Matthew T Rondina1, BreAnna Brewster2, Colin K Grissom3, Guy A Zimmerman4, Diana H Kastendieck2, Estelle S Harris4, Andrew S Weyrich5. 1. Division of General Internal Medicine, University of Utah School of Medicine, Salt Lake City; Department of Internal Medicine, and the Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City. Electronic address: matthew.rondina@hsc.utah.edu. 2. Department of Internal Medicine, and the Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City. 3. The Division of Pulmonary and Critical Care Medicine, University of Utah School of Medicine, Salt Lake City; The Intermountain Medical Center, Division of Critical Care, Murray, UT. 4. The Division of Pulmonary and Critical Care Medicine, University of Utah School of Medicine, Salt Lake City. 5. The Division of Pulmonary and Critical Care Medicine, University of Utah School of Medicine, Salt Lake City; Department of Internal Medicine, and the Program in Molecular Medicine, University of Utah School of Medicine, Salt Lake City.
Abstract
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).
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).
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