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- Matthew T Rondina, BreAnna Brewster, Colin K Grissom, Guy A Zimmerman, Diana H Kastendieck, Estelle S Harris, and Andrew S Weyrich.
- Division of General Internal Medicine, University of Utah, Salt Lake City, UT 84132, USA. matthew.rondina@hsc.utah.edu
- Chest. 2012 Jun 1;141(6):1490-5.
BackgroundChanges in platelet reactivity during 2009 influenza A(H1N1) (A[H1N1]) have not been characterized.MethodsWe 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).ResultsPlatelet-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.ConclusionsThese 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).
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