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Vascular endothelial growth factor gene polymorphism and acute respiratory distress syndrome
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  1. A R L Medford1,
  2. L J Keen2,
  3. J L Bidwell2,
  4. A B Millar1
  1. 1Lung Research Group, Division of Medicine, University of Bristol, Southmead Hospital, Bristol BS10 5NB, UK
  2. 2Department of Pathology and Microbiology, Homeopathic Hospital Site, University of Bristol, Bristol BS6 6JU, UK
  1. Correspondence to:
    Dr A B Millar
    Lung Research Group, Department of Clinical Science at North Bristol, University of Bristol, Southmead Hospital, Westbury-on-Trym, Bristol BS10 5NB, UK; Ann.Millarbristol.ac.uk

Abstract

Background: Non-cardiogenic pulmonary oedema is a characteristic feature of the acute respiratory distress syndrome (ARDS). The properties of vascular endothelial growth factor (VEGF) as a potent vascular permogen and mitogen have led to investigation of its potential role in this condition. Lower VEGF plasma levels have been linked to the presence of the T allele in the +936 CT polymorphism. We hypothesised that the presence of the T allele would be associated with the development and severity of ARDS.

Methods: A cohort of 137 normal subjects, 117 ventilated patients with ARDS, and 103 “at risk” of ARDS were genotyped for the VEGF+936 CT polymorphism. The severity of physiological disturbance and mortality was determined in the ventilated cohorts.

Results: The CT and TT genotype frequencies were increased in ARDS patients compared with both normal subjects (OR 2.01, 95% CI 1.13 to 3.58, p = 0.02) and those “at risk” (OR 2.05, 95% CI 1.02 to 2.20, p = 0.03). In patients with ARDS but not those “at risk”, CT and TT genotypes were associated with a higher mean APACHE III score (80.9 (4.3) v 69.3 (2.9), p<0.05).

Conclusion: These data support a role for VEGF in the pathogenesis of ARDS and its associated physiological derangement.

  • acute lung injury
  • vascular endothelial growth factor
  • polymorphism

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Footnotes

  • This study was supported by a grant from the British Lung Foundation.

  • The authors have no competing interests.

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