Giuseppe
Emeritus
[Source: Chest, full text: (LINK). Abstract, edited.]
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In Vivo Platelet Activation in Critically Ill Patients With Primary 2009 Influenza A(H1N1)
Matthew T. Rondina, MD, BreAnna Brewster, Colin K. Grissom, MD, FCCP, Guy A. Zimmerman, MD, Diana H. Kastendieck, BA, Estelle S. Harris, MD, FCCP and Andrew S. Weyrich, PhD
Author Affiliations: From the Division of General Internal Medicine (Dr Rondina) and the Division of Pulmonary and Critical Care Medicine (Drs Grissom, Zimmerman, Harris, and Weyrich), Department of Internal Medicine, and the Program in Molecular Medicine (Drs Rondina and Weyrich and Mss Brewster and Kastendieck), University of Utah School of Medicine, Salt Lake City; and the Intermountain Medical Center (Dr Grissom), Division of Critical Care, Murray, UT.
Correspondence to: Matthew T. Rondina, MD, University of Utah, Department of Internal Medicine, 50 N Medical Dr, Room 4B120, Salt Lake City, UT 84132; e-mail: matthew.rondina@hsc.utah.edu
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<SUB>IIb</SUB>β<SUB>3</SUB>) 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).
Footnotes
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.
Funding/Support: This work was supported by the National Institutes of Health [Grants HL091754, HL066277, and K23HL092161] and the National Center for Research Resources public health service [Grant ULI-RRO25764].
Abbreviations: A(H1N1), 2009 influenza A(H1N1) - ALI, acute lung injury - APACHE, Acute Physiology and Chronic Health Evaluation - FITC, fluorescein isothiocyanate - PAC-1, antibody that binds to the active conformation of integrin α<SUB>IIb</SUB>β<SUB>3</SUB> ? PMA, platelet-monocyte aggregate ? SSC, side scatter - TRAP, thrombin-receptor activating peptide - TNF-α, tumor necrosis factor-α
Received November 9, 2011. Accepted February 4, 2012. ? 2012 American College of Chest Physicians
-Matthew T. Rondina, MD, BreAnna Brewster, Colin K. Grissom, MD, FCCP, Guy A. Zimmerman, MD, Diana H. Kastendieck, BA, Estelle S. Harris, MD, FCCP and Andrew S. Weyrich, PhD
Author Affiliations: From the Division of General Internal Medicine (Dr Rondina) and the Division of Pulmonary and Critical Care Medicine (Drs Grissom, Zimmerman, Harris, and Weyrich), Department of Internal Medicine, and the Program in Molecular Medicine (Drs Rondina and Weyrich and Mss Brewster and Kastendieck), University of Utah School of Medicine, Salt Lake City; and the Intermountain Medical Center (Dr Grissom), Division of Critical Care, Murray, UT.
Correspondence to: Matthew T. Rondina, MD, University of Utah, Department of Internal Medicine, 50 N Medical Dr, Room 4B120, Salt Lake City, UT 84132; e-mail: matthew.rondina@hsc.utah.edu
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<SUB>IIb</SUB>β<SUB>3</SUB>) 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).
Footnotes
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.
Funding/Support: This work was supported by the National Institutes of Health [Grants HL091754, HL066277, and K23HL092161] and the National Center for Research Resources public health service [Grant ULI-RRO25764].
Abbreviations: A(H1N1), 2009 influenza A(H1N1) - ALI, acute lung injury - APACHE, Acute Physiology and Chronic Health Evaluation - FITC, fluorescein isothiocyanate - PAC-1, antibody that binds to the active conformation of integrin α<SUB>IIb</SUB>β<SUB>3</SUB> ? PMA, platelet-monocyte aggregate ? SSC, side scatter - TRAP, thrombin-receptor activating peptide - TNF-α, tumor necrosis factor-α
Received November 9, 2011. Accepted February 4, 2012. ? 2012 American College of Chest Physicians
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