Article

Labor and infection. II. Bacterial endotoxin in amniotic fluid and its relationship to the onset of preterm labor

Yale University School of Medicine, Department of Obstetrics and Gynecology, New Haven, CT 06510-8063.
American Journal of Obstetrics and Gynecology (Impact Factor: 3.97). 06/1988; 158(5):1044-9.
Source: PubMed

ABSTRACT We have previously reported the detection of endotoxin in the amniotic fluid of patients with gram-negative intraamniotic infection. Endotoxin or lipopolysaccharide is a potent biologic product capable of inducing prostaglandin release from several cell types and, therefore, may be involved in the onset of human parturition in the presence of intraamniotic infection. This article describes a technique for the quantification of endotoxin in amniotic fluid. The method uses a computer-assisted quantification of the turbidimetric reaction between the Limulus amebocyte lysate and endotoxin. Serial dilutions of Escherichia coli endotoxin in culture-negative amniotic fluid were prepared, and the samples were run in the assay. Amniotic fluid was found to enhance the reaction, and a dilution of 1:20 was required for this biologic fluid to behave similarly to pyrogen-free water. The sensitivity of this kinetic turbidimetric technique in the detection of endotoxin in amniotic fluid was 40 pg/ml. This method was applied to the quantification of endotoxin concentration in amniotic fluid in 26 patients with intraamniotic infection and premature rupture of membranes. Patients in active labor had higher concentrations of endotoxin (median = 47,514 pg/ml) than nonlaboring patients (median = 635 pg/ml) (p less than 0.025). Therefore, women with preterm labor had a higher median concentration of endotoxin in amniotic fluid than patients who were not in labor.

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    • "High levels of LPS have also been detected in women with bacterial vaginosis [3]. In human, Gram-negative bacterial infections are recognized as a cause of fetal loss and preterm labor [4], [5]. Mimicking maternal infection by exposing the pregnant rodents to LPS during the first trimester resulted in embryonic resorption and fetal death [6], [7]. "
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    • "LPS stimulated activin A secretion from AEC at doses of 10 μg/mL or higher. The endotoxin concentrations in the amniotic fluid of women with premature rupture of membranes were between several hundred pg/mL to several μg/mL, as determined by the Limulus amebocyte lysate assay with E.coli LPS as the standard [30]. Compared to the endotoxin concentrations in the amniotic fluid, the LPS doses that stimulated activin A secretion from AEC were higher. "
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