Genetic variation and coronary atherosclerosis in patients with systemic lupus erythematosus

C P Chung1, J F Solus2, A Oeser2

  • 1Departments of Medicine, Vanderbilt University, Nashville, TN, USA c.chung@vanderbilt.edu.

Lupus
|April 5, 2014
PubMed

Insights

Genetic variations may influence coronary artery disease in systemic lupus erythematosus (SLE) patients. Researchers identified potential gene links to coronary atherosclerosis, but further studies are needed for confirmation.

Area of Science:

  • Genetics
  • Cardiovascular Medicine
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) significantly increases mortality due to coronary artery disease (CAD).
  • Traditional cardiovascular risk factors do not fully explain the elevated risk in SLE patients.
  • The role of genetic predisposition in CAD development within SLE is under investigation.

Purpose of the Study:

  • To investigate the hypothesis that genetic variations contribute to coronary atherosclerosis in patients with SLE.
  • To identify specific single-nucleotide polymorphisms (SNPs) associated with coronary artery calcium (CAC) in SLE.

Main Methods:

  • Genotyping of 152 candidate genes related to autoimmune or cardiovascular risk in 125 SLE patients.
  • Detection of coronary artery calcium (CAC) using electron-beam computed tomography.
  • Statistical analysis of SNP genotypes and CAC presence, adjusting for age, sex, and race.

Main Results:

  • Coronary artery calcium (CAC) was detected in 26% of the SLE patients studied.
  • Polymorphisms in 20 candidate genes showed nominal association with CAC presence (p-values 0.001-0.047).
  • No associations remained significant after false discovery rate adjustment, indicating a need for replication.

Conclusions:

  • Genetic variations in genes like ADAM33, ADIPOQ, and IRF5 may be nominally associated with coronary atherosclerosis in SLE.
  • Some identified genes are known SLE susceptibility genes or have been linked to cardiovascular disease in other populations.
  • Replication studies in larger SLE cohorts are essential to validate these findings and clarify the genetic contribution to CAD in SLE.

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