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Changes in the plasma levels of type 1 and type 2 plasminogen activator
inhibitors in normal pregnancy and in patients with severe preeclampsia
A Estelles, J Gilabert, J Aznar, DJ Loskutoff and RR Schleef
Department of Obstetrics and Gynecology, Hospital La Fe, Valencia, Spain.
This report defines the nature of the molecules responsible for the
increased plasma plasminogen activator inhibitor (PAI) activity in
preeclamptic patients and the relationship of these inhibitors to the
severity of placental damage in preeclampsia. Clinical groups consisting of
pregnant women with either severe preeclampsia or chronic hypertension with
superimposed severe preeclampsia, as well as normal pregnant and
nonpregnant women, were analyzed in a panel of functional and immunologic
assays for PAI-1 and PAI-2. Pure severe preeclamptic patients in their
third trimester showed a significant increase in both antigenic (136 ng/mL)
and functional (5.76 U/mL) type 1 PAI (PAI-1) as compared with normal
third-trimester pregnant women (34.8 ng/mL and 2.57 U/mL, respectively). In
contrast, antigenic (186 ng/mL) and functional (5.76 U/mL) levels of type 2
PAI (PAI-2) were significantly lower in the pure severe preeclampsia group
as compared with the values of the normal pregnant group (269 ng/mL and
9.58 U/mL, respectively). The patients with chronic hypertension and
superimposed severe preeclampsia exhibited PAI-2 levels comparable to those
of the pure preeclamptic group, whereas their antigenic and functional
PAI-1 levels were intermediate (94 ng/mL and 3.25 U/mL, respectively)
between the normal pregnant and the pure preeclamptic groups. During early
puerperium of both normal pregnant women and patients, plasma PAI-1 antigen
and activity decreased within one day to approximately the levels detected
in normal nonpregnant women, while PAI-2 levels remained elevated for over
11 days. Similar results were obtained in plasma samples obtained from
citrated blood and blood collected with an anticoagulant/antiplatelet
mixture, suggesting that increased PAI-1 levels in preeclamptic patients
were not due to platelet activation in vitro. In preeclamptic patients, a
positive correlation between birth weight and PAI-2 values was observed (r
= .64, P less than .05), whereas birth weight was inversely correlated with
both PAI-1 levels and total PAI activity (r = -.6, P less than .005 and r =
-.76, P less than .005 respectively). Preeclamptic patients with extensive
placental infarction exhibited higher plasma PAI activity (24.1 U/mL v 11.6
U/mL) and PAI-1 values (305 ng/mL v 80.9 ng/mL) than preeclamptic patients
without extensive placental infarction. In contrast, PAI-2 levels were
reduced in preeclamptic patients with infarction in comparison with those
of patients without infarction (141 ng/mL v 212.9 ng/mL). Our data indicate
that increases in the level of PAI-1 accounts for the high plasma PAI
activity in severe preeclampsia as measured using single-chain t-PA.
Volume 74,
Issue 4,
pp. 1332-1338,
09/01/1989
Copyright © 1989 by The American Society of Hematology
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