Angiotensin-converting enzyme genotype may predict survival following major trauma. Issue 11 (27th October 2008)

• Record Type: Journal Article
• Authors: Kehoe, A D; Eleftheriou, K I; Heron, M; Coats, T J; Montgomery, H E
• Is Part Of: Emergency medicine journal. Volume 25:Issue 11(2008)
• Page Start: 759
• Page End: 761
• Publication Date: 2008-10-27
• Subjects: Emergency medicine -- Periodicals; 616.02505
• DOI: 10.1136/emj.2006.045336
• Languages: English
• ISSNs: 1472-0205

Abstract

Abstract : Background: As a key component of the endocrine renin-angiotensin system (RAS), angiotensin-converting enzyme (ACE) regulates circulatory homeostasis. Meanwhile, the local RAS influences tissue growth, inflammatory and metabolic responses. The absence (deletion, D) rather than the presence (insertion, I) of a 287 base pair fragment in the ACE gene is associated with higher circulating and tissue ACE activity, with excess mortality in critical illness (including adult acute respiratory distress syndrome and paediatric meningococcal infection) and with worse functional outcome from traumatic brain injury. Objective: To determine if the ACE genotype is associated with mortality following major trauma. Methods: 41 subjects with major trauma admitted to the Royal London Hospital over a 2-year period via the Helicopter Emergency Medical Service were enrolled. ACE genotype was available in 36. Injury Severity Score (ISS), Revised Trauma Score (RTS), age, sex and outcome data were recorded for each. ACE genotype was determined from leucocyte DNA using well described techniques. Results: The presence of one or more D alleles was associated with a mortality of 36.4% compared with 7.1% for II alleles (p = 0.048). Age (p = 0.044) also predicted mortality whereas RTS (p = 0.08) and ISS (p = 0.46) did not. ACE genotype was significantly associated with RTS but not age or ISS. Conclusion: The ACE D allele may be associated with mortality from major trauma. Replication of these findings in larger studies may aid definition of high-risk subgroups that would benefit from early intensive management. New therapeutic targets might also be suggested.