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(Chest. 2002;121:85S-86S.)
© 2002 American College of Chest Physicians

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 and Richard G. Wunderink, MD, FCCP

* 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

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-{alpha} 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.

A prospective cohort study of 289 adults with CAP was performed. Genotyping of the ICAM-1 G241R site was done using allele-specific polymerase chain reaction. Outcome measures included mortality, septic shock (SS), ARDS, and respiratory failure (RF). Heterozygotes at the G241R site demonstrated a frequency of 8.3% in the entire study group; no RR homozygotes were detected.

The frequency of the heterozygotes in patients with SS (6.7%) and RF (5.7%) was not different from patients without these complications of CAP. Ten patients in the cohort had ARDS, and 22 patients died; all had homozygotes for the GG phenotype. We conclude that unlike the associations we have reported between tumor necrosis factor-{alpha} polymorphisms and outcome in patients with CAP, the ICAM-1 polymorphism that results in the glycine-to-arginine substitution at position 241 does not appear to play a role in SS, RF, ARDS, or mortality in adults with CAP.


   Footnotes
 
Abbreviations: CAP = community-acquired pneumonia; ICAM = intracellular adhesion molecule; RF = respiratory failure; SS = septic shock

Dr. Quasney is supported in part by the Children’s Foundation of Memphis and by the American Lung Association.





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