Polymorphisms in the angiotensin I converting enzyme (ACE) gene are associated with multiple sclerosis risk and response to Interferon-β treatment

Int Immunopharmacol. 2018 Nov:64:275-279. doi: 10.1016/j.intimp.2018.09.014. Epub 2018 Sep 13.

Abstract

Background: Multiple sclerosis (MS) as a chronic autoimmune demyelinating disorder of the central nervous system has been associated with numerous genetic and environmental factors among them are functional variants within the angiotensin I converting enzyme (ACE) gene.

Methods: In the present study, we genotyped the rs4359 (C/T) and rs1799752 (Insertion (I)/Deletion (D)) of this gene in 391 MS patients and 380 age- and sex-matched controls.

Results: We found significant overrepresentation of the I allele of the rs1799752 in MS patients compared with healthy subjects (Adjusted P value = 0.03, OR (95% CI) = 1.28 (1.05-1.57). The same allele was associated with MS risk in co-dominant and dominant models (Adjusted P values of 0.007 and 0.002 respectively). The allele and genotype frequencies of the rs4359 were not significantly different between cases and controls. Moreover, the I allele of the rs1799752 was significantly overrepresented in MS patients who were irresponsive to IFN-β compared with healthy subjects (Adjusted P value = 0.04, OR (95% CI) = 1.57 (1.08-2.29)). The same allele was associated with irresponsiveness to IFN-β in dominant model (Adjusted P value = 0.02, OR (95% CI) = 2.32 (1.22-4.42)).

Conclusion: The present study provides further evidences for the role of ACE in MS risk or response of patients to IFN-β treatment.

Keywords: Angiotensin I converting enzyme; Multiple sclerosis; Polymorphism.

MeSH terms

  • Adult
  • Alleles
  • Female
  • Haplotypes
  • Humans
  • Interferon-beta / therapeutic use*
  • Male
  • Middle Aged
  • Multiple Sclerosis / drug therapy
  • Multiple Sclerosis / etiology*
  • Multiple Sclerosis / genetics
  • Peptidyl-Dipeptidase A / genetics*
  • Peptidyl-Dipeptidase A / physiology
  • Polymorphism, Genetic*
  • Risk

Substances

  • Interferon-beta
  • Peptidyl-Dipeptidase A