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Rheumatology Advance Access originally published online on January 30, 2007
Rheumatology 2007 46(5):772-775; doi:10.1093/rheumatology/kel433
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Angiotensin-converting enzyme I/D polymorphism and macrovascular disease in systemic sclerosis

F. Bartoli1, C. Angotti1, C. Fatini2, M. L. Conforti1, S. Guiducci1, J. Blagojevic1, D. Melchiorre1, G. Fiori1, S. Generini1, N. Damjanov1,3, S. Rednic1,4, A. Pignone5, S. Castellani6, R. Abbate2 and M. Matucci Cerinic1

1Department of Medicine and Surgery, Division of Medicine I and Rheumatology, 2Department of Medical and Surgical Critical Care, Atherothrombotic Disease Unit, University of Florence, Florence, Italy, 3Institute of Rheumatology, University of Belgrade, Belgrade, Serbia, 4Department of Medicine, Division of Rheumatology, University of Cluj Napoca, Romania, 5Department of Medicine & Surgery, Division on Medicine II and 6Department of Medical and Surgical Critical Care, Section of Angiology, University of Florence, Florence, Italy.

Correspondence to: M. M. Cerinic, Department of Medicine Section of Rheumatology, Villa Monna Tessa, Viale Pieraccini 18, 50122 Firenze, Italy. E-mail: cerinic{at}unifi.it


   Abstract

Objective. Systemic sclerosis (SSc) is characterized by microvascular and macrovascular alterations. The D allele of the ACE I/D polymorphism is known to be associated with an increased incidence of atherosclerosis and has been recently proposed as associated with increased risk of SSc. This study evaluates the relationship between intima-media thickness (IMT), ankle-brachial pressure measurements (ABPI) and ACE I/D polymorphism in SSc patients.

Methods. According to the presence of ACE D allele (analysed by PCR), 53 SSc patients (47 females and 6 males; median age was 60.4 ± 10.68 yrs; range 40–75 yrs) were divided in carriers of the D allele (DD + ID) (n = 46) and carriers of the I allele (II) (n = 7). In these patients, IMT and ABPI [calculated as the posterior tibial artery pressure (mmHg) divided by the brachial pressure] were obtained. Forty-three healthy controls (40 women and 13 men; median age 56.3 ± 10.23; range 40–70 yrs) of the same ethnicity were recruited.

Results. SSc patients had IMT significantly higher than controls (0.85 ± 0.03 vs 0. 68 ± 0.01; P < 0.03). No significant differences (P > 0.3) in ABPI values between patients (1.018 ± 0.10) and controls (1.091 ± 0.11) were found. SSc patients with ACE DD and ID genotype showed an IMT significantly greater (0.89 ± 0.03) than those carrying the II genotype (0.61 ± 0.01) (P < 0.04). ABPI was not different among ACE gene genotypes.

Conclusion. Our findings confirm an increased prevalence of macrovascular disease in SSc patients and show that IMT is greater in patients carrying the ACE DD and ID genotype in comparison with II homozygotes. This suggests that, in SSc, the presence of ACE D allele may predispose to an involvement of the macrovascular system.

KEY WORDS: Systemic sclerosis, Macrovascular disease, ACE polymorphism, Intima media thickness

Submitted 27 June 2006; revised version accepted 5 December 2006.
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