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ACUTE LUNG INJURY |
1 Lung Research Group, Division of Medicine, University of Bristol, Southmead Hospital, Bristol BS10 5NB, UK
2 Department of Pathology and Microbiology, Homeopathic Hospital Site, University of Bristol, Bristol BS6 6JU, UK
Correspondence to:
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.Millar{at}bristol.ac.uk
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.
Keywords: acute lung injury; vascular endothelial growth factor; polymorphism
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