246 Abstracts / Pregnancy Hypertension: An International Journal of Women’s Cardiovascular Health 4 (2014) 241–247

The role of angiogenic factors in pre-eclampsia the uteroplacental circulation, which previously has been
Bambang Abimanyu closed by trophoblast plugs in the spiral arteries, begins to
open. Defective placentation may arise from premature
Preeclampsia is best described as a Pregnancy specific
opening, and perfusion of the intervillous space by oxygen-
syndrome that can affect virtually every organ system. Pre-
ised arterial blood before the placenta is equipped to cope
eclampsia, a systemic syndrome of pregnancy clinically
with the stress. Placentation extends over about 10 weeks
characterized by new onset of proteinuria and hypertension,
and, when it is defective, constitutes stage 3 of pre-
is associated with significant morbidity and mortality to
eclampsia.
both mothers and fetuses. Preeclampsia originates in the
Stages 4–6 all occur in the second half of pregnancy.
placenta, starting within adequate cytotrophoblast invasion
Stage 4 is associated with excessive or deficient placental
and ending with widespread maternal endothelial dysfunc-
derived factors in the mother’s blood, secondary to placental
tion. Production of placental anti-angiogenic factors, specif-
damage, before the appearance of clinical signs. When the
ically soluble fms-related tyrosine kinase 1 and soluble
diagnosis of pre-eclampsia can be made stage 5 has begun.
endoglin, have been shown to be upregulated in preeclamp-
Stage 6 affects less than half of women with pre-eclampsia.
sia. These placental anti-angio-genic factors are released
It is the superimposition of a second and later spiral artery
into the maternal circulation; their actions disrupt the
lesion called acute atherosis, which has some resemblance
maternal endothelium and result in hypertension, protein-
to atherosclerosis, which is suffered by middle and old-aged,
uria, and the other systemic manifestations of preeclampsia.
non-pregnant adults. Its importance is that it further
The molecular basis for placental dysregulation of these
reduces uteroplacental perfusion and predisposes to spiral
pathogenic factors remains unknown, remains unknown.
artery thrombosis, which underlies the occurrence of pla-
Hypoxia is likely an important regulator. Other factors such
cental infarcts. The evidence for and the mechanisms of
as alterations in the renin–angiotensin–aldosterone axis,
these multiple stages will be briefly presented.
immune maladaption, excessive shedding of trophoblast
debris, oxidative stress, and genetic factors likely contribute doi:10.1016/j.preghy.2014.04.020
to the pathogenesis of the abnormal placentation. The only
successful treatment for preeclampsia is delivery. No defin-
itive preventive strategies have been identified.
Management of preeclampsia
doi:10.1016/j.preghy.2014.04.019 Gustaaf Albert Dekker

Most patients with a pregnancy-induced hypertensive

disorder have no clinical symptoms. So it can only be reli-
The six stages of pre-eclampsia ably detected by repetitive searches (screening) for the early
CWG Redman (Nuffield Department of Obstetrics and signs and symptoms in the 2nd half of pregnancy. Adequate
Gynaecology, John Radcliffe Hospital, Oxford 0X3 9DU, and proper prenatal care is the most important part of man-
UK) agement of preeclampsia. Maternal antenatal monitoring
includes identifying women at increased risk, early detec-
For many years pre eclampsia has been considered to be
tion of preeclampsia by recognizing clinical signs and symp-
a two-stage disease. The first stage comprises poor placenta-
toms, and to observe progression of the condition to the
tion. The second stage is the clinical expression of the dis-
severe state. As the etiology of preeclampsia remains in
ease namely new hypertension and new proteinuria. The
question, the only effective treatment is to deliver the infant
first stage is preclinical and symptomless, which evolves
and placenta; ancillary therapy is predominantly symptom-
between weeks 8 and 18 of pregnancy, when the uteropla-
atic and not directed at underlying causes. Once the diagno-
cental circulation is established by spiral artery remodelling.
sis of preeclampsia is made, subsequent therapy will depend
Its consequence is dysfunctional perfusion of the intervillous
on the results of initial maternal and fetal evaluation. The
space of the placenta with oxidative and haemodynamic
primary objective of management of preeclampsia must
stress. The damaged placenta releases excessive pro-inflam-
always be safety of the mother. Although delivery is always
matory and antiangiogenic factors into the maternal
appropriate for the mother, it may not be optimal for the
circulation.
fetus that is extremely premature. The decision between
With increasing knowledge, this model has become inad-
delivery and expectant management depends on fetal gesta-
equate. First the antecedents of poor placentation have
tional age, maternal and fetal status at time of initial evalu-
become clearer and are immunological in origin, reflecting
ation, presence of labor or rupture of fetal membranes, and
the mother’s ability to accommodate to the genetic foreign-
level of available neonatal and maternal services.
ness of her unborn child. They begin, as discussed already in
It is important to emphasize that hypertension is merely
this meeting, with preconceptual tolerisation of the mother
one manifestation of this disease, albeit directly related to
to the semen of the prospective father of her child. A lack of
one of the most serious consequences for the mother, i.e
tolerisation, arising from a short interval between first
cerebral involvement, which may manifest itself as convul-
coitus and conception increases the likelihood of poor pla-
sions, focal neurological events such as cortical blindness,
centation and pre-eclampsia (Stage 1). This is presumed to
and even cerebral hemorrhage. The benefits of acute
affect the health and growth of the embryo immediately
pharmacologic control of severe hypertension prior to deliv-
after implantation but there is little evidence of this at the
ery are generally accepted. The more contentious issues are
moment (Stage 2). Placentation begins after week 8 when
the role of pharmacologic therapy in allowing prolongation