Oral anticoagulant treatment: risk factors involved in 500 intracranial hemorrhages.

Intracranial bleeding is the most severe complication caused by anticoagulant or antiplatelet treatment. The increasing use of this therapy, especially in older people, makes the balance between clinical benefit and bleeding risk an important consideration. A retrospective study of all consecutive 500 intracranial hemorrhages in the West Valladolid area, approximately 220,000 people, during the period 1998 to 2004, was performed. In relation to mortality, predisposing conditions were included, such as age, antithrombotic treatment, arterial hypertension, cancer, blood diseases, vascular malformations, and traumatisms. The incidence of intracranial hemorrhage was 310 per 100,000 per year with a mortality of 30%. Higher mortality was found in antiplatelet-treated patients (44.9%) than in anticoagulated patients (31.1%). This may be related to a different mean age of 78 vs. 71 years. Arterial hypertension was the most frequent risk factor (45.1% in nontreated patients, 60% anticoagulated, and 75.5% antiplatelet). The relative risk of intracranial bleeding in anticoagulated patients was 11.2 (p < 0.001) with an incidence of 0.03% and a median of 14 months since treatment began. The median INR was 3.3. In 40% of the patients the previous five controls were in range. Strict consideration of indications criteria joined to a better control of risk factors may avoid intracranial bleeding episodes.

Patrón de hemostasia de alto riesgo en pacientes con sobrepeso y diabetes tipo 2 / High risk haemostasis patterns in overweight patients with type 2 diabetes mellitus

Introducción. Algunos estudios han demostrado un estado de hipercoagulabilidad en los pacientes diabéticos. Objetivo. Comparar el patrón de hemostasia entre pacientes diabéticos con sobrepeso y controles. Diseño. Un total de 23 pacientes con diabetes mellitus tipo 2 y sobrepeso atendidos en nuestra unidad fueron incluidos en el estudio (16 varones/7 mujeres). Las características clínicas de los pacientes fueron: 61,3 ñ 12,3 años, índice de masa corporal (IMC) 27,2 ñ 3,9 kg /m2 y duración de la diabetes 8,4 ñ 6,7 años. Un grupo de 23 voluntarios sanos fue elegido al azar entre donantes de sangre sin diabetes mellitus (15 varones/8 mujeres). Las características clínica de estos pacientes fueron: 62 + 13 años a IMC 27,6 ñ 3,1 kg/m2. A todos los sujetos, casos y controles, se les realizaron las siguientes pruebas: inhibidor del activador del plasminógeno: tipol (PAI-1), complejo trombina/antitrombina 111 (TAT), activador tisular del palsminógeno (t-PA), antígeno Von Willebrand (vW), proteína C (PC), proteína S (PS), trombomodulina (TH), factor Vi¡ activado, dímero D (DD), plasmina-antiplasmina (PAP) y fragmento activado protrombina Fl + 2 (F12). Estos parámetros fueron comparados en ambos grupos y dentro de los diabéticos en los grupos con y sin micro y macroangiopatía. En ambos grupos; se realizó un análisis de correlación entre los parámetros clínicos y los hemostásicos. Resultados. Los pacientes diabéticos con sobrepeso evidenciaron un incremento en los factores procoagulantes (F12 1,38 ñ 0,4 frente a 1,21 ñ 0,25 nmol/i; p < 0,05); VII[a] 94,6 ñ 48 frente a 81,7ñ 28 (MU/m]); p < 0,05), y un descenso en los parámetros fibrinolíticos (PAP 262,9 ñ 107,5 frente a 348,5 ñ 143 ng/I; p < 0,05), así como en los parámetros anticoagulantes (trombomodulina 27,4 ñ 11,7 frente a 45,1 ñ 21,7 ng/ml; p < 0,05), con un incremento en los niveles de dímero D (DD 22;3 ñ 26;8 frente a 9,7 ñ 5,4 ug/l; p < 0.05) v (t-PA 12.6 ñ 5.1 frente a 7.4 ñ 3.1 ng/ml; p < 0,05). En los pacientes diabéticos no hubo diferencia en función de la ausencia o presencia de micro o macroangiopatía. La proteína C y tPA mostraron una correlación negativa (r = -0,34; p < 0,01; y r = -0,32; p < 0,05, respectivamente) con la hemoglobina glucosilada (HbA1c) 1 FVW se correlacionó de una manera positiva con el IMC (r = 0,32; p < 0,05). No se encontraron correlaciones entre los parámetros de hemostasia, con el IMC y HbA1c en los sujetos control. Conclusión. En los pacientes con diabetes tipo 2, hay un estado de hipercoagulabilidad que puede influir en las complicaciones crónicas de esta población (AU)

[Familial thrombophilia due to resistance to activated protein C]. / Trombofilia familar debida a resistencia a la proteína C activada.

Resistance to activated protein C (RAPC) has been described recently as a cause of trombophilia; this may justify up to 50% of thromboembolic disease without predisposing cause in patients under 45 years. A 29 years-old male with a previous deep venous thrombosis (DVT) in the lower left limb three years earlier, developed a DVT in the right lower limb after a trauma of the knee that required immobilization, was associated to pulmonary thromboembolism diagnosed by gammagraphic methods. The phlebographic study showed femoro-iliaco-caval venous thrombosis. The proband's father and a younger brother had a previous history of thrombotic episodes. The following tests, were performed in the proband and relatives: prothrombin time, aPTT, thrombin time, fibrinogen, (Von Clauss), antithrombin III (chromogenic), protein C and protein S (coagulometry and ELISA), plasminogen (chromogenic) and lupus anticoagulant (ITT, dRVVT, aCL). RAPC was evaluated in two different samples. The proband study was performed under oral anticoagulation treatment (OAT). Control groups were: 21 blood donors and 12 OAT patients. The results showed a decreased response to APC in the proband (ratio 1.5) and relatives: father (1.4), brothers (1.5 and 1.5), while the mother was within the normal range (> or = 2). In normal controls and OAT patients the ratio was over 2. No other abnormalities were detected in the assays performed. It is concluded that RAPC is the cause of this familial trombophilia. RAPC should be included in the evaluation study of trombophilia.