[Anticoagulation treatment withdrawal in primary antiphospholipid syndrome when anticardiolipin antibodies become negative]. / Retirada de la anticoagulación en el síndrome antifosfolípido primario cuando se negativizan los anticuerpos anticardiolipina.

OBJECTIVES: The recommended treatment in patients with primary antiphospholipid syndrome (APS) after a thrombotic event is long-term anticoagulation. However, it is still not exactly known how to manage patients who remain stable for years and whose antiphospholipid antibodies (APA) decrease until becoming negative. This study aims to assess the course of the primary APS in a group of patients after anticoagulation therapy is discontinued. PATIENTS AND METHOD: Ten patients with primary APS who had developed deep venous thrombosis in the limbs (9) or in the aorta (1) were included. After a minimum period of 12 months of anticoagulation therapy, this was discontinued if the patients were negative APA during the follow-up in two consecutive measurements. RESULTS: Six patients (60%) developed persistent negative APA. Four had transient risk factors (2 pregnant, 1 immobilization, 2 oral contraceptives). No new thrombosis episode was observed after a follow-up period of 21 +/- 4.9 months. CONCLUSIONS: Our data suggest that anticoagulation can be discontinued in those patients with primary APS and persistent negative APA, especially if the thrombotic event was venous and occurred in association with a transient risk factor, such as immobilization or pregnancy. Extensive studies are required to confirm these results.

Retirada de la anticoagulación en el síndrome antifosfolípido primario cuando se negativizan los anticuerpos anticardiolipina / Anticoagulation treatment withdrawal in primary antiphospholipid syndrome when anticardiolipin antibodies become negative

Objetivos. La anticoagulación a largo plazo es el tratamiento recomendado en el síndrome antifosfolípido primario (SAF) tras un evento trombótico. Sin embargo, no se conoce con precisión cómo se deben manejar los enfermos que permanecen estables durante años, y cuos anticuerpos antifosfolípido (AAF) descienden hasta negativizarse. El objetivo de este trabajo es valorar la evolución del SAF primario, tras la suspensión de la anticoagulación, en este grupo de pacientes. Población y métodos. Se incluyeron diez pacientes diagnosticados de SAF primario que habían sufrido una trombosis venosa profunda en las extremidades (9) y en la aorta(1). Tras un período mínimo de 12 meses de anticoagulación se retiró el tratamiento a los pacientes que presentaron AAF negativos a lo largo del seguimiento en dos determinaciones consecutivas. Resultados. Los AAF se negativizaron de forma persistente en seis enfermos (60%). Cuatro presentaban factores de riesgo transitorios (2 gestación, 1 inmovilización, 2 anticonceptivos), y tras la retirada de la coagulación ninguno desarrolló nuevos eventos trombóticos. Conclusiones. Nuestros datos sugieren que la retirada del tratamiento anticoagulante puede ser adecuada en un grupo de pacientes con SAF primario que, tras un periodo prolongado de anticoagulación, negativizan los AAF de forma estable. Esta actitud sería más segura si el evento trombótico era venoso y ocurrió durante la presencia de un factor de riesgo transitorio. No obstante, son necesarios estudios más amplios que confirmen estos hallazgos

Objectives. The recommended treatment in patients with primary antiphospholipid syndrome (APS) after a thrombotic event is long-term anticoagulation. However, it is still not exactly known how to manage patients who remain stable for years and whose antiphospholipid antibodies (APA) decrease until becoming negative. This study aims to assess the course of the primary APS in a group of patients after anticoagulation therapy is discontinued. Patients and method. Ten patients with primary APS who had developed deep venous thrombosis in the limbs (9) or in the aorta (1) were included. After a minimum period of 12 months of anticoagulation therapy, this was discontinued if the patients were negative APA during the follow-up in two consecutive measurements. Results. Six patients (60%) developed persistent negative APA. Four had transient risk factors (2 pregnant, 1 immobilization, 2 oral contraceptives). No new thrombosis episode was observed after a follow-up period of 21 ± 4.9 months. Conclusions. Our data suggest that anticoagulation can be discontinued in those patients with primary APS and persistent negative APA, especially if the thrombotic event was venous and occurred in association with a transient risk factor, such as immobilization or pregnancy. Extensive studies are required to confirm these results

A carbohydrate-rich diet reduces LDL size in QQ homozygotes for the Gln 192Arg polymorphism of the paraoxonase 1 gene.

Paraoxonase 1 (PON 1) is an esterase with antioxidant properties that is present in HDL. Gln192Arg polymorphism (also named Q192R or Q/R) of the PON 1 gene that encodes this protein defines two alleles (Q and R). The R allele has been associated with higher cardiovascular risk. LDL size and susceptibility to oxidation also have been identified as cardiovascular risk factors. Our objective was to determine whether genetic variations in the Gln192Arg polymorphism influence LDL size and susceptibility to oxidation after the consumption of diets with different fat content. In our experiments, the participants (n = 98) underwent three 4-wk diets--one, saturated fat-enriched (SAT); another, monounsaturated fat-enriched (MONO); and a third, carbohydrate-enriched (CHO). We observed that LDL were smaller in the QQ group after the CHO diet vs. the SAT (P < 0.01) and MONO diets (P < 0.03). No differences in LDL size were found in QR/RR subjects. When we analyzed lag time of oxidation of LDL, we found that when carriers of the R allele (QR/RR) received the MONO diet, the lag period of LDL oxidation was longer as compared with the CHO diet. Otherwise, we found no differences in QQ homozygotes when we evaluated the lag time of oxidation of LDL after the three diets. These results suggest that the Glnl92Arg polymorphism of the paraoxonase gene influences LDL size and susceptibility to oxidation in response to diet.