting that LTalpha+250 is a marker, rather than a causative polymorphism. Carriage of the G:G haplotype had a significant protective effect against the development of septic shock (p = 0.011). T1RF was not associated with LTalpha+250 AA genotype. In the absence of septic shock, there was a significant trend to greater T1RF in patients with LTalpha+250 GG (TNFalpha hyposecretor) genotype (p = 0.03). Our finding of different genotype associations for SS and T1RF has important implications for immunotherapy in both CAP and sepsis, as well as for the definition of the systemic inflammatory response syndrome (SIRS).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1073-449X
pubmed:author
pubmed:issnType
Print
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1599-604
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11401880-Adolescent, pubmed-meshheading:11401880-Adult, pubmed-meshheading:11401880-Aged, pubmed-meshheading:11401880-Aged, 80 and over, pubmed-meshheading:11401880-Cohort Studies, pubmed-meshheading:11401880-Community-Acquired Infections, pubmed-meshheading:11401880-Female, pubmed-meshheading:11401880-Genotype, pubmed-meshheading:11401880-Haplotypes, pubmed-meshheading:11401880-Humans, pubmed-meshheading:11401880-Lymphotoxin-alpha, pubmed-meshheading:11401880-Male, pubmed-meshheading:11401880-Middle Aged, pubmed-meshheading:11401880-Pneumonia, Bacterial, pubmed-meshheading:11401880-Polymorphism, Genetic, pubmed-meshheading:11401880-Prospective Studies, pubmed-meshheading:11401880-Respiratory Insufficiency, pubmed-meshheading:11401880-Risk Factors, pubmed-meshheading:11401880-Shock, Septic, pubmed-meshheading:11401880-Survival Rate, pubmed-meshheading:11401880-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
Septic shock and respiratory failure in community-acquired pneumonia have different TNF polymorphism associations.
pubmed:affiliation
Department of Medicine, University of Western Australia, Royal Perth Hospital, Perth, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't