J.'.~"";i'

Review ofLiterature
proved by studies showing PGI2 biosynthesis preceding the development
ofclinical disease (Fitzgerled et al, 1987).
Schiff et al., (1988) reported a reduced incidence ofP.E.T. with
low dose aspirin treatment which can selectively suppress the synthesis of
platelet TxA2 without inhibiting the production of vascular PGI2.
So, evidence from maternal plasma, maternal urine, fetal plasma,
fetal vessels, amniotic fluid, and fetoplacental units has all supported the
concept that P.I.H. is associated with a functional imbalance between
PGI2 and TxA2(Schiff et al., 1988).
Gong et al., (1993) demonstrated, by using peripheral blood
mononuclear cells as a study model, increased TxA2 production in P.I.H.
patients both with and without proteinuria and this may playa role in the
development of hypertension and decreased placental blood flow. Of
primary importance in his study was that the sera from P.E.T. woman
with proteinuria contained a factor(s) that suppresses PGh production and
enhances TxA2 synthesis in peripheral blood mononuclear cells.
The cause of the imbalance between PGh and TXA2 seems to be
complicated and multifactorial. _To date there are several substances that
have been reported to be changed in P.I.H. and are also known to affect
the production of prostaglandins (PGs) in the humans (Gong et al.,
1993).
The first of these substances is progesterone which is capable of
inhibiting POI2 production and its level is found to be increased in P.I.H.
placentas (Walsh, 1988). The second is reactive oxygen species. It has
been reported that the activity ofreactive oxygen species is increased in
P.LH. and can change the pattern ofPGs production in favor of TxA2,
synthesis (Dekker et al., 1991 and Wisdom et al., 1991). The third is
mitogenic factor(s) which was recently discovered in the serum ofP.I.H.
patient by Taylor et al., (1990) and has the ability to stimulate fibroblasts
14
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