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We sought to determine whether midtrimester amniotic fluid levels of matrix metalloproteinase- 8 were associated with subsequent preterm premature rupture of membranes. We conducted a case- control study examining 57 asymptomatic women who underwent genetic amniocentesis from 14 to 21 weeks’ gestation and subsequently had preterm premature rupture of membranes (< 35 wk) and 58 women with subsequent term delivery. Measurement of total matrix metalloproteinase- 8 level in amniotic fluid was conducted using a commercially available enzyme- linked immunosorbent assay and association with preterm birth due to preterm premature rupture of membranes was assessed. The overall distribution of matrix metalloproteinase- 8 concentrations was similar in women who had preterm premature rupture of membranes and term controls (median 2.39 ng/mL, 25th to 75th percentile 1.1- 10.1 vs 2.37 ng/mL, 25th to 75th percentile 1.5- 4.7, P =. 94). However, 26% of women who had preterm premature rupture of membranes had a matrix me- talloproteinase- 8 concentration above the 90th percentile (8.7 ng/mL), compared with only 10% of term controls (odds ratio 3.1, 95% CI 1.1- 8.7; P =. 03). Elevated matrix metallopro- teinase- 8 remained associated with preterm premature rupture of membranes after adjustment for maternal age, race, parity, gestational age, and year of amniocentesis (odds ratio 3.4, 95% CI 1.2- 9.9; P =. 03). The overall distribution of midtrimester amniotic fluid matrix metalloproteinase- 8 levels did not differ between women who had preterm premature rupture of membranes and those delivered at term. However, marked elevations of midtrimester amniotic fluid matrix metalloproteinase- 8 were highly associated with subsequent preterm premature rupture of membranes, suggesting that the pathophysiologic processes that contribute to preterm premature rupture of membranes may begin in early pregnancy.
We sought to determine whether midtrimester amniotic fluid levels of matrix metalloproteinase-8 were associated with subsequent preterm premature rupture of membranes. We conducted a case-control study examining 57 asymptomatic women who underwent genetic amniocentesis from 14 to 21 weeks’ gestation and subsequently had preterm Premature rupture of membranes (<35 wk) and 58 women with subsequent term delivery. Measurement of total matrix metalloproteinase-8 level in amniotic fluid was conducted using a commercially available enzyme-linked immunosorbent assay and association with preterm birth due to preterm premature rupture of membranes were assessed. The overall distribution of matrix metalloproteinase- 8 concentrations was similar in women who had preterm premature rupture of membranes and term controls (median 2.39 ng / mL, 25th to 75th percentile 1.1-10.1 vs 2.37 ng / mL, 25th to 75th percentile 1.5-4.7, P = .94). However, 26% of women who had preterm premature rupture of memb ranes had a matrix me- talloproteinase- 8 concentration above the 90th percentile (8.7 ng / mL), compared with only 10% of term controls (odds ratio 3.1, 95% CI 1.1- 8.7; P = .03) Elevated matrix metallopro - teinase- 8 remained associated with preterm premature rupture of membranes after adjustment for maternal age, race, parity, gestational age, and year of amniocentesis (odds ratio 3.4, 95% CI 1.2-9.9; P = .03). The overall distribution of midtrimester amniotic fluid matrix metalloproteinase- 8 levels did not differ between women who had preterm premature rupture of membranes and those delivered at term. However, marked elevations of midtrimester amniotic fluid matrix metalloproteinase-8 were highly associated with subsequent preterm premature rupture of membranes, suggests that the pathophysiologic processes that contribute to preterm premature rupture of membranes may begin in early pregnancy.