Estudios de hipercoagulabilidad en oftalmología¿Qué pedir y cuándo?

  1. F.J. Muñoz-Negrete
  2. P. Casas-Lleras
  3. M. Pérez-López
  4. G. Rebolleda
Zeitschrift:
Archivos de la Sociedad Española de Oftalmologia

ISSN: 0365-6691

Datum der Publikation: 2009

Ausgabe: 84

Nummer: 7

Seiten: 325-332

Art: Artikel

DOI: 10.4321/S0365-66912009000700003 DIALNET GOOGLE SCHOLAR lock_openOpen Access editor

Andere Publikationen in: Archivos de la Sociedad Española de Oftalmologia

Zusammenfassung

Most ophthalmologic disorders secondary to hypercoagulabe state are due to the confluence of congenital and adquired factors. A systematic workup is mandatory. Most of congentital coagulation disorders cause venous trombosis and are inherited autosomal dominantly. In order of frequency these are factor V Leiden mutation (activated protein C resistance), G20210A mutation of the prothrombin gen and protein C, protein S, and antithrombin III deficiencies. Sickle cell anemia can determine arerial and venous thrombosis. In relation with arterial occlusion, the markers most frequently involved are homcysteine fasting levels and the markers of antiphospholipid antibody syndrome. Both of them can also determine venous thrombosis. Several acquired factors can lead to hypoercoagulable state, especially hyperhomocysteinemia, antiphospholipid antibody syndrome, hepatic disease, alcohol and tobacco intake, oral contraceptives, immobilization, surgeries and malignancies. In central venous occlusion is only necessary to rule out hyperhomocysteinemia and antiphospholipid antibody syndrome in young patients without known risk factors. In central artery occlusion, hypercoagulable workup is only recommended for patients less than 50 years-old with unknown emboli source. In this cases protein C, protein S, and antithrombin III deficiencies, homocystein, sickle cell diseae and antiphospholipid antibody syndrome will ruled out. In non arteritic ischemic optic neuropathy hypercoagulable work up is not necessary. In amaurosis fugax without known emboli source, it is recommended to rule out etiologies of arterial occlusion, especially antithrombin III deficiencies, homocystein, sickle cell diseae and antiphospholipid antibody syndrome.

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Fuente de los datos: Dialnet