Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure

<p>Abstract</p> <p>Background</p> <p>Exposure to mustard gas frequently results in long-term respiratory complications. However the factors which drive the development and progression of these complications remain unclear. The Renin Angiotensin System (RAS) has been imp...

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Main Authors: Humphries Steve E, Soroush Mohammad, Khoshbaten A, Hopkinson Nicholas S, Kehoe Anthony, Thompson Julian, Hosseini-khalili Ali, Montgomery Hugh, Ghanei Mostafa
Format: Article
Language:English
Published: BMC 2008-08-01
Series:BMC Pulmonary Medicine
Online Access:http://www.biomedcentral.com/1471-2466/8/15
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spelling doaj-7d2ecf218b7d44429289f86e113c74d42020-11-24T21:53:27ZengBMCBMC Pulmonary Medicine1471-24662008-08-01811510.1186/1471-2466-8-15Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposureHumphries Steve ESoroush MohammadKhoshbaten AHopkinson Nicholas SKehoe AnthonyThompson JulianHosseini-khalili AliMontgomery HughGhanei Mostafa<p>Abstract</p> <p>Background</p> <p>Exposure to mustard gas frequently results in long-term respiratory complications. However the factors which drive the development and progression of these complications remain unclear. The Renin Angiotensin System (RAS) has been implicated in lung inflammatory and fibrotic responses. Genetic variation within the gene coding for the Angiotensin Converting Enzyme (ACE), specifically the Insertion/Deletion polymorphism (I/D), is associated with variable levels of ACE and with the severity of several acute and chronic respiratory diseases. We hypothesized that the ACE genotype might influence the severity of late respiratory complications of mustard gas exposure.</p> <p>Methods</p> <p>208 Kurdish patients who had suffered high exposure to mustard gas, as defined by cutaneous lesions at initial assessment, in Sardasht, Iran on June 29 1987, underwent clinical examination, spirometric evaluation and ACE Insertion/Deletion genotyping in September 2005.</p> <p>Results</p> <p>ACE genotype was determined in 207 subjects. As a continuous variable, FEV<sub>1 </sub>% predicted tended to be higher in association with the D allele 68.03 ± 20.5%, 69.4 ± 21.4% and 74.8 ± 20.1% for II, ID and DD genotypes respectively. Median FEV<sub>1 </sub>% predicted was 73 and this was taken as a cut off between groups defined as having better or worse lung function. The ACE DD genotype was overrepresented in the better spirometry group (Chi<sup>2 </sup>4.9 p = 0.03). Increasing age at the time of exposure was associated with reduced FEV<sub>1 </sub>%predicted (p = 0.001), whereas gender was not (p = 0.43).</p> <p>Conclusion</p> <p>The ACE D allele is associated with higher FEV<sub>1 </sub>% predicted when assessed 18 years after high exposure to mustard gas.</p> http://www.biomedcentral.com/1471-2466/8/15
collection DOAJ
language English
format Article
sources DOAJ
author Humphries Steve E
Soroush Mohammad
Khoshbaten A
Hopkinson Nicholas S
Kehoe Anthony
Thompson Julian
Hosseini-khalili Ali
Montgomery Hugh
Ghanei Mostafa
spellingShingle Humphries Steve E
Soroush Mohammad
Khoshbaten A
Hopkinson Nicholas S
Kehoe Anthony
Thompson Julian
Hosseini-khalili Ali
Montgomery Hugh
Ghanei Mostafa
Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
BMC Pulmonary Medicine
author_facet Humphries Steve E
Soroush Mohammad
Khoshbaten A
Hopkinson Nicholas S
Kehoe Anthony
Thompson Julian
Hosseini-khalili Ali
Montgomery Hugh
Ghanei Mostafa
author_sort Humphries Steve E
title Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
title_short Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
title_full Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
title_fullStr Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
title_full_unstemmed Angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
title_sort angiotensin-converting enzyme genotype and late respiratory complications of mustard gas exposure
publisher BMC
series BMC Pulmonary Medicine
issn 1471-2466
publishDate 2008-08-01
description <p>Abstract</p> <p>Background</p> <p>Exposure to mustard gas frequently results in long-term respiratory complications. However the factors which drive the development and progression of these complications remain unclear. The Renin Angiotensin System (RAS) has been implicated in lung inflammatory and fibrotic responses. Genetic variation within the gene coding for the Angiotensin Converting Enzyme (ACE), specifically the Insertion/Deletion polymorphism (I/D), is associated with variable levels of ACE and with the severity of several acute and chronic respiratory diseases. We hypothesized that the ACE genotype might influence the severity of late respiratory complications of mustard gas exposure.</p> <p>Methods</p> <p>208 Kurdish patients who had suffered high exposure to mustard gas, as defined by cutaneous lesions at initial assessment, in Sardasht, Iran on June 29 1987, underwent clinical examination, spirometric evaluation and ACE Insertion/Deletion genotyping in September 2005.</p> <p>Results</p> <p>ACE genotype was determined in 207 subjects. As a continuous variable, FEV<sub>1 </sub>% predicted tended to be higher in association with the D allele 68.03 ± 20.5%, 69.4 ± 21.4% and 74.8 ± 20.1% for II, ID and DD genotypes respectively. Median FEV<sub>1 </sub>% predicted was 73 and this was taken as a cut off between groups defined as having better or worse lung function. The ACE DD genotype was overrepresented in the better spirometry group (Chi<sup>2 </sup>4.9 p = 0.03). Increasing age at the time of exposure was associated with reduced FEV<sub>1 </sub>%predicted (p = 0.001), whereas gender was not (p = 0.43).</p> <p>Conclusion</p> <p>The ACE D allele is associated with higher FEV<sub>1 </sub>% predicted when assessed 18 years after high exposure to mustard gas.</p>
url http://www.biomedcentral.com/1471-2466/8/15
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