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LSC 2013 abstract - Hypoxia-inducible factor 1 alpha polymorphisms in relation to pulmonary involvement in systemic sclerosis

Harpreet Lota, Carmel Stock, Hiroe Sato, Carmen Fonseca, Athol Wells, Christopher Denton, David Abraham, Gisela Lindahl, Elisabetta Renzoni
European Respiratory Journal 2013 42: 3522; DOI:
Harpreet Lota
1Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom
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Carmel Stock
1Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom
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Hiroe Sato
1Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom
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Carmen Fonseca
2Centre for Rheumatology, Royal Free Hospital, London, United Kingdom
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Athol Wells
1Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom
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Christopher Denton
2Centre for Rheumatology, Royal Free Hospital, London, United Kingdom
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David Abraham
2Centre for Rheumatology, Royal Free Hospital, London, United Kingdom
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Gisela Lindahl
1Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom
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Elisabetta Renzoni
1Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom
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Abstract

Introduction: Transcription factor hypoxia-inducible factor 1 (HIF1) upregulates the expression of angiogenic genes including vascular endothelial growth factor. Systemic sclerosis (SSc) is a multisystem disease characterised by organ fibrosis and widespread vasculopathy. We assessed the association of two transcriptionally active, single nucleotide polymorphisms (SNPs) of the hypoxia-inducible factor 1 alpha gene (HIF1A) in SSc.

Methods: Using a case-control study design, HIF1A SNPs (rs11549465 C/T, rs12434438 A/G) were genotyped in SSc patients (n=426) and UK controls from the Wellcome Trust Case-Control Consortium (n=5564 and 5659). The SSc cohort was subdivided according to the presence or absence of pulmonary fibrosis (PF) (n=227 v. 199), pulmonary hypertension (PH) on echocardiography (n=17 v. 129) and autoantibody subsets; anti-topoisomerase I antibodies (n=108) and anti-centromere antibodies (n=105).

Results: Genotype distribution in all groups conformed to Hardy-Weinberg equilibrium. There were no significant differences in genotype or allele frequencies between SSc and controls (SSc: CC:82.1%, CT:16.7%, TT:1.2% v. controls: CC:81.3%, CT:17.8%, TT:0.9% and SSc: AA:63.9%, AG:32.6%, GG:3.5% v. controls: AA:63.4%, AG:32.5%, GG:4.1%). On subgroup analysis, no significant differences were observed according to PF, autoantibodies, or in the group with available echocardiography (n=146), according to PH.

Conclusion: An association was not detected between HIF1A SNPs and SSc. Due to limited power in the PH subgroup, an association with pulmonary vascular involvement cannot be excluded and requires further evaluation and longitudinal analysis.

  • © 2013 ERS
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LSC 2013 abstract - Hypoxia-inducible factor 1 alpha polymorphisms in relation to pulmonary involvement in systemic sclerosis
Harpreet Lota, Carmel Stock, Hiroe Sato, Carmen Fonseca, Athol Wells, Christopher Denton, David Abraham, Gisela Lindahl, Elisabetta Renzoni
European Respiratory Journal Sep 2013, 42 (Suppl 57) 3522;

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LSC 2013 abstract - Hypoxia-inducible factor 1 alpha polymorphisms in relation to pulmonary involvement in systemic sclerosis
Harpreet Lota, Carmel Stock, Hiroe Sato, Carmen Fonseca, Athol Wells, Christopher Denton, David Abraham, Gisela Lindahl, Elisabetta Renzoni
European Respiratory Journal Sep 2013, 42 (Suppl 57) 3522;
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