**Part 3**

**Cerebral Venous Thrombosis and Venous Thrombosis of the Eye** 

110 Venous Thrombosis – Principles and Practice

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**7** 

*Czech Republic* 

**Cerebral Venous Thrombosis in** 

Procházka Václav1, Procházka Martin2,

*1Radiodiagnostic Institute FN Ostrava-Poruba* 

*4Neurosurgery Department FN Ostrava-Poruba* 

**Patients Using Oral Contraceptives** 

Ľubušký Marek2, Procházková Jana3 and Hrbáč Tomáš4

*2Gynaecology and Obstetrics Department FN and LF UP Olomouc* 

Cerebral venous thrombosis is a relatively rare, however life-threatening condition. Current studies show that around 10% of the patients die. Earlier works proved that most of the thromboses originated secondarily, as a consequence of local or systemic infection, more than 30% of the cases were considered to be idiopathic. More recent studies also mention other risk factors, which may contribute to the onset of thrombosis. These include thrombophilic states or use of oral contraceptives. A number of hypercoagulation states or thrombophilic conditions, which contribute to the onset of thromboembolic disease, have

Thrombophilia is a congenital or acquired disorder of the haemostatic mechanism, characterized with an increased tendency towards blood clotting and thrombotization. Typical manifestations of the condition include frequent occurrence of lower extremities thromboses in young age, with frequent recurrence, or localization in unusual places. Congenital forms of the disorder are characterized with family occurrence. The most frequent conditions associated with congenital form of the disease are mutation of genes coding VLeiden factor (Leiden mutation), prothrombin G20210A, hyperhomocysteinemia and furthermore also autosomal

The point mutation of the factor V gene usually occurs in the place of protein C binding, which results in its cleavage and inactivation. The changes are associated with substitution of guanine with adenine at the 1691st nucleotide of the factor V, this substitution results in further substitution of glutamine with arginine on the 506th position of the factor V chain (FV Q506). The mutation is also known as "Leiden mutation", based on the place of its discovery (Leiden, Holland). Substitution of amino acids in the factor V chain causes resistance against the activated protein C, resulting in a higher tendency towards thrombosis. The mutation is considered to be autosomal dominant hereditary. It affects 5-9% of the European population. The mechanism of resistance against the activated protein C

Another possible predisposition factor of venous thrombosis is a mutation of gene for prothrombin - G20210A variant. It is present in about 2% of the population. The mutation

**1. Introduction** 

been discovered and described in the recent years.

inheritance of antithrombin III (AT III), protein C and protein S deficit.

(APC resistance) was first described by Dahlbäck in 1993 in Sweden.

*3Haemato-oncology Department FN and LF UP Olomouc* 
