A link between a hemostatic disorder and preterm PROM: a role for tissue factor and tissue factor pathway inhibitor.
OBJECTIVE
Vaginal bleeding is a risk factor for preterm PROM (PPROM). A disorder of decidual hemostasis has been implicated in the genesis of PROM. Indeed, excessive thrombin generation has been demonstrated in PPROM both before and at the time of diagnosis. Decidua is a potent source of tissue factor (TF), the most powerful natural pro-coagulant. A decidual hemostatic disorder may link vaginal bleeding, PPROM and placental abruption. This study was conducted to determine the behaviour of maternal TF and its natural inhibitor, the tissue factor pathway inhibitor (TFPI) in PPROM.


METHODS
This cross-sectional study included women with PPROM (n = 123) and women with normal pregnancies (n = 86). Plasma concentrations of TF and TFPI were measured by a sensitive immunoassay. Non-parametric statistics were used for analysis.


RESULTS
(1) The median maternal plasma TF concentration was significantly higher in patients with PPROM than in women with normal pregnancies (median: 369.5 pg/mL; range: 3.27-2551 pg/mL vs. median: 291.5 pg/mL; range: 6.3-2662.2 pg/mL respectively, p = 0.001); (2) the median maternal TFPI plasma concentration was significantly lower in patients with PPROM than in women with normal pregnancies (median: 58.7 ng/mL; range: 26.3-116 ng/mL vs. median: 66.1 ng/mL; range: 14.3-86.5 ng/mL respectively, p = 0.019); (3) there was no correlation between the plasma concentration of TF and TFPI and the gestational age at sample collection; and (4) among patients with PPROM there was no association between the presence of intra-amniotic infection or inflammation and median plasma concentrations of TF and TFPI.


CONCLUSIONS
(1) Patients with PPROM have a higher median plasma concentration of TF and a lower median plasma concentration of TFPI than women with normal pregnancies. (2) These findings suggest that PPROM is associated with specific changes in the hemostatic/coagulation system.
Erez
Offer
O
Perinatology Research Branch, NICHD, NIH, DHHS, Detroit, Michigan, USA. oerez@med.wayne.edu
Espinoza
Jimmy
J
Chaiworapongsa
Tinnakorn
T
Gotsch
Francesca
F
Kusanovic
Juan Pedro
JP
Than
Nandor Gabor
NG
Mazaki-Tovi
Shali
S
Vaisbuch
Edi
E
Papp
Zoltan
Z
Yoon
Bo Hyun
BH
Han
Yu Mi
YM
Hoppensteadt
Debra
D
Fareed
Jawed
J
Hassan
Sonia S
SS
Romero
Roberto
R
D000653:Amniotic Fluid / Q000737:chemistry / Q000276:immunology / Q000382:microbiology; D002821:Chorioamnionitis / Q000097:blood / Q000209:etiology / Q000382:microbiology; D003430:Cross-Sectional Studies; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000097:blood / Q000209:etiology*; D005865:Gestational Age; D020141:Hemostatic Disorders / Q000097:blood / Q000150:complications* / Q000209:etiology; D006801:Humans; D008074:Lipoproteins / Q000097:blood / Q000502:physiology*; D009035:Mothers; D011247:Pregnancy; D011250:Pregnancy Complications, Hematologic / Q000097:blood / Q000209:etiology; D011251:Pregnancy Complications, Infectious / Q000097:blood / Q000382:microbiology / Q000473:pathology; D013925:Thromboplastin / Q000032:analysis / Q000502:physiology*; D014592:Uterine Hemorrhage / Q000097:blood / Q000209:etiology
D008074:Lipoproteins; C051928:lipoprotein-associated coagulation inhibitor; D013925:Thromboplastin