Angiotensin-converting enzyme gene polymorphism in Kuwaiti patients with systemic lupus erythematosus

Clin Exp Rheumatol. 2007 May-Jun;25(3):437-42.

Abstract

Objective: To investigate the frequency of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism genotypes in patients with systemic lupus erythematosus (SLE), and to study the correlation between I/D polymorphism of the ACE gene and the clinical manifestations of SLE, especially vascular involvement, lupus nephritis and disease severity.

Methods: The frequency of ACE gene I/D polymorphism genotypes was determined in 92 patients with SLE from Kuwait, and compared to that in 100 ethnically matched healthy controls using the polymerase chain reaction.

Results: The distribution of ACE I/D polymorphism and allele frequencies in SLE patients was not significantly different from controls. Further analyses of SLE patients showed that there was a significant association between DD genotype and Raynaud's phenomenon (p=0.008, odd ratio=5.4, 95% confidence interval: 1.6-18.6). However, there was no significant association between the ACE genotype and lupus nephritis or disease severity.

Conclusion: No difference was found between the distribution of the ACE genotype in SLE patients and the general pop-ulation in Kuwait. However, the presence of the DD genotype may confer susceptibility to the development of vascular morbidity.

MeSH terms

  • Adult
  • Case-Control Studies
  • Female
  • Gene Expression Regulation, Enzymologic
  • Gene Frequency
  • Genetic Predisposition to Disease / ethnology
  • Genetic Predisposition to Disease / genetics
  • Genotype
  • Humans
  • Kuwait
  • Lupus Erythematosus, Systemic / ethnology
  • Lupus Erythematosus, Systemic / genetics*
  • Lupus Nephritis / ethnology
  • Lupus Nephritis / genetics
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Raynaud Disease / ethnology
  • Raynaud Disease / genetics
  • Severity of Illness Index

Substances

  • Peptidyl-Dipeptidase A