Abstract
polymorphisms: the prothrombin 20210 G→A, factor V Leiden G 1691A, plasminogen activator inhibitor (PAI) −6754G/5G, fibrinogen −455G→A, platelet receptors: GPIB (−5) T→C, GPIIIA L33P T→ C, GP IA C807T, SELPLG M621 G→A, methylenetetrahydrofolate reductase (MTHFR) C677T, methionine synthase reductase (MTRR) A66G, coagulation factor VII 10976 G→A. At stroke pts studied data coagulogram tests and homocysteine level before anticoagulant therapy. REsults: Total frequency of prothrombin gene G20210A, factor V Leiden, MTHFR (C677T) and MTRR (A66G) mutations at stroke pts in 2.8 times is higher, than at healthy children. The polymorphisms in homocysteine metabolism genes met more often: MTRR (66GG) in 30.6% of cases, MTHFR (677TT) in 8.3% of cases. The homocysteine level at stroke pts exceeded the upper limit of normal age level and also was significantly elevated in at carriers of these genes: 10.29±1.55 mcmol/l vs 7.33±0.6 mcmol/l (p = 0.018). In coagulogram the anticoagulant system disorders (decrease of a protein C activity – in 22.7% of cases, protein S activity – in 13.6% and antithrombin III – in 12.5% of cases), and also increase of D-dimer level – in 21% of cases are found out. Conclusions: The impact prothrombotic disorders must be examined in relation to other established risk factors and potentially new therapeutic strategies. It is reasonable to measure the serum homocysteine level at ischemic stroke pts.
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