The present study was the first study in Iran to evaluate the impact of prothrombin gene mutation (G20210A) as an independent risk factor in incidence of ischemic stroke. After reporting the cause of prothrombin gene mutation (G20210A) in 1994,9
several studies examined its effect on coagulation disorders. Considering the known effect of this mutation on developing venous thrombosis, several studies were designed to evaluate the prevalence of it in various races and communities including Iran. The next step was investigating the possible role of this mutation in arterial vascular events. Several case controlstudies assessed the existence of prothrombin gene mutation (G20210A) in patients with myocardial infarction and ischemic stroke and its comparison with control group.10
In the present study, exclusion of patients with classical risk factors for stroke, made it more possible to judge about the pathogenicity of this mutation. In addition, since there was no similar study for the prevalence of this factor in Esfahan Province, this case-control study provided an estimation of it in healthy population of this province. The frequency of 1.85% which was obtained in our study was in accordance with studies which discussed the higher prevalence of this mutation in Caucasians; the theory which says this mutation has been derived from the Middle East, and then spread to Western and North Europe.14
According to studies in different nations, variable prevalence has been reported for this mutation. Accordingly, the prevalence of this gene is varied from 3.1% in Sweden,13
1.8% in Germany to 0.5% in Serbia.16
This mutation has a low prevalence in East Asia such as Thailand, China, Korea and Japan and also Africa.16
The obtained relative frequency in this study in comparison with its high prevalence in Turkey (2.6%) in North West of Iran in the one hand, and its near-zero frequency in east Asian courtiers and east parts of Iran on the other hand, placed Iran in the middle of an intermediate region with high prevalence and areas with low prevalence of this mutation.
Prothrombin gene mutation (G20210A) were not found among the 22 studied samples. Therefore, to some extent this study can be in accordance with many studies which mentioned that existence of prothrombin gene mutation (G20210A) has no role in increased arterial thrombosis risk factor.17
However, some studies even have found a strong correlation between the existence of prothrombin gene mutation (G20210A) and incidence of myocardial infarction.
Despite the known effect of prothrombin gene mutation (G20210A) on incidence of venous thrombosis, this mutation is considered as a relatively weaker risk factor in incidence of thrombotic events. The present study provided data that the pathogenicity of this factor could be analyzed. A case control study20
which was done on American female youths with myocardial infarction made a 25-fold risk for them who were prothrombin gene mutation (G20210A) carrier in addition with smoking. The women, who had this factor but did not smoke, had no higher risk compared to others. Not finding the prothrombin gene mutation (G20210A) in our selected patients made us realized that this mutation perhaps can increase the risk of stroke in terms of hypertension, diabetes mellitus or other stroke risk factors and cannot be a potential risk by itself; a finding which was confirmed by other studies.20