Cardiovascular Journal of Africa: Vol 24 No 2 (March 2013)

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CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 2, March 2013 AFRICA 5
Editorial
Impact of HIV on the incidence of pre-eclampsia
J MOODLEY
Pre-eclampsia, a condition unique to human pregnancy, is
defined as new-onset hypertension (BP ≥ 140/90 mmHg) in the
second half of pregnancy, associated with significant proteinuria
(≥ 30 mgms). The aetiology of this condition remains elusive
but recent findings suggest that pre-eclampsia is a two-stage
disorder. The first stage is thought to be due to failure of the spiral
arterioles in the placental bed to undergo vascular remodelling
into wide-bore channels. This vascular maladaptation of the
placental bed results in a marked reduction in blood flow to the
placenta and sets the scene for the second stage.
Reduction in blood flow to the placenta induces cellular
hypoxia, which results in the release of trophoblastic debris,
necrotic tissue and a variety of anti-angiogenic circulating
factors such as soluble fms-like tyrosine kinase 1 and soluble
endoglin. It is believed that these excessive anti-angiogenic
factors bind with pro-angiogenic factors (vascular endothelial
factor and placental growth factors), inhibiting their biological
activities and subsequently resulting in widespread endothelial
damage and the clinical disorder of pre-eclampsia.1
The current view of the pathophysiology of pre-eclampsia
as described above is that this pregnancy disorder is a multi-
organ endothelial disorder. Therefore it is important to recognise
that although hypertension and proteinuria are the dominant
clinical signs, pre-eclampsia may present with signs of isolated
thrombocytopenia, liver enzyme abnormalities, intra-uterine
foetal growth restriction or seizures. The exact cause however
remains unknown and management is based on delaying delivery
long enough for the foetus to mature, and expediting delivery of
the placenta to avoid significant maternal and neonatal morbidity
and mortality.2
However, what is generally not recognised is that hypertension
may get worse following delivery or that women may present
with hypertension for the first time in the immediate postpartum
period (usually the first 72 hours following delivery). This is
thought to reflect mobilisation of fluid accumulated in the extra-
vascular space following delivery.
Minimal rises inbloodpressureoccur innormal pregnanciesbut
more than one-third of pre-eclamptics have sustained high blood
pressures in the puerperium and they may also develop pulmonary
oedema. The clinical implications of this is that close monitoring
of blood pressure levels must continue following delivery and it
may be safer to keep all pre-eclamptics in hospital for at least
three days to detect any early signs of complications and take
timeous measures to prevent maternal morbidity and mortality.3
The initiator of the vascular maladaptation is not known but
it is believed that immunological abnormalities may be involved.
Similarly, HIV is an immune-dysfunction disorder and in the
initial stages of this infection, when few symptoms are present,
there may be a slight depression in CD4 T cells.4 It is plausible
that the impaired immunity associated with HIV could lower the
risk of pre-eclampsia. The current data on this matter however,
are conflicting.5,6
Kalumba et al. took a different approach from earlier studies
to establish whether HIV infection had a protective effect on
the incidence of pre-eclampsia.7 These authors performed a
retrospective case–control study by comparing HIV rates in
pre-eclamptics and normotensive healthy women. Previous
studies have just compared the rate of pre-eclampsia between
uninfected and HIV-infected pregnant women.5,8,9 Kalumba et
al. found a lower rate of HIV infection in pre-eclamptics in
comparison to a control group.7
This study suggests that the rates of pre-eclampsia are
lower in HIV-positive pregnant women. Because this study
was retrospective and CD4 counts were not available for a large
number of the study patients, there is a need for a prospective
study involving large numbers of patients to confirm the findings
of Kalumba et al.7
J MOODLEY, MD,
Department of Obstetrics and Gynaecology; Women’s Health
and HIV Research Group, Department of Obstetrics and
Gynaecology, University of KwaZulu-Natal, Durban, South
Africa
References
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decreases sFlt-1 and sEng in pregnant I-NAME treated Sprague-
Dawley rats. Eur J Obstet Gynecol Reprod Biol 2011; 157(2): 136–140.
Doi.10.1016/j.ejogrb.2011.03.005.
2. Moodley J for the National Committee on Confidential Enquiries
into Maternal Deaths. Maternal deaths associated with hypertension
in South Africa: lessons to learn from the Saving Mothers Report
2005–2007. Cardiovasc J Afr 2010; 21(6): 10–14.
3. Smith M, Waugh J, Nelson-Piercy C. Management of postpartum hyper-
tension. Obstet Gynaecol. DOI;10.1111/j.1744-4667.2012.00144.x.
Accessed 14 January 2013.
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5. Mattar R, Abes M A, Prescill CL, Nelson S, et al. Pre eclampsia and
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Immunol 2007; 76: 75–77.
7. Kalumba VM, Moodley J, Naidoo, TD. Is the prevalence of pre-
eclampsia affected by HIV/AIDS? A retrospective case-controlled
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Increased risk of pre-eclampsia and fetal death in HIV infected women
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pre-eclampsia/eclampsia? Obstet Gynecol 2004; 104(2): 238–242.