Activated Protein C Anticoagulant System Dysfunction and Thrombophilia in Asia

Thrombophilia that is common among Caucasians is caused by genetic polymorphisms of coagulation factor V Leiden (R506Q) and prothrombin G20210A. Unlike that in Caucasians, thrombophilia that is common in the Japanese and Chinese involve dysfunction of the activated protein C (APC) anticoagulant system caused by abnormal protein S and protein C molecules. Approximately 50% of Japanese and Chinese individuals who develop venous thrombosis have reduced activities of protein S. The abnormal sites causing the protein S molecule abnormalities are distributed throughout the protein S gene, PROS1. One of the most common abnormalities is protein S Tokushima (K155E), which accounts for about 30% of the protein S molecule abnormalities in the Japanese. Whether APC dysfunction occurs in other Asian countries is an important aspect of mapping thrombophilia among Asians. International surveys using an accurate assay system are needed to determine this.

Evaluation of the role of thrombophilia associated factors in pre-eclampsia

To evaluate the role of thrombophilia associated factors in pre-eclamptic pregnant women. A case control study was conducted on 30 severe pre-eclamptic pregnant women [group A], and 30 normotensive pregnant women [group B] from Shatby University Maternity Hospital. Routine laboratory tests, protein C, protein S, antithrombin III, factor V Leiden and anticardiolipin antibodies [IgM, IgG] were measured for both groups. Informed consent of the patients was taken. There was not any significant difference in the values of factor V Leiden, protein C, protein S, antithrombin III, and anticardiolipin IgG between pre-eclamptic and normotensive pregnant women. However, anticardiolipin IgM was shown to be significantly higher in the pre-eclamptic patients. Severe pre-eclamptic patients were 3.5 times more likely to develop elevated levels of anticardiolipin IgM. Routine screening for inherited thrombophilia disorders is not recommended in pre-eclamptic females

Factor XII deficiency and habitual abortion: the Haegman connection

To evaluate the role of factor XII deficiency in cases of habitual abortions. A case control study was conducted on 50 women with history of three or more consecutive first-trimester abortions [group A] of unexplained nature from outpatient clinic of Shatby Maternity University Hospital, and 25 healthy women with no history of recurrent miscarriage, thrombotic disease or adverse pregnancy outcomes [group B]. Blood sample was taken from each patient to assay the following parameters: protein S [PS], protein C [PC], antithrombin III [ATIII], and coagulation factor XII [FXII]. The subsequent miscarriage rate with abnormal FXII is significantly higher than that with normal FXII. However, there were no statistically significant differences in the subsequent miscarriage rates between normal and abnormal PC, PS and ATIII values. Factor XII deficiency might play a role in recurrent miscarriages

deficiencia de la antitrombina III, la proteína C, la proteína S y resistencia a la proteina C activada en pacientes con trombosis venosa profunda

Objetivo. Establecer la frecuencia de la deficiencia de la antitrombina III (Ant III), proteina C, proteina S y de la resistencia a la proteina C activadas (RPCA) en pacientes con trombosis venosa profunda (TVP). diseño. Estudio prospectivo descriptivo desde julio de 1995 a julio de 1997. Lugar. salas de medicina interna y consulta de anticoagulación del Hospital San Vicente de Paúl. Pacientes. Se estudiaron 17 pacientes menores de 45 años con TVP confirmada por dúplex o pletismografía venosa. Los criterios de exclusión fueron: ser mayor de 45 años, tener síndrome nefrótico o hepatopatía, o estar anticoagulado. Intervención. Se hizo medición cuantitativa de la antitrombina III (valor de referencia (VR): 88-131 por ciento), la proteina C (VR: 66-129 por ciento) y la proteina S (VR: 61.9-145.3 por ciento). La RPCA se determinó por la medición del tiempo de coagulación en el plasma en la respuesta a la proteina C activada. El APTT se determinó en presencia y ausencia de la proteina C activada. El resultado se expresó como una razón entre dos tiempos de coagulación (APTT/APTT2) y se consideró la presencia si dicha razón era menor o igual a 2. Resultados. La edad prometio fue de 32.05 años. El 70.5 por ciento fueron mujeres. La frecuencia de la deficiencia de la ant III y de la proteína C en 17 pacientes fue de 5.88 por ciento. En 16 pacientes la frecuencia de la deficiencia de la proteina S fue de 6.25 por ciento y de la RPCA 37.5 por ciento. Conclusiones. La RPCA fue la causa más comín de trombofilina en los pacientes estudiados. Las frecuencias de las deficiencias de estas proteínas y la RPCA concordaron con lo publicado en la literatura. En nuestro medio se deberian estudiar los pacientes para trombofilia heredada si la TVP ocurre en personasd menores de 45 años, especialmente la RPCA