Genetic Variant of the C-reactive Protein Gene and Prevalence of Peripheral Arterial Disease in Patients with Type 2 Diabetes MellitusStavroula Papaoikonomou1*#, Dimitris Tousoulis2#, Nicholas Tentolouris1, Nikolaos Papageorgiou2, Antigoni Miliou2, Emmanuel Androulakis2, Charalambos Antoniades2 and Christodoulos Stefanadis2
- *Corresponding Author:
- Stavroula Papaoikonomou
14 Lefkosias Street, 14123
Likovrisi - Attiki, Greece
Tel: +30 210 2829405, 6932428960
E-mail: [email protected]
Received date December 24, 2014; Accepted date March 24, 2015; Published dateMarch 30, 2015
Citation: Papaoikonomou S, Tousoulis D, Tentolouris N, Papageorgiou N, Miliou A, et al. (2015) Genetic Variant of the C-reactive Protein Gene and Prevalence of Peripheral Arterial Disease in Patients with Type 2 Diabetes Mellitus. J Diabetes Metab 6:529. doi:10.4172/2155-6156.1000529
Copyright: ©2015 Papaoikonomou S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: Diabetes mellitus is strongly associated with inflammatory procedures, obesity and macrovascular complications, while genetic factors are involved in the disease pathogenesis and its complications. The aim of this study was to examine the impact of A3872G polymorphism on C-reactive protein (CRP) gene on the prevalence of peripheral arterial disease (PAD) in Greek Caucasian subjects with type 2 diabetes mellitus (T2DM).
Methods: The study population consisted of 423 patients with T2DM. The A3872G polymorphism was detected by polymerase chain reaction and appropriate restriction enzyme digestion (HpyCH4III). High sensitivity CRP was assayed by particle-enhanced immunonephelometry. PAD was diagnosed using clinical or ultrasonography criteria and/or ankle brachial index <0.9.
Results: The genotype distribution (%) in PAD patients (GG: 48.1, AG: 29.1, AA: 22.8) did not differ significantly compared to non-PAD disease subjects (GG: 53.8, AG: 26.7, AA: 19.5), (P=0.258). After adjustment for classical risk factors, carriers of “A” allele (AG+AA) compared with GG homozygotes had higher odds (OR) for PAD, (AG+AA): 82 (40.0) vs. GG: 76 (34.2), (OR 1.622, 95% confidence intervals 1.029-2.536, P=0.037).
Conclusions: In Caucasian subjects with T2DM, the GG homozygotes of the A3872G genetic polymorphism on the C-reactive protein gene may be protected from the risk of peripheral arterial disease compared to carriers of the “A” allele. These results indicate a potential genetic role of inflammation in atherosclerosis in patients with type 2 diabetes mellitus.