Chest · 2012
In vivo platelet activation in critically ill patients with primary 2009 influenza A(H1N1).
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
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Rondina Matthew T, Brewster BreAnna, Grissom Colin K, Zimmerman Guy A, Kastendieck Diana H, Harris Estelle S, Weyrich Andrew S
Аннотация
BACKGROUND: Changes in platelet reactivity during 2009 influenza A(H1N1) (A[H1N1]) have not been characterized.
METHODS: We prospectively examined platelet activation and cytokine responses in patients with A(H1N1) (n = 20), matched patients with bacterial pneumonia (n = 15), and nonhospitalized, healthy control subjects (n = 10).
RESULTS: Platelet-monocyte aggregation was higher in patients with A(H1N1) (21.4% ± 4.7%) compared with patients with pneumonia (10.9% ± 3.7%) and control subjects (8.1% ± 4.5%, P < .05). Similarly, PAC-1 (antibody that binds to the active conformation of integrin α(IIb)β(3)) binding to platelets is increased in patients with A(H1N1) (9.5% ± 4.7%) compared with patients with pneumonia (1.0% ± 0.7%) and healthy subjects (0.61% ± 0.15%, P < .10). PAC-1 binding was twofold higher in patients with A(H1N1) with shock vs those without shock. IL-6 levels were elevated in patients with A(H1N1), indicating systemic inflammation consistent with activation of circulating platelets.
CONCLUSIONS: These findings, derived from a small but documented cohort of patients, demonstrate that platelet activation responses during A(H1N1) are enhanced-exceeding responses in patients with bacterial pneumonia-and provide new evidence that platelets may contribute to inflammatory responses during A(H1N1).
METHODS: We prospectively examined platelet activation and cytokine responses in patients with A(H1N1) (n = 20), matched patients with bacterial pneumonia (n = 15), and nonhospitalized, healthy control subjects (n = 10).
RESULTS: Platelet-monocyte aggregation was higher in patients with A(H1N1) (21.4% ± 4.7%) compared with patients with pneumonia (10.9% ± 3.7%) and control subjects (8.1% ± 4.5%, P < .05). Similarly, PAC-1 (antibody that binds to the active conformation of integrin α(IIb)β(3)) binding to platelets is increased in patients with A(H1N1) (9.5% ± 4.7%) compared with patients with pneumonia (1.0% ± 0.7%) and healthy subjects (0.61% ± 0.15%, P < .10). PAC-1 binding was twofold higher in patients with A(H1N1) with shock vs those without shock. IL-6 levels were elevated in patients with A(H1N1), indicating systemic inflammation consistent with activation of circulating platelets.
CONCLUSIONS: These findings, derived from a small but documented cohort of patients, demonstrate that platelet activation responses during A(H1N1) are enhanced-exceeding responses in patients with bacterial pneumonia-and provide new evidence that platelets may contribute to inflammatory responses during A(H1N1).
Предметные рубрики MeSH
APACHEAdultAnalysis of VarianceCase-Control StudiesChi-Square DistributionComorbidityCritical IllnessDual Specificity Phosphatase 2Enzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansInfluenza A Virus, H1N1 SubtypeInfluenza, HumanInterleukin-6Length of StayMaleMiddle AgedPlatelet ActivationProspective StudiesReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alpha