Possíveis mecanismos trombogênicos da hiper-homocisteinemia e o seu tratamento nutricional
Palavras-chave:
doenças cardiovasculares, doenças vasculares, homocisteína, nutricionistaResumo
A hiper-homocisteinemia é um fator de risco independente para as doenças vasculares oclusivas. Os mecanismos exatos pelos quais a hiper-homocisteinemia favorece o desenvolvimento dessas doenças não são totalmente compreendidos. Sugere-se que o dano ao endotélio vascular, promovido pelas espécies de oxigênio reativas, oriundas da oxidação da homocisteína, seja a causa dos eventos tromboembólicos. Estudos indicam que a homocisteína interfere em vários mecanismos anticoagulantes mediados pelo endotélio vascular, tais como: redução da ativação da proteína C, inibição da trombomodulina e supressão da expressão do sulfato de heparan. Sabe-se que os níveis de homocisteína são influenciados por diversos fatores, dentre eles destaca-se a deficiência de vitaminas do complexo B (especialmente folato, cobalamina e piridoxina). A suplementação de folato, isoladamente ou em combinação com a cobalamina e piridoxina, reduz os níveis de homocisteína plasmática mesmo em pessoas que não apresentam deficiência dessas vitaminas. Esta revisão tem como objetivos abordar os possíveis mecanismos pelos quais a hiper-homocisteinemia poderia levar ao desenvolvimento de eventos tromboembólicos e o tratamento nutricional da hiper-homocisteinemia.
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