The impact of factor V Leiden and G20210A prothrombin mutations on carotid stenosis in type 2 diabetes mellitus
Journal Title: Αρχεία Ελληνικής Ιατρικής - Year 2010, Vol 27, Issue 4
Abstract
OBJECTIVE Diabetes mellitus (DM) is an independent risk factor for arterial thrombosis. Patients with DM have severe carotid stenosis and increased intima-media thickness (IMT). Factor V (Leiden) and factor II (G20210A prothrombin) mutations are responsible mainly for venous thrombosis, but in some cases for arterial thrombosis also. Studies have concluded that carriers of these thrombophilic mutations present increased carotid stenosis. This is a study of the effect of Leiden and G20210A prothrombin mutations on carotid stenosis and carotid IMT in patients with type 2 diabetes mellitus (T2DM). METHOD A total of 362 patients with T2DM, 145 male and 217 female, mean age 65.8±10 years, from the General Hospital of Kilkis and the "AHEPA" Hospital of Thessaloniki were examined for Leiden and G20210A prothrombin mutation by polymerase chain reaction (PCR). Ultrasonography (US) was used to measure carotid IMT in 55 of the patients: 20 patients with normal genotype, 10 with factor II G20210A mutation, 23 with factor V Leiden mutation, and 2 who were carriers of both mutations. The diabetic patients on whom US was performed had the same risk factors for development of cardiovascular disease. RESULTS Six carriers of the factor II G20210A mutation (50%, p=0.258), 6 carriers of the factor V Leiden mutation (24%, p=0.651) and 6 patients (30%) with the wild genotype had an increased volume of atherosclerosis in the carotid arteries, while 6 carriers of the factor II G20210A mutation (50%), 19 carriers of the factor V Leiden mutation (76%) and 14 patients (70%) with the wild genotype did not have increased carotid atherosclerosis. CONCLUSIONS The factor V Leiden and factor II G20210A mutations do not appear to have a direct impact on carotid stenosis and carotid IMT in patients with T2DM.
Authors and Affiliations
T. FRENGIDIS, A. THEODORIDIS
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