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Problema newynashiwaniq beremennosti prodolzhaet sohranqt' swoü aktual'nost' i prioritetnost' w sowremennom akusherstwe. Cel'ü prowedennogo issledowaniq bylo ustanowit' rol' polimorfnyh wariantow genow metabolizma folatow (MTHFR, MTRR, MTR) i gena faktora angiogeneza (VEGF-A) u zhenschin s nerazwiwaüschejsq beremennost'ü i ämbrionow w formirowanii riska poteri beremennosti rannih srokow. Materialy. Osnownaq gruppa sostoqla iz 117 zhenschin s nerazwiwaüschejsq beremennost'ü I trimestra, gruppa srawneniq - 117 zhenschin bez sluchaew newynashiwaniq beremennosti, s fiziologicheskim techeniem nastoqschej beremennosti I trimestra, normal'nym kariotipom ploda. Vywody. U zhenschin s priwychnym newynashiwaniem chasche wstrechaetsq genotip 66AA polimorfizma MTRR 66 A>G (p=0,035). U zhenschin s nerazwiwaüschejsq beremennost'ü i hromosomnoj anomaliej u ploda chasche wstrechaetsq allel' 2756G polimorfizma MTR 2756 A>G (p=0,047). U zhenschin i plodow sluchaew nerazwiwaüschejsq beremennosti dostowerno chasche wstrechaütsq genotipy 936ST i 936TT polimorfizma VEGF-A 936S>T, p=0,048. U zhenschin s nerazwiwaüschejsq beremennost'ü i narusheniem waskulqrizacii horiona chasche wstrechaütsq genotipy -634SS i -634GC polimorfizma VEGF-A -634 G>C, p=0,04.
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