Monitoring anticoagulant therapy with vitamin K antagonists in patients with antiphospholipid syndrome.

Because of the possible interference of antiphospholipid antibodies (APL) with the phospholipid component of thromboplastin reagents, concerns have been raised about the validity of international normalized ratio (INR) testing to monitor anticoagulant therapy with vitamin K antagonists in patients with antiphospholipid syndrome (APS). To investigate the reliability of the INR, we determined the INR using various prothrombin time (PT) assays and compared the results with those of a chromogenic factor X (CFX) assay. The study cohort consisted of 40 APS patients and 100 APL-negative patients who were on anticoagulant therapy for reasons other than APS. The agreement (i.e. the percentage of patients with a difference ≤0.5 INR units) between the PT-derived INR and CFX-derived INR equivalents was only moderate in both patient groups. The best agreement with CFX-derived INR equivalents was observed for the Thromborel S reagent in APS patients (69.1 %) and for Neoplastin Plus in APL-negative patients (72.0 %). Regarding the results for the point-of-care system CoaguChek XS, an agreement between the INR and the CFX-derived INR equivalent was less frequently observed in the APS patients (55.6 vs. 67.8 %; p = 0.050). When considering all 3058 pairs of INR tests within the international sensitivity index (ISI)-calibrated range of 1.5 to 4.5 s, we did not observe a higher variability of INR values in either the APS patient group or the subgroup of APS patients positive for lupus coagulants compared with the APL-negative controls. In conclusion, monitoring vitamin K antagonists (VKA) therapy with laboratory INR measurements seems to be suitable for the majority of APS patients.

Prevalence of thrombophilia according to age at the first manifestation of venous thromboembolism: results from the MAISTHRO registry.

Thrombophilia is a well-established risk factor for a venous thromboembolic event (VTE), and it has been proposed that hereditary thrombophilia may substantially contribute to the development of VTE in young patients. We aimed to analyse the prevalence of thrombophilia with special regard to the age of VTE manifestation. The study cohort consisted of 1490 patients (58% females) with a median age 43 years at the time of their first VTE. At least one thrombophilic disorder was identified in 50·1% of patients. The probability of detecting a hereditary thrombophilia declined significantly with advancing age (from 49·3% in patients aged 20 years and younger to 21·9% in patients over the age of 70 years; P < 0·001). This may be primarily attributed to the decreasing frequencies of the F5 R506Q (factor V Leiden) mutation and deficiencies of protein C or protein S with older age at the time of the initial VTE event. Moreover, thrombophilia was more prevalent in unprovoked compared with risk-associated VTE (57·7% vs. 47·7%; P = 0·001). The decline in the prevalence of hereditary thrombophilia with older ages supports the use of a selected thrombophilia screening strategy dependent on age and the presence or absence of additional VTE risk factors.

Prevalence of established risk factors for venous thromboembolism according to age.

OBJECTIVE: To date, the factors that contribute to the rise in venous thromboembolism (VTE) risk observed with higher ages remain unknown. Therefore, the aim of the present analysis was to study the distribution of established VTE risk factors in categories of manifestation age in a large cohort of VTE patients. METHODS: Data were taken from the MAISTHRO (MAin-ISar-THROmbosis) registry, a cross-sectional study of patients with acute or documented history of VTE. The registry enrolled 1500 consecutive patients (869 females; median age, 43 years) with a first lower-extremity deep vein thrombosis or pulmonary embolism. RESULTS: VTE was attributed to established risk factors in 76.6% of cases. By classifying patients into categories of VTE manifestation age, we observed a steep rise in the prevalence of malignancies with advancing age (ie, 1.3% of cases of VTE occurred under the age of 30 and 34.0% of VTE cases manifested over the age of 70; P < .001). In contrast, VTE was more likely to be related to thrombophilia, a family history of VTE, oral contraceptives, and pregnancy in younger patients. Hereditary thrombophilia was detected in 50% of VTE patients younger than 20 and in 21.8% over the age of 70 (P < .001). With regard to other VTE risk factors, the results were insignificant. In addition, we were unable to demonstrate an accumulation of common VTE risk factors among patients at higher ages. CONCLUSIONS: The distribution of established VTE risk factors varies with the age of VTE manifestation. Future studies are needed to clarify the role of age-specific risk factors in the development of VTE and in the incidence gradient with aging.