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Intracellular Adhesion Molecule Gly241Arg Polymorphism Has No Impact on ARDS or Septic Shock in Community-Acquired Pneumonia*

Michael W. Quasney, MD, PhD; Grant W. Waterer, MBBS, FCCP; Mary K. Dahmer, PhD; Dawn Turner, MD; Qing Zhang, BS; Rita M. Cantor, PhD; Richard G. Wunderink, MD, FCCP
Author and Funding Information

*From the Departments of Pediatrics and Molecular Sciences, Crippled Children’s Foundation Research Center, University of Tennessee; and Methodist LeBonheur Healthcare Foundation, Memphis, TN.

Correspondence to: Michael W. Quasney, MD, PhD, College of Medicine, Department of Pediatrics, Crippled Children’s Foundation Research Center, 50 North Dunlap, Room 301, Memphis, TN 38103



Chest. 2002;121(3_suppl):85S-86S. doi:10.1378/chest.121.3_suppl.85S
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The clinical presentation and outcome following inflammatory stimuli are determined in part by the type and degree of the stimulus as well as host factors. We have previously demonstrated associations between genetic polymorphisms in the regulatory regions of tumor necrosis factor-α with both the severity of community-acquired pneumonia (CAP) and the type of clinical presentation. A recent polymorphism has been described in the gene coding for intracellular adhesion molecule (ICAM) type 1, which alters a glycine at position 241 to an arginine. This polymorphism is associated with polymyalgia rheumatica and giant-cell arteritis, common inflammatory diseases involving the synovium and extracranial branches of the aorta. Both of these disorders have elevated levels of ICAM-1, and it is hypothesized that the G241R mutation might allow for more effective binding of ICAM-1 to Mac-1, thereby enhancing the inflammatory response. We hypothesized that this mutation may be involved in some of the complications of CAP in adults.

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