Background: Thromboembolic disease (TED) represents one of many factors of morbitity and mortality in THE CCNA2 BURKHA. FV Leiden G1691A-FVL and FII G20210A-PTM and?to assess ?the ?variations between?venous arterial and combined thrombotic events. Tests ?for polymorphism MTHFR C677T and? antithrombin ?proteins ?C ?and ?proteins? S was performed also. Correlations with? dyslipidemia cigarette smoking weight problems homocysteine and antiphospholipid antibodies had been made. Strategies: 515 individuals with unprovoked TED 263 men median age group 44 years had been studied. Patients had been split into three organizations: 258 with venous thrombosis (group A) 239 with arterial (group B) and 18 with combined shows (group C). All individuals were interviewed regarding genealogy of TED origin dyslipidemia and cigarette smoking. Body mass index (BMI) have been calculated. Molecular assessment from the FVL MTHFR and PTM C677T was performed. Antithrombin proteins C proteins S APCR homocysteine antiphospholipid antibodies and lipid profile had been also measured. Outcomes: The populace researched was homogenous among three organizations as regards age group (p=0.943) lipid profile (p=0.271) BMI (p=0.506) homocysteine (p=0.177) antiphospholipid antibodies (p=0.576) and positive genealogy (p=0.099). There is no difference in MKT 077 the prevalence of FVL between venous and arterial disease (p=0.440). Significant relationship of PTM with venous TED was discovered (p=0.001). The amount of negative and positive for MTHFR shown statistically factor with a support in arterial disease (p=0.05). Moreover a 2-fold increase in the risk of venous thrombosis in FVL positive patients (odds ratio: 2.153) and a positive correlation of homocysteine levels with MTHFR C677T (p<0.001) was found. Conclusions: Correlation of PTM MKT 077 with venous thrombosis was established. Analysis showed no difference in prevalence of FVL between venous and arterial thrombosis indicating that FVL might be a MKT 077 predisposing factor for arterial disease. A MKT 077 significant increase in MTHFR C677T prevalence in arterial disease was found. In conclusion young patients with unprovoked arterial disease should undergo evaluation for thrombophilic genes. Identification of these mutations is important in the overall assessment and management of patients at high risk. Findings will influence the decisions of stratified approaches for antithrombotic therapy either primary or secondary thromboprophylaxis the duration of therapy the potential for avoiding clinical thrombosis by risk factor modification and the genetic counselling of family members. However further studies are needed to clarify the nature of the association regarding venous and arterial thrombotic events. Keywords: thrombophilic mutations unprovoked thromboembolic disease arterial thromboembolic disease venous thromboembolic disease Introduction Thromboembolic disease (TED) is multifactorial and represents one of the major causes of morbitity and mortality in developed countries. Thrombosis can occur in the arterial or the venous circulation and has a major medical impact. The most frequent clinical manifestations include either pulmonary embolism and/or deep venous thrombosis (venous TED) or acute coronary syndromes and ischemic cerebrovascular disease (arterial TED) together the leading causes of death in Western World1 2 Thrombophilia is a hypercoagulable state predisposing to thrombosis3-6. Thrombosis is a multifactorial disease resulting from the dynamic interaction MKT 077 between genetic and acquired risk factors1. Despite considerable progress in identifying important genetic risk factors underlying predisposition to venous thrombosis the genetic factors contributing to the risk for arterial thrombosis remain largely unknown. Although inherited thrombophilia’s predominant clinical manifestation is venous thrombosis its contribution to arterial thrombosis still remains controversial7. The pathogenic changes that occur in the blood vessel wall and in the blood itself resulting in thrombosis are not fully understood. Venous and arterial thrombotic disorders have traditionally been considered MKT 077 as separate pathophysiological entities partly as a result of the.