Anticoagulación extendida en la enfermedad tromboembólica venosa. A favor / Extended anticoagulation in venous thromboembolism disease. In favour

La enfermedad tromboembólica venosa puede considerarse una enfermedad crónica ya que, tras un primer episodio, el riesgo de recurrencia permanece toda la vida. La recurrencia es una complicación grave. La anticoagulación es eficaz mientras se mantiene, pero al suspenderla el riesgo de nuevos eventos trombóticos persiste indefinidamente. Las guías de práctica clínica ofrecen recomendaciones específicas sobre la duración del tratamiento en pacientes con enfermedad provocada o recurrente, pero son poco precisas para aquellos con un primer episodio no provocado. La decisión debe tomarse tras una cuidadosa valoración individual del riesgo-beneficio de la anticoagulación. Este artículo repasa las evidencias a favor de prolongar la anticoagulación y las opciones terapéuticas actuales (AU)

Venous thromboembolism disease can be considered a chronic disease because, after the first episode, there is a life-long risk of recurrence. Recurrence is a severe complication. Anticoagulation is effective while it is maintained, but when it is discontinued, the risk of new thrombotic events persists indefinitely. Clinical practice guidelines offer specific recommendations on the treatment duration for patients with provoked or recurrent disease but are not specific for those with a first unprovoked episode. The decision should be made after a careful individual assessment of the risk-benefit of anticoagulation. This article reviews the evidence in favour of extending the anticoagulation and the current therapeutic options (AU)

Valores de colesterol HDL en la población infantil y riesgo trombótico / Values of high-density lipoprotein cholesterol in the pediatric population and risk of thrombosis

Introducción Existen evidencias del papel protector que el colesterol unido a lipoproteínas de alta densidad (c-HDL) puede ejercer frente a la formación de la placa de ateroma y de su implicación en el transporte reverso de colesterol, así como de sus propiedades antioxidantes y moduladoras de la respuesta inflamatoria. También se han relacionado concentraciones bajas con un estado protrombótico. Objetivo Determinar la relación existente entre el c-HDL y los parámetros lipídicos y hemostáticos. Pacientes y métodos Un total de 110 niños (50 niñas, 60 niños) de entre 6 y 7 años. Se determinó el perfil lipídico, dímero-D, inhibidor del activador del plasminógeno y fibrinógeno. Resultados Los valores medios de los parámetros estudiados fueron colesterol total (192,92 ± 26,01 mg/dl), c-HDL (72,87 ± 15,69 mg/dl), colesterol unido a lipoproteínas de baja densidad (c-LDL) (109,46 ± 23,30 mg/dl), triglicéridos (56,24 ± 20,35 mg/dl), apolipoproteína B (apo B) (91,96 ± 14,93 mg/dl), apo A1 (168,4 ± 24,55 mg/dl), logaritmo lipoproteína(a) (1,76 ± 1,36 mg/dl), logaritmo del inhibidor del activador del plasminógeno tipo 1 (PAI-1) (3,77 ± 3,93 U/ml), logaritmo del dímero-D (5,53 ± 0,49 ng/ml) y fibrinógeno (268,61 ± 48,59 mg/dl). Al dividir la muestra en dos grupos, atendiendo a las concentraciones de c-HDL, los niños con valores más bajos presentaron concentraciones más elevadas y estadísticamente significativas de colesterol total/c-HDL, fibrinógeno y PAI. Los valores de c-HDL se asociaron directa y significativamente con colesterol total y apo A1 e inversa y significativamente con el cociente colesterol total/c-HDL, fibrinógeno y el PAI. Conclusión La población infantil estudiada presentó valores elevados de c-HDL, y éstos pudieron ser los responsables del incremento de colesterol total. Aumentos en su concentración se asociaron de manera significativa con una disminución del riesgo trombótico

Introduction There is evidence of the protective effect of high-density lipoprotein (HDL)-cholesterol against atheroma plaque formation and of its role in cholesterol efflux from cells, as well as its anti-oxidative and inflammatory modulating response properties. Low HDL-cholesterol levels have been associated with a prothrombotic state. Objective To determine the relationship between HDL-cholesterol and lipidic and hemostatic parameters. Patients and methods We studied 110 children (50 girls, 60 boys) aged between 6 and 7 years old. Lipid profile, D-dimer, plasminogen activator inhibitor (PAI) and fibrinogen were determined. Results The mean values of the studied parameters were as follows: total cholesterol (192.92 ± 26.01 mg/dl), HDL-cholesterol (72.87 ± 15.69 mg/dl), low-density lipoprotein-cholesterol (109.46 ± 23.30 mg/dl), triglycerides (56.24 ± 20.35 mg/dl), apolipoprotein B (91.96 ± 14.93 mg/dl), apolipoprotein A1 (168.4 ± 24.55 mg/dl), lipoprotein(a) logarithm (1.76 ± 1.36 mg/dl), plasminogen activator inhibitor-1 logarithm (PAI-1) (3.77 ± 3.93 U/ml), D-dimer logarithm (5.53 ± 0.49 ng/ml) and fibrinogen (268.61 ± 48.59 mg/dl).When the sample was divided into two groups according to HDL-cholesterol levels, children with lower levels showed significantly higher values of total cholesterol/HDL-cholesterol, fibrinogen and PAI. HDL-cholesterol levels were directly and significantly associated with total cholesterol and apolipoprotein A1 and negatively and significantly associated with the total cholesterol/HDL-cholesterol ratio, fibrinogen and PAI. Conclusion The children studied had high HDL-cholesterol levels, which could be responsible for the high total cholesterol levels. High values of HDL-cholesterol are significantly associated with a reduction in thrombotic risk

An oligonucleotide microarray for the monitoring of repair enzyme activity toward different DNA base damage.

Characterization of DNA-N-glycosylase activities in cell extract is a challenging problem and could represent a major concern for medical applications. Synthetic oligonucleotides which contain base lesions located on specific sites constitute suitable substrates for their study. An in vitro miniaturized assay was developed that allows the measurement of cleavage activities of DNA repair enzymes on a set of oligonucleotides (ODNs) that contained different lesions. The modified ODNs were indirectly hybridized onto probes chemically fixed at defined sites on a circular format within each well of a 96-well microtiter plate (Oligo Sorbent Array, OLISA). The lesions were selected among oxidative damage (8-oxo-7,8-dihydroguanine, formylamine), deaminated bases (uracil, hypoxanthine) and alkylated base (N(6)-etheno-adenine). Cleavage specificity was checked using different enzymes: Fapy-DNA-N-glycosylase, 3-methyladenine DNA glycosylase II, uracil-N-glycosylase, endonuclease V and endonuclease VIII. The extent of excision could be monitored simultaneously for the selected base damage. For this purpose, we used automated fluorescence imaging analysis of the residual ODNs that contained lesions and remained on the support after release of the cleaved ODNs recognized by the repair enzymes. The results indicated that this assay could advantageously replace the analysis of glycosylase activities by PAGE techniques. Finally we show that this in vitro repair assay represents an interesting tool for the determination of cellular repair activities.