Relationship between dimethylarginine dimethylaminohydrolase gene variants and asymmetric dimethylarginine in patients with rheumatoid arthritis

Theodoros Dimitroulas, Aamer Sandoo, James Hodson, Jacqueline Smith, Vasileios F. Panoulas, George D. Kitas

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)
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Abstract

Objective

The aim of our study was to determine whether Dimethylarginine Dimethylaminohydrolase (DDAH) 1 and 2 gene polymorphisms – the main enzyme involved in ADMA degradation – are associated with high Asymmetric Dimethylarginine (ADMA) levels in Rheumatoid Arthritis (RA).

Methods

Serum ADMA levels were measured in 201 individuals with RA [155 females median age 67 (59–73)]. Four tag SNPs in DDAH1 gene and 2 in the DDAH2 gene were genotyped by using the LightCycler™ System. ADMA was initially compared across the genetic variables using one-way ANOVA and then multivariate analysis examined each of the genes after adjustment for parameters of systemic inflammation and insulin resistance, namely erythrocyte sedimentation rate (ESR) and homeostatic model assessment (HOMA), which we have previously shown affect ADMA levels in RA.

Results

No significant relationship between DDAH genetic variables and ADMA levels was established in ANOVA analysis. Multivariate model adjusted for age, HOMA and ESR did not demonstrate any significant association between DDAH variants and ADMA.

Conclusion

The results of our study give no evidence to suggest that increased ADMA levels in RA relate to DDAH genetic polymorphisms. Better understanding of disease-related factors and their interactions with traditional CV risk factors may represent mechanisms responsible for ADMA accumulation in this population.
Original languageEnglish
Pages (from-to)38-44
JournalAtherosclerosis
Volume237
Issue number1
Early online date27 Aug 2014
DOIs
Publication statusPublished - 1 Nov 2014

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