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

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CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 2, March 2013 26 AFRICA
the HIV-negative group (39.2%) than in the HIV-positive group
(27.9%) (p = 0.022). This correlates with the fact that the
mean serum total protein and albumin levels were lower in the
HIV-negative than the HIV-positive group (p < 0.0001, p = 0.013,
respectively) and could suggest that immunity plays a role in the
pathogenesis of proteinuria in pre-eclampsia.
Our findings are different from those of Frank et al. who
found no significant association between HIV infection and
pre-eclampsia; the rate of pre-eclampsia in their study was not
different between HIV-infected (5.7%) and uninfected women
(5.2%). In their study the CD4 count was known in only 13 cases
out of 704 HIV-infected women.7
The main difference between our study and that of Frank et
al. is the fact that they included women with underlying medical
conditions.7 This group with underlying medical conditions may
have had other independent risk factors for pre-eclampsia and
the immune maladaptation was less likely to be the initial event.
Underlying medical conditions constituted an exclusion criterion
from our study.
Also, the power was estimated assuming a reduction in the
rate of pre-eclampsia from 8% (in uninfected women) to 5%
in HIV-infected women. This margin was very narrow if we
consider the wide variability in the rate of pre-eclampsia from
one geographical area to another, and even from one period of
time to another in the same area. The findings can easily swing
for or against the hypothesis. Our findings are less likely to have
been affected by minimal variations in the rate.
Frank et al. did raise the fact that the pre-term birth rate is
high in HIV-infected women and it is possible that a proportion
may have delivered prior to the onset of pre-eclampsia.7 Data on
the rate of pre-term births in HIV-infected women is, however,
conflicting with some studies showing no differences between
HIV-infected and uninfected women.12,13 This confounding factor
is less likely to have affected our results since the mean
gestational age at delivery was not significantly different
between uninfected and HIV-infected women (34.86 weeks and
33.65 weeks, respectively).
The AmRo study found no difference in pre-eclampsia rate
between HIV-positive and HIV-negative women.12 The incidence
of pre-eclampsia was 2.8% among 143 HIV-positive women.
This sample size was too small to demonstrate a possible
statistical difference and 93 out of 143 women were already on
HAART (highly active antiretroviral therapy), hence they were
possibly immune competent.12
Suy et al.13 found a very low rate of pre-eclampsia among 258
HIV-infected women who were not on HAART. In 140 women on
HAART, however, the pre-eclampsia rate was significantly higher
(11%). In the same group, the rate of pre-eclampsia in uninfected
women was 2.8%. These results suggested that HIV-infected
women are at a lower risk of developing pre-eclampsia than
uninfected women, but at a higher risk when on HAART.13
In our study, we could not evaluate for replication of the
rate of pre-eclampsia in women on HAART because of its
different approach. However, the findings also suggested that
immunosuppression could be protective against pre-eclampsia.
Immune reconstitution could alleviate this protection and even
possibly increase the risk of developing pre-eclampsia.
Wimalasundera et al.9 also found a low rate of pre-eclampsia
in HAART-naïve, HIV-infected women but a higher rate in those
on HAART. A retrospective study by Mattar et al.4 found a low
rate of pre-eclampsia among 123 HIV-positive women (0.8%)
compared to 1 708 controls (10.6%); this was a significant
difference. The median CD4 count in HIV-infected women was
531 cells/µl.
As illustrated above, the results from various studies are
conflicting. This is probably due to differences in study design
and approach. Some studies included patients with underlying
chronic medical conditions.4,9
Our approach was unique in comparing the rate of HIV
infection in pre-eclamptic women with that in a control group.
Because of the high rate of HIV in South Africa, this is the
most important study so far on HIV and pre-eclampsia. We
excluded women with underlying chronic medical conditions
and evaluated the level of immunity as per the CD4 count level,
and correlated proteinuria and other parameters of pre-eclampsia
with the HIV status.
There were some limitations to our study and this included
the fact that it was a retrospective study. The CD4 counts were
available in only a few cases of both pre-eclamptics and the
control group (small sample size). Also, in many cases, these
were not recent results; the testing had been carried out up to
six months earlier. In these cases, this did not reflect the actual
immune status of the women at the time of recruitment.
For the same reason, we could not make a correlation between
the severity of proteinuria and the level of immunity as expressed
by the CD4 count. A more accurate quantification of proteinuria
(by 24-hour urine protein levels or spot protein:creatinine
ratio) and recently obtained CD4 counts could provide a better
evaluation.
Conclusion
Our study revealed a significantly lower rate of HIV/AIDS
infection in pre-eclamptic women compared to those without
pre-eclampsia. This finding suggests that women with HIV/
AIDS are less likely to develop pre-eclampsia.
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