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Letter
Lack of association between angiotensin converting enzyme gene polymorphism and Korean Behçet’s disease
  1. H K Chang1,
  2. J U Kim2,
  3. S S Lee3,
  4. D H Yoo4
  1. 1Department of Internal Medicine, Dankook University, Cheonan, South Korea
  2. 2Department of Laboratory Medicine, Ulsan University, Kangnung, South Korea
  3. 3Department of Internal Medicine, Chonnam National University Medical School, Gwangju, South Korea
  4. 4Department of Internal Medicine, The Hospital for Rheumatic Diseases, Hanyang University, Seoul, South Korea
  1. Correspondence to:
    Dr H K Chang
    Division of Rheumatology, Department of Internal Medicine, Dankook University, 16-5 Anseo-Dong, Cheonan, Chungcheongnamdo, 330-715, South Korea; hanks22dankook.ac.kr

https://doi.org/10.1136/ard.2003.011007

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    The histological hallmark of Behçet’s disease (BD) is a vasculitis, and endothelial dysfunction has a role in the development of the vascular lesions in BD.1,2 Angiotensin converting enzyme (ACE) plays a part in the renin-angiotensin and kallikrein-kininogen systems by producing angiotensin II from angiotensin I and by inactivating bradykinin. The ACE gene is located on the long arm of chromosome 17, and insertion and deletion (I/D) polymorphism of this gene is strongly related to the levels of circulating ACE: the serum levels of ACE in the DD genotype, homozygote for the deletion allele, are about twice as high as those in the II genotype, homozygote for the insertion allele.3 In addition, the DD genotype is associated with endothelial dysfunction, as the stimulated endothelial or donated nitric oxide response is blunted.4 Moreover, angiotensin II may participate in the vascular pathogenesis …

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    Footnotes

    • This study was supported by the research fund of Dankook University in 2003.