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American journal of obstetrics and gynecology v.217 no.6, 2017년, pp.695.e1 - 695.e14   SCI SCIE
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In an in-vitro model using human fetal membranes, 17-α hydroxyprogesterone caproate is not an optimal progestogen for inhibition of fetal membrane weakening

Kumar, Deepak (Department of Pediatrics, Case Western Reserve University, Cleveland, OH ) ; Moore, Robert M. (Department of Pediatrics, Case Western Reserve University, Cleveland, OH ) ; Mercer, Brian M. (Department of Reproductive Biology, Case Western Reserve University, Cleveland, OH ) ; Mansour, Joseph M. (Department of Mechanical and Aerospace Engineering, Case Western Reserve University, Cleveland, OH ) ; Mesiano, Sam (Department of Reproductive Biology, Case Western Reserve University, Cleveland, OH ) ; Schatz, Frederick (Department of Obstetrics and Gynecology, South Florida University, Tampa, FL ) ; Lockwood, Charles J. (Department of Obstetrics and Gynecology, South Florida University, Tampa, FL ) ; Moore, John J. (Department of Pediatrics, Case Western Reserve University, Cleveland, OH ) ;
  • 초록  

    Background The progestogen 17-α hydroxyprogesterone caproate (17-OHPC) is 1 of only 2 agents recommended for clinical use in the prevention of spontaneous preterm delivery, and studies of its efficacy have been conflicting. We have developed an in-vitro model to study the fetal membrane weakening process that leads to rupture in preterm premature rupture of the fetal membranes (pPROM). Inflammation/infection associated with tumor necrosis factor-α (TNF-α) induction and decidual bleeding/abruption associated thrombin release are leading causes of preterm premature rupture of the fetal membranes. Both agents (TNF-α and thrombin) cause fetal membrane weakening in the model system. Furthermore, granulocyte-macrophage colony-stimulating factor (GM-CSF) is a critical intermediate for both TNF-α and thrombin-induced fetal membrane weakening. In a previous report, we demonstrated that 3 progestogens, progesterone, 17-alpha hydroxyprogesterone (17-OHP), and medroxyprogesterone acetate (MPA), each inhibit both TNF-α– and thrombin-induced fetal membrane weakening at 2 distinct points of the fetal membrane weakening pathway. Each block both the production of and the downstream action of the critical intermediate granulocyte-macrophage colony-stimulating factor. Objective The objective of the study was to characterize the inhibitory effects of 17-OHPC on TNF-α– and thrombin-induced fetal membrane weakening in vitro. Study Design Full-thickness human fetal membrane fragments from uncomplicated term repeat cesarean deliveries were mounted in 2.5 cm Transwell inserts and cultured with/without 17-alpha hydroxyprogesterone caproate (10 –9 to 10 –7 M). After 24 hours, medium (supernatant) was removed and replaced with/without the addition of tumor necrosis factor-alpha (20 ng/mL) or thrombin (10 U/mL) or granulocyte-macrophage colony-stimulating factor (200 ng/mL). After 48 hours of culture, medium from the maternal side compartment of the model was assayed for granulocyte-macrophage colony-stimulating factor and the fetal membrane fragments were rupture strength tested. Results Tumor necrosis factor-alpha and thrombin both weakened fetal membranes (43% and 62%, respectively) and increased granulocyte-macrophage colony-stimulating factor levels (3.7- and 5.9-fold, respectively). Pretreatment with 17-alpha hydroxyprogesterone caproate inhibited both tumor necrosis factor-alpha– and thrombin-induced fetal membrane weakening and concomitantly inhibited the induced increase in granulocyte-macrophage colony-stimulating factor in a concentration-dependent manner. However, contrary to our prior reports regarding progesterone and other progestogens, 17-alpha hydroxyprogesterone caproate did not also inhibit granulocyte-macrophage colony-stimulating factor–induced fetal membrane weakening. Conclusion 17-Alpha hydroxyprogesterone caproate blocks tumor necrosis factor-alpha– and thrombin-induced fetal membrane weakening by inhibiting the production of granulocyte-macrophage colony-stimulating factor. However, 17-alpha hydroxyprogesterone caproate did not also inhibit granulocyte-macrophage colony-stimulating factor–induced weakening. We speculate that progestogens other than 17-alpha hydroxyprogesterone caproate may be more efficacious in preventing preterm premature rupture of the fetal membranes–related spontaneous preterm birth.


  • 주제어

    17-alpha hydroxyprogesterone caproate .   biomechanical weakening .   fetal membranes .   granulocyte-macrophage colony–stimulating factor .   medroxyprogesterone acetate .   preterm premature rupture of the fetal membranes .   progesterone .   progestogens .   thrombin .   tumor necrosis factor-alpha.  

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