Increased coagulation factor levels have been demonstrated to be a risk factor for venous thromboembolism in patients of Caucasian origin. Coagulation factors, hereditary thrombophilia, and ABO blood group were evaluated for venous thrombosis risk in a heterogeneous Brazilian population consisting of 122 women and 53 men, with a median age of 36 years (range 13-63), matched to a control group by age, sex, and ethnicity. Increased levels of factor VIII (odds ratio [OR], 3.1; 95% confidence interval [CI], 1.6-6.0), von Willebrand factor (OR, 2.8; 95% CI, 1.4-5.4), non-O blood group (OR, 2.1; 95% CI, 1.3-3.4), and thrombophilia (OR, 3.4; 95% CI, 1.6-7.1) emerged as independent risk factors for venous thromboembolism. The interaction of high levels of factor IX and factor XI with other independent variables increased the potential for thrombosis synergistically. Therefore, the ability of identifying underlying thrombophilia risk factors in our population was enhanced by the inclusion of these factors in the prothrombotic laboratory workup.

Thrombosis is a major clinical feature of the antiphospholipid syndrome. Interactions between genetic and acquired factors could contribute to thrombosis development. In this study, we evaluated 40 patients with antiphospholipid syndrome and thrombosis, 31 primary and nine secondary to systemic lupus erythemathosus, to estimate the carrier rates of factor V Leiden, 20210A --> G prothrombin variant and 677C --> T in the MTHFR gene. Protein C, protein S and antithrombin were measured in 30 patients, with a median of 100.66 +/- 23.86, 93.57 +/- 36.44 and 98.8 +/- 5.67%, respectively. None of the patients were deficient on these natural anticoagulants. No significant variation was found between the patient group and the controls, regarding the prevalence of homozygotes for the mutated 677T allele (2.5 versus 5.4%), or heterozygotes for factor V Leiden (0 versus 0.7%). Despite the fact that these mutations are relatively common in Brazilian thrombophilic patients, its low prevalence in this cohort of patients suggest that these genetic alterations are not risk factors for thrombosis in antiphospholipid syndrome. The prevalence of the mutated allele 20210A of the prothrombin gene was higher in patients when compared with controls (5 versus 0.7%; P = 0.01), suggesting that prothrombin variant could increase the risk of thrombosis in patients with antiphospholipid syndrome.

The home prothrombin time/international normalized ratio (PT/INR) self-management could be convenient for patients, enhancing treatment compliance and improving the quality of the oral anticoagulation. However, patient self-management (PSM) of oral anticoagulation may not be feasible for up to half of the patients due to cognitive or educational issues. In the present study, we aimed to evaluate the feasibility of a PSM program in a public health medical center that provides care for low-income patients. We also aimed to determine the accuracy of individual point-of-care devices (CoaguChek XS(®)) during long-term of home manipulation. Patients' time-in-therapeutic range (TTR) and perception of quality of life, were evaluated at scheduled study-visits to the center. Additionally, the accuracy of individual CoaguChek XS(®) was evaluated in comparison to the standard automated coagulometer at scheduled study-visits to the center. Twenty-five patients were included in the PSM program. The median TTR of patients was 75 % before inclusion, 72 % at 3 months, 75 % at 6 months and 100 % at 12 months after the beginning of self-management (P = 0.14).The median DASS scores were 64, 63, 61.5 and 71.5 before inclusion and at 3, 6 and 12 months, respectively (P = 0.09). One hundred paired INR values were obtained. Correlation between INR values delivered by individual CoaguChek XS(®) and the automated coagulometer was 94 % and the mean result bias was 0.07 INR units. The coefficient of correlation and the mean bias between methods was stable during 24 months of follow-up. The present study suggests that PSM is feasible for patients treated in the public health system and that the results delivered by CoaguChek XS(®) have long-term reliability.

5064 Introduction Livedoid vasculopathy is a rare skin disease caused by the extensive formation of microthrombi in dermis vessels, which leads to infarction and ulceration of the epidermis. The pathogenesis of livedoid vasculopathy is unknown, and hypercoagulation states have been implicated. Moreover, success using anticoagulation was reported in some patients. We hypothesized that decreased levels of ADAMTS13 activity and Von Willebrand factor (vWF) levels could contribute to the pathogenesis of local thrombus formation in livedoid vasculopathy. Objective Here we evaluated the levels of ADAMTS13 activity and vWF in patients with livedoid vasculopathy. Patients and methods Fourteen patients (93% female) with livedoid vasculopathy, median age of 41.5 years (22 - 48) were included in the study. All patients were evaluated for the presence of classical acquired and hereditary thrombophilia markers. In addition, vWF antigen levels (Elisa) and activity (collagen binding assays), as well as ADAMTS13 activity (evaluated by residual collagen binding) were evaluated. Results nine patients (64%) were carriers of the MTHFR C677T mutation (6 heterozygous and 3 homozygous); 1 patient was a carrier of factor V Leiden mutation, and 1 patient was a carrier of the FII G20210A mutation. None of the patients presented deficiency of antithrombin, protein C or S, and antiphospholipid antibodies were not identified in our study population. ADAMTS13 and VWF activities were normal in all patients. Median vWF antigen was 120.5U/dl (reference value of 40.0 - 232.0%), and vWF activity was 102.3% (reference value of 45.5 - 203.7%). ADAMTS13 activity was 138.9% (reference value of 56.0 - 227.2 %). Two patients had a history of thromboembolic diseases: one patient with 2 strokes and one patient with central retinal artery occlusion. Conclusion We show here that ADAMTS13 activity and vWF levels are not altered in patients with livedoid vasculopathy. The MTHFR C677T mutation is frequent in patients with livedoid vasculopathy but quantification of homocysteine levels is necessary to consider any relationship with this disease. Disclosures No relevant conflicts of interest to declare.

Our results demonstrate that POC devices present good correlation with standard laboratory methods for PT determination in supra-therapeutic INRs and that differences in clinical management do not support the need for systematic confirmation of these results in nonbleeding patients.