Nowe spojrzenie na patomechanizm porodu przedwczesnego

Jan Urban, Adam Lemancewicz

Streszczenie
Initiation of labor is a complex process that involves fetal-maternal communication. Although the mechanism for the initiation of preterm labor has not been elucidated fully, it may differ from that in normal labor. Preterm labor may be caused by the activation of the cell-mediated immune system, which is induced by bacteria or their components. Endotoxins may lead to cytokine production and subsequent synthesis and release of PGs. The defense mechanism of the mother and fetus against infection is partially controlled through the production of cytokine inhibitors. Urinary trypsin inhibitor (UTI) is an example of the naturally occuring substances that inhibits cytokines. UTI significantly inhibits the production of PGE₂ in the myometrial cell cultures stimulated by IL-1 and LPS and supresses myometrial contraction by regulation of intracellular Ca⁺⁺. UTI also inhibits cervical maturation induced by IL-8, prevents the the morphologic and functional changes in fetal membranes, prevents endothelial cell damage caused by serum from preeclamptic women and counteracts amniotic cell damage induced by IL-1β or TNF-β. So UTI plays role in maintaining normal pregnancy and preventing preterm delivery which is due mainly to complicated biological phenomena, including cervical ripening, fragility of fetal membranes, and uterine contraction induced by inflammatory cytokines.

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