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Michael Feingold, MD; Anthony J. Sbarra, PhD
St Margaret's Hospital for Women Tufts University School of Medicine Boston

JAMA. 1987;257(11):1475.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Gravett and associates¹ are to be congratulated for their work on the association of bacterial vaginosis and premature rupture of the membranes. They suggest that the mechanism by which maternal cervical or vaginal infection may cause preterm labor or preterm premature rupture of the membranes may involve bacterial phospholipase A₂ and subsequent cleaving of bound arachidonic acid from the phospholipid components of fetal membranes. The resulting free arachidonic acid, an obligate precursor of prostaglandin, would now be available for prostaglandin synthesis and the initiation of labor and preterm premature rupture of the membranes. Some recent work in our laboratory supports this concept.

Study.—

We have developed an in vitro experimental model that has allowed us to study amniotic lysosomal enzyme release (ie, phospholipase A₂) under controlled conditions.² A layer of human amniotic membranes was mounted on a specially designed reaction vessel serving as . . . [Full Text PDF of this Article]

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