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Endothelial dysfunction in childhood infection

Charakida, M. (författare)
Donald, A. E. (författare)
Terese, M. (författare)
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Leary, S. (författare)
Halcox, J. P. (författare)
Ness, A. (författare)
Davey Smith, G. (författare)
Golding, J. (författare)
Friberg, Peter, 1956 (författare)
Gothenburg University,Göteborgs universitet,Hjärt-kärlinstitutionen,Cardiovascular Institute
Klein, N. J. (författare)
Deanfield, J. E. (författare)
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 (creator_code:org_t)
2005
2005
Engelska.
Ingår i: Circulation. - 1524-4539. ; 111:13, s. 1660-5
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • BACKGROUND: Atherosclerosis begins in early life, and endothelial dysfunction is recognized as a key initiating event in the development of atherosclerosis. Although infection has been implicated in endothelial dysfunction and atherogenesis, the impact of acute common childhood infections on the vascular endothelium is unknown. METHODS AND RESULTS: We studied 600 children aged 10 years drawn from the Avon Longitudinal Study of Parents and Children. The children were divided into 3 groups: those with current acute infection (AI; n=135; 73 boys and 62 girls); a convalescent group with infection in the past 2 weeks (n=166; 78 boys and 88 girls), and a healthy control group (n=299; 131 boys and 168 girls). Endothelial function was determined in all subjects by high-resolution ultrasound to measure brachial artery flow-mediated dilation (FMD) and was expressed as the percentage change in diameter from baseline after reactive hyperemia. FMD was repeated in 40 children in the AI group and 50 in the control group after a mean interval of 1 year. FMD was lower in both the AI group (6.3+/-2.7%, mean+/-SD) and the convalescent group (8.1+/-3.1%) than in the control group (9.7+/-2.5%; P<0.001 for both). The observed differences in FMD remained after adjustment for potential confounding variables. At the repeat visit, FMD was unchanged in controls (P=0.85) but improved in the AI group (P<0.001). CONCLUSIONS: Acute infection in childhood is associated with impaired endothelium-dependent vasodilation. These findings support a potential role for previously unsuspected extrinsic inflammatory stimuli in the pathogenesis of early atherosclerosis.

Nyckelord

Arteriosclerosis/etiology
Case-Control Studies
Child
Endothelium
Vascular/*physiopathology
Female
Follow-Up Studies
Humans
Infection/*physiopathology
Male
Risk Factors
Socioeconomic Factors
Vasodilation

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