A RELAXIN-MEDIATED PATHWAY TO PRETERM PREMATURE RUPTURE OF THE FETAL MEMBRANES THAT IS INDEPENDENT OF INFECTION

Citation
Lk. Millar et al., A RELAXIN-MEDIATED PATHWAY TO PRETERM PREMATURE RUPTURE OF THE FETAL MEMBRANES THAT IS INDEPENDENT OF INFECTION, American journal of obstetrics and gynecology, 179(1), 1998, pp. 126-134
Citations number
25
Categorie Soggetti
Obsetric & Gynecology
ISSN journal
00029378
Volume
179
Issue
1
Year of publication
1998
Pages
126 - 134
Database
ISI
SICI code
0002-9378(1998)179:1<126:ARPTPP>2.0.ZU;2-S
Abstract
OBJECTIVE: This study was designed to show whether the overexpression of relaxin in the decidua of patients with preterm premature rupture o f the membranes is independent of or a consequence of chorioamnionitis . STUDY DESIGN: Two experiments were conducted. In the first experimen t fetal membranes and decidua were collected from patients with preter m premature rupture of the membranes (n = 17) or preterm labor (n = 17 ) and were divided according to their degree of histologic infection. Messenger ribonucleic acid was isolated from the tissues and quantitat ive, sequential Northern analyses were carried out for the expression of human relaxin, interleukin-1 beta, interleukin-6, and interleukin-8 . The second experiment was aimed at increasing the numbers of messeng er ribonucleic acid preparations in the two extreme categories, uninfe cted and severely infected tissues, with preterm premature rupture of the membranes and preterm labor. Some samples of messenger ribonucleic acid from the first experiment were rerun with the Northern analyses in the second experiment. These repeat samples showed no statistical d ifferences in the results run at different times. Therefore the data f rom the respective groups of patients in both experiments were pooled for statistical analysis. RESULTS: In both the first experiment and in the pooled data of the two experiments the expression of the relaxin genes was significantly greater (P < .005) in the tissues from patient s with preterm premature rupture of the membranes compared with those with preterm labor, in the absence of infection. No effect of the leve l of infection on the expression of relaxin was noted. In contrast, in terleukin-6 gene expression was significantly increased (P < .05) in s everely infected tissues, which was independent of whether the deliver y was from preterm premature rupture of the membranes or preterm labor . The expression of the interleukin-1 beta and interleukin-8 genes wer e only marginally increased even in severe infection. Marked patient v ariability in expression of the interleukin genes, especially in sever e infection, was noted. CONCLUSION: A relaxin-mediated pathway that le ads to preterm premature rupture of the membranes may exist independen t of infection.