[Premature rupture of amniotic membranes: a new view of pathomechanism: the role of plasmin, cytokines and metalloproteinases].
The paper surveys current studies on fibrinolytic components, plasmin, cytokines and metalloproteinases in human foetal membranes, and, on the basis of new findings, reviews the mechanism of premature rupture of foetal membranes. Plasmin, which can be formed in foetal membranes, causes a transformation of procollageneses into collageneses, and thus initiates a cascade enzymatic process called a proteolytic (collagenolytic) cascade of plasmin. In the case of foetal membranes inflammation at the lower pole (ascending inflammation from the vagina and cervical canal of uterus), the so-called inflammatory cytokines can be created, initiating a local collagenolytic process, forming in that place punctum minoris resistentiae.
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Katedry i Zakładu Propedeutyki Medycyny AM w Bydgoszczy.
D016207:Cytokines / Q000378:metabolism*; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000175:diagnosis* / Q000378:metabolism*; D005341:Fibrinolysin / Q000378:metabolism*; D006801:Humans; D008666:Metalloendopeptidases / Q000378:metabolism*; D011247:Pregnancy
D016207:Cytokines; D005341:Fibrinolysin; D008666:Metalloendopeptidases