American Journal of Epidemiology Vol. 155, No.

3
Copyright 2002 by the Johns Hopkins Bloomberg School of Public Health Printed in U.S.A.
All rights reserved

Preeclampsia and Gestational Hypertension and Birth Weight Xiong et al.

Impact of Preeclampsia and Gestational Hypertension on Birth Weight by
Gestational Age

Xu Xiong,1,2,5 Nestor N. Demianczuk,3 L. Duncan Saunders,2 Fu-Lin Wang,4 and William D. Fraser1

The predominant etiologic theory of preeclampsia is that reduced uteroplacental perfusion is the unique
pathogenic process in the development of preeclampsia. Decreased uteroplacental blood flow would result in lower
birth weights. To date, no study has assessed the effect of preeclampsia on birth weight by gestational age. Thus,
the authors conducted a retrospective cohort study based on 97,270 pregnancies that resulted in delivery between
1991and 1996 at 35 hospitals in northern and central Alberta, Canada. Differences in mean birth weight between
women with preeclampsia and normotensive women ranged from 547.5 g to 239.5 g for gestational age
categories ranging from 32 weeks to 42 weeks. The birth weights were statistically significantly lower among

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mothers with preeclampsia who delivered at 37 weeks, with an average difference of 352.5 g. However, the birth
weights were not lower among preeclamptic mothers who delivered after 37 weeks (average difference of 49.0 g).
In Alberta, 61.2% of preeclamptic patients gave birth after 37 weeks of gestation. The authors conclude that babies
born to mothers with preeclampsia at term have fetal growth similar to that of babies born to normotensive mothers.
This finding does not endorse the currently held theory that reduced uteroplacental perfusion is the unique
pathophysiologic process in preeclampsia. Am J Epidemiol 2002;155:2039.

birth weight; gestational age; hypertension; pre-eclampsia; pregnancy

Hypertensive disorders in pregnancy, especially pre-
eclampsia, remain a major cause of maternal and infant mor-
bidity and mortality worldwide (1). Despite numerous basic,
clinical, and epidemiologic studies that have been conducted
over the past half-century, knowledge of the etiology and
pathogenesis of preeclampsia remains elusive (2). Because
the pathophysiology of preeclampsia has not yet been eluci-
dated, clinical trials have failed to demonstrate any effective
prevention or treatment strategies, apart from early delivery in
cases where the disorder is severe (2, 3).
A prevailing hypothesis regarding the pathogenesis of
preeclampsia is the ischemic model. Decreased uteropla-
cental perfusion is hypothesized to be the primary step and the
point of convergence of diverse pathogenic processes in the
development of preeclampsia (46). It is intuitive that reduced
Received for publication April 12, 2001, and accepted for publica-
tion August 15, 2001.
Abbreviations: LGA, large for gestational age; SGA, small for
gestational age.
1
Department of Obstetrics and Gynecology, Faculty of Medicine,
Laval University, Quebec City, Quebec, Canada.
2
Department of Public Health Sciences, Faculty of Medicine,
University of Alberta, Edmonton, Alberta, Canada.
3
Department of Obstetrics and Gynecology, Faculty of Medicine,
University of Alberta, Edmonton, Alberta, Canada.
4
Health Surveillance, Alberta Health and Wellness, Edmonton,
Alberta, Canada.
5
Current affiliation: St.-Franois dAssise Hospital, Quebec City,
Quebec, Canada.
Reprint requests to Dr. Xu Xiong, Hpital Saint-Franois dAssise,
Centre de rechercheD1-724, 10 rue de lEspinay, Qubec,
Qubec G1L 3L5, Canada (e-mail: Xu.Xiong@crsfa.ulaval.ca).
placental blood flow should result in decreased fetal growth,
with an increased risk of intrauterine growth restriction and
low birth weight. However, epidemiologic studies have not
conclusively established an association between preeclampsia
or gestational hypertension and poor fetal growth (7).
Birth weight is determined by both duration of gestation
and rate of fetal growth. Preeclampsia significantly
increases the risk of iatrogenic preterm birth (delivery) for
maternal indications. To study the effect of preeclampsia
and gestational hypertension on fetal growth, it is important
to compare the fetal growth of babies born to mothers with
preeclampsia or gestational hypertension with that of
babies born to mothers without these conditions at the same
gestational ages. To our knowledge, no study to date has
examined the impact of preeclampsia and gestational
hypertension on mean birth weight by gestational week,
and no previous study has examined whether the effect of
preeclampsia or gestational hypertension on fetal growth
differs according to gestational age. Using an existing peri-
natal database, we conducted a study to assess the effect of
preeclampsia and gestational hypertension on fetal growth
according to gestational age.
MATERIALS AND METHODS
Study population
The Northern and Central Alberta Perinatal Audit and
Education Program commenced data collection in 1991 to
monitor the impact of educational strategies designed to
decrease the incidence of obstetric interventions (8, 9). The

203
204 Xiong et al.
database is derived directly from the standard labor and
delivery record used in Alberta. Every effort is made to
ensure accuracy of the data. Records received in paper for-
mat from participating hospitals are reviewed by an audit
coordinator to check for discrepancies before being entered
into the database by a data clerk. Data validation is per-
formed at three levels: The registry is checked for missing
or incomplete data; programmed computer checks and
cross-tabulations are used to reduce the risk of typing errors;
and an ongoing manual review of a random sample of charts
is performed to check the accuracy of information. A mini-
mum of one out of every 20 records is verified against the
actual data entered.
Data included in this study were collected from 35
Alberta hospitals in which 97,270 deliveries occurred
between July 1, 1991, and December 31, 1996. Women with
the following characteristics were excluded from the analy-
sis: multiple pregnancies (2,528 cases); preexisting chronic
hypertension (695 cases); use of antihypertensive drugs
before pregnancy (208 cases); any type of prior diabetes
(753 cases); gestational diabetes (2,456 cases); cardiovascu-
lar disease (546 cases); and chronic renal disease (102
cases). Women who had had transient hypertension during
labor but had experienced no hypertension during preg-
nancy were also excluded (809 cases). These conditions
were excluded mainly because they are potentially con-
founding variables known to be associated with both
preeclampsia or gestational hypertension and birth weight.
After exclusion of an additional 1,375 cases with missing
antenatal information, 87,798 pregnancies remained for the
analysis.
Definition of exposure and outcome
The Northern and Central Alberta Perinatal Audit and
Education Program defines gestational hypertension (8, 9) as
a blood pressure of 140/90 mmHg without or with protein-
uria of no greater than trace levels after 20 weeks of gestation.
Preeclampsia is defined as a blood pressure of 140/90
mmHg with proteinuria of 1 on dipstick in two samples
taken 6 hours apart, or >0.3 g in a 24-hour urine collection.
Eclampsia is diagnosed when convulsions occur in a woman
with preeclampsia. Because we restricted our focus to gesta-
tional hypertension and preeclampsia, pregnancies
complicated by chronic hypertension and preeclampsia super-
imposed on chronic hypertension were not studied.
Birth weight was measured shortly after delivery.
Gestational age was based on the last menstrual period, con-
firmed by early pelvic examination, and verified by first-
trimester or early second-trimester ultrasound when available.
If the date of the last menstrual period was not thought to be
accurate, gestational age was based solely on the first-
trimester or early second-trimester ultrasound findings.
Definition of potentially confounding variables
Potentially confounding variables were selected on the
basis of our review of the literature and the biologic plausi-
bility of an association with both exposure and outcome.
The potentially confounding variables included in the analy-
sis were maternal smoking, maternal age, parity, obesity
(maternal prepregnancy weight 91 kg), maternal prepreg-
nancy weight 45 kg, prior spontaneous and induced abor-
tion, prior small-for-gestational-age (SGA) newborn, prior
large-for-gestational-age (LGA) newborn, anemia, and pre-
mature rupture of membranes.
Statistical analysis
Analysis of variance was performed to compare mean
birth weights by gestational week between women with ges-
tational hypertension or preeclampsia and normotensive
women. Post hoc pairwise multiple comparisons that
assessed which specific mean values differed significantly
from the others were performed using Tukey and Bonferroni
procedures (10). To adjust for confounding effects, we
applied multiple linear regression using birth weight as the
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dependent variable and preeclampsia (preeclampsia  1,
normotensive  0), gestational hypertension (gestational
hypertension  1, normotensive  0), and other confound-
ing variables as the independent variables. The regression
() coefficients for preeclampsia, gestational hypertension,
and other variables were estimated by the method of least
squares (10, 11). For example, the coefficient for the vari-
able preeclampsia represents the average change in birth
weight (g) associated with a change from preeclampsia
(code 1) to normotensive status (code 0) adjusted for all
other variables included in the regression (10). Finally, we
also analyzed the impact of preeclampsia and gestational
hypertension on birth weight by gestational age by separat-
ing nulliparous and multiparous women to examine whether
the effect differed by parity. The statistical significance
( p value) of the coefficients was also tested by t test; the
p value was two-tailed, and 0.05 was the critical alpha level.
All statistical analyses were performed with SPSS 10.0 for
Windows (SPSS, Inc., Chicago, Illinois).
RESULTS
The initial population in the database consisted of 97,270
women. Table 1 shows the characteristics of the study pop-
ulation before exclusions. Overall, 8.2 percent of the women
were teenagers and 37.4 percent were over 30 years old;
40.5 percent were nulliparous, and 26.6 percent smoked dur-
ing pregnancy. The incidences of gestational hypertension,
preeclampsia, and chronic hypertension were 3.9 percent,
1.7 percent, and 0.9 percent, respectively. The incidences of
preterm birth, low birth weight, and stillbirth were 9.0 per-
cent, 6.9 percent, and 0.3 percent, respectively.
Figure 1 and table 2 show the impact of gestational hyper-
tension and preeclampsia on birth weight by gestational age.
Babies born to women at gestational ages 32 weeks were
pooled, as were those born at gestational ages 42 weeks,
producing categories of sufficient sample size to allow
meaningful comparisons. With respect to the gestational age
categories from 32 weeks to 42 weeks, differences in
mean birth weight between the gestational hypertension and
normotensive groups ranged from 434.2 g to 55.1 g. For
Am J Epidemiol Vol. 155, No. 3, 2002
 Preeclampsia and Gestational Hypertension and Birth Weight 205

TABLE 1. Characteristics of the study population The differences in mean birth weight between the
(n = 97,270) in a study of the effects of preeclampsia and preeclamptic and normotensive groups ranged from 547.5
gestational hypertension on birth weight by gestational age, g to 239.5 g. For women delivering at 37 weeks, birth
Alberta, Canada, 19911996 weights were statistically significantly lower among women
Characteristic* No. % with preeclampsia than among women with normal blood
Maternal age (years) pressure, both prior to and after adjustment for confounding
19 7,708 8.2 variables ( < 0, p < 0.01). The average unadjusted birth
2030 51,025 54.4 weight difference at 37 weeks was 352.5 g. However, for
>30 35,047 37.4
women delivering after 37 weeks, the differences in mean
Parity birth weights between women with preeclampsia and
Nulliparity 38,408 40.5 women with normal blood pressure were not statistically
Multiparity 56,312 59.5 significant. In fact, mean birth weights were higher among
Maternal smoking women with preeclampsia than among women with normal
Yes 25,285 26.6 blood pressure at 41 and 42 weeks, but the differences
No 69,677 73.4 were not statistically significant ( > 0, p > 0.05). The aver-
Hypertensive disorders age unadjusted birth weight difference after 37 weeks was
in pregnancy 49.0 g.
Normotensive 89,714 93.5 In Alberta, 38.8 percent of women with preeclampsia

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Gestational gave birth at 37 weeks or less, and 61.2 percent gave birth
hypertension 3,713 3.9 after 37 weeks.
Preeclampsia 1,651 1.7 Table 3 shows the results of multivariable analyses of the
Chronic hypertension 877 0.9
impact of preeclampsia and gestational hypertension on birth
Infants sex weight by gestational age among nulliparous and multiparous
Male 48,521 51.0 women separately. There was no significant difference in the
Female 46,554 49.0 effect of preeclampsia and gestational hypertension on birth
Cesarean delivery weight between nulliparous and multiparous women.
Yes 16,280 17.1 However, in the upper gestational age categories (41 and 42
No 78,798 82.9 weeks), the effects pointed in different directions.
Preterm birth
Yes 8,558 9.0
No 86,520 91.0
DISCUSSION

Low birth weight To our knowledge, no previous study has examined the
Yes 6,602 6.9 effect of preeclampsia and gestational hypertension on mean
No 88,476 93.1 birth weight by gestational week. These results contrast with
Stillbirth our previous findings, in which, on the basis of the same
Yes 303 0.3 data, we observed that the overall mean birth weight was
No 94,775 99.7 markedly lower among babies born to mothers with
Mean gestational age preeclampsia than among babies born to normotensive
(weeks) 39.0 (2.4) mothers (8). In the present study, 61.2 percent of babies born
to mothers with preeclampsia were delivered after 37 weeks.
Mean birth weight (g) 3,390.0 (627.2)
When we compared the birth weight of babies born to moth-
* Cases with missing information are excluded. ers with preeclampsia after 37 weeks to that of babies born
Includes 12 cases of eclampsia.
Numbers in parentheses, standard deviation. to normotensive mothers at the same gestational age, there
was no statistically significant difference. Thus, most babies
born to mothers with preeclampsia at term actually have
women delivering before 37 weeks, birth weights were sta- normal birth weight for their expected gestational age. The
tistically significantly lower among women with gestational effect of gestational hypertension on birth weight by gesta-
hypertension than among women with normal blood pres- tional age was similar to that of preeclampsia.
sure. However, for women delivering at 37 weeks, the birth This study demonstrates that the effect of preeclampsia
weights were generally higher among women with gesta- and gestational hypertension on birth weight is a function of
tional hypertension than among women with normal blood gestational age. The effect of decreased birth weight is found
pressure. After adjustment for confounding factors, for mostly among preterm births. This may explain the contra-
women delivering before 37 weeks, birth weights remained dictory findings of previous epidemiologic studies that have
significantly lower among babies born to women with ges- examined the relation between preeclampsia or gestational
tational hypertension than among babies born to women hypertension and birth weight (7, 8, 12). For example, we
with normal blood pressure ( < 0, p < 0.01). For women recently reported results from two separate studies of the
delivering at 37 weeks, there was no statistically signifi- effects of preeclampsia on birth weight (8, 12). These studies
cant difference in mean birth weights between women with were carried out in separate populations. The first study, in
gestational hypertension and normal blood pressure. which we found no difference in mean birth weight between

Am J Epidemiol Vol. 155, No. 3, 2002

206 Xiong et al.

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FIGURE 1. Impact of preeclampsia and gestational hypertension on birth weight (n = 87,798), Alberta, Canada, 19911996.

the preeclamptic group (3,213.1 g) and the normotensive
group (3,241.8 g), had a relatively small proportion of
preeclamptic patients (6.7 percent) who delivered preterm
(12). In the second study, where we observed a significantly
decreased mean birth weight among babies born to mothers
with preeclampsia (2,952.4 g) as compared with those born
to normotensive mothers (3,380.5 g), the proportion of
preterm births among preeclamptic patients was high (27.5
percent) (8). The observed overall effect on birth weight may
depend on the relative proportions of full-term and preterm
deliveries among patients with preeclampsia in the study.
The finding that most babies born to preeclamptic women
at term have normal fetal growth cannot be reconciled with
the currently held belief that reduced uteroplacental perfu-
sion is the unique pathophysiologic process in preeclampsia
(46). There is increasing literature supporting the hypothe-
ses of considerable pathophysiologic heterogeneity in
preeclampsia. The limitations of the ischemic model as
the sole genesis of preeclampsia have been discussed (13).
In longitudinal studies, Easterling et al. (14) demonstrated
an increase in blood flow among preeclamptic patients sec-
ondary to increased maternal cardiac output. By studying

TABLE 2. Impact of preeclampsia and gestational hypertension on birth weight, by week of gestation, in univariable analysis and
multivariable linear regression analysis (n = 87,798), Alberta, Canada, 19911996
Gestational hypertension (n = 2,395) Preeclampsia (n = 745)
versus versus
normotensive status (n = 84,658) normotensive status (n = 84,658)
Week
of Study sample Study sample
gestation Mean birth Mean birth
No. with weight B SE weight B SE
No. No. with No.
gestational difference (g) difference (g)
normotensive preeclampsia normotensive
hypertension

32 41 1,676 248.1 363.2 161.1** 59 1,676 464.2** 665.1 135.6**

33 29 417 434.2** 484.9 106.2** 21 417 547.5** 608.5 125.2**
34 22 668 312.8* 332.6 112.4** 28 668 462.8** 522.8 100.8**
35 43 1,097 317.2** 317.5 69.1** 36 1,097 222.7** 245.6 76.9**
36 107 2,293 189.7** 227.4 44.4** 61 2,293 178.7** 224.4 57.8**
37 238 5,007 19.7 54.9 29.9 84 5,007 239.1** 255.2 49.3**
38 432 12,617 5.9 19.2 21.1 141 12,617 45.9 61.4 36.4
39 632 20,841 55.1** 24.7 17.3 116 20,841 9.0 6.9 40.0
40 622 26,642 45.3* 18.4 18.0 145 26,642 32.5 46.1 16.9
41 198 11,929 22.4 11.7 32.0 47 11,929 74.8 67.6 65.4
42 31 1,471 59.3 103.2 85.8 7 1,471 239.5 226.2 178.1
* p < 0.05; ** p < 0.01.
Adjusted for maternal smoking, maternal age, parity, maternal prepregnancy weight of 91 kg, maternal prepregnancy weight of 45 kg,
prior spontaneous and induced abortions, prior small-for-gestational-age newborn, prior large-for-gestational-age newborn, anemia, and pre-
mature rupture of membranes.
SE, standard error.

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 Preeclampsia and Gestational Hypertension and Birth Weight 207

TABLE 3. Impact of preeclampsia and gestational hypertension on birth weight, by week of gestation and parity, in multivariable
linear regression analysis (n = 87,798), Alberta, Canada, 19911996
Gestational hypertension (n = 2,395) Preeclampsia (n = 745)
versus versus
normotensive status (n = 84,658) normotensive status (n = 84,658)
Week
of Nulliparous women Multiparous women Nulliparous women Multiparous women
gestation (n = 34,929) (n = 52,124) (n = 33,943) (n = 51,460)

B SE B SE B SE B SE

32 451.5 192.6** 170.9 285.9 523.7 162.7** 832.7 239.3**

33 396.7 121.7** 622.0 199.7** 466.8 133.0** 1,024.7 300.1**
34 304.3 140.3* 290.6 184.7** 467.8 120.5** 593.9 196.9**
35 254.4 82.4** 414.2 120.1** 280.9 92.4** 121.8 133.8
36 244.0 55.9** 192.2 71.2** 169.0 68.5** 261.6 104.1**
37 29.3 38.4 68.5 47.7 305.1 57.9** 88.6 91.6
38 0.1 27.0 19.4 33.6 43.3 23.8 67.2 66.3
39 27.7 22.3 39.3 27.3 0.3 45.1 21.9 84.9
40 33.0 21.5 36.5 32.3 53.7 28.7 78.1 46.9
41 67.9 37.3 213.0 62.3 103.7 67.6 158.3 254.7
42 137.7 103.8 1.1 151.9 403.1 209.3 183.6 336.2

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* p < 0.05; ** p < 0.01.
Adjusted for maternal smoking, maternal age, maternal prepregnancy weight of 91 kg, maternal prepregnancy weight of 45 kg, prior
spontaneous and induced abortions, prior small-for-gestational-age newborn, prior large-for-gestational-age newborn, anemia, and premature
rupture of membranes.
SE, standard error.

the placental clearance of dehydroisoandrosterone sulfate,
an indicator of uteroplacental perfusion, Gant et al. (15)
noted that women who became preeclamptic in the third
trimester had substantially greater uteroplacental blood
flows throughout most of their pregnancies than those who
remained normotensive. In a study of 1,650 Caucasian
women, Kingdom et al. (16) found that 85 percent and 94
percent of women who developed preeclampsia at term had
normal uterine Doppler flow indices as measured at 20
weeks and 3034 weeks, respectively. In our recent studies
(8, 12), we observed a significant association between ges-
tational hypertension and preeclampsia and LGA infants. In
addition, significant associations were noted between these
variables and low birth weight and SGA infants. Indeed,
approximately 90 percent of babies born to preeclamptic
mothers were appropriate-for-gestational-age or LGA,
which suggests that uteroplacental blood flow may be nor-
mal or increased in the majority of preeclamptic patients (8).
A further challenge to the ischemic model in
preeclampsia arises from the findings of a reduced risk of
cerebral palsy among preterm or low birth weight infants
born to mothers with preeclampsia (17). Cerebral palsy risk
is markedly increased in infants born significantly preterm
or in those of very low birth weight. If uteroplacental hypo-
perfusion were the sole pathophysiologic mechanism, then
infants born to preeclamptic mothers, under such ischemic
conditions, would be expected to be at higher risk of devel-
oping cerebral palsy. However, the results of our recent
meta-analysis suggest that preeclampsia may be protective
against cerebral palsy in preterm and low birth weight
infants (17). Finally, most previous studies on the etiology
of preeclampsia were of a cross-sectional or case-control
design in which women selected for study have already had
preeclampsia. It is therefore difficult to know whether
decreased uteroplacental perfusion was the cause of the dis-
ease or the result of the disease. Uteroplacental hypoperfu-
sion may be the result of preeclampsia occurring after the
clinical expression of the disease. In order to detect changes
in uteroplacental perfusion before the onset of preeclampsia,
prospective or longitudinal studies are warranted.
Mean birth weight is influenced by both the right and left
tails of the birth weight curve. Although preeclampsia sig-
nificantly increases the risk of low birth weight and SGA
babies (the left tail of the birth weight curve), preeclampsia
also increases the risk of high birth weight and LGA babies
(the right tail of the birth weight curve) (8, 12). The lower
weights on the left side of the curve may be offset by higher
weights on the right side of curve, resulting in a flattening
out of the normal distribution, without displacement of the
mean birth weight (12). The group of preeclamptic women
who have LGA babies are probably mostly among those
who gave birth after 37 weeks. The phenomenon of LGA
and high birth weight infants born to preeclamptic patients
may be the result of earlier growth-enhancing effects by an
increased uteroplacental blood flow due to higher blood
pressure (8, 18).
Another possible explanation for these findings is that
preeclampsia that is of early onset (37 weeks) may be more
likely to be severe, more likely to have a detrimental effect
on fetal growth, and more likely to lead to iatrogenic pre-
mature delivery. Preeclampsia that is of late onset (>37
weeks) may be more likely to be mild and less likely to lead
to iatrogenic premature delivery. Uteroplacental hypoper-
fusion, if present, may be of too short a duration to affect
fetal size (8). Indeed, it would seem likely that preterm birth
is a marker of disease severity and fetal growth restriction.
Early-onset preeclampsia and late-onset preeclampsia may
be different diseases. Unfortunately, our data set did not

Am J Epidemiol Vol. 155, No. 3, 2002

208 Xiong et al.
include information on the onset and severity of preeclamp-
sia or on whether the preterm births were spontaneous or
medically induced. Further studies are needed to examine
this hypothesis.
As is true for other studies based on a large database, our
data were subject to nondifferential misclassification bias.
To limit the number of false-positive cases in the preeclamp-
sia and gestational hypertension groups, we excluded
women with hypertension that occurred only during labor.
Many of these women may not have had true hypertensive
disorders but rather may have represented the normal
response to stress at the time of delivery. Because the sam-
ple size was so large for the normotensive group, the false-
negative cases were unlikely to have biased our findings.
It should be noted that the control group for preterm
births does not necessarily represent a normal control
group and that patients who deliver their babies prematurely
from causes other than preeclampsia probably have a higher
proportion of SGA infants than women whose babies remain
in utero. The data presented here may underestimate the
detrimental effects of preeclampsia on birth weight among
preterm births.
The incidence of preeclampsia in our data was 1.7 per-
cent, which is lower than a previously reported rate of 5
percent (1, 2). The incidence of preeclampsia varies
greatly according to the characteristics of the population
studied and the criteria used for the diagnosis of
preeclampsia. There is also great geographic variation in
the incidence of preeclampsia (19). Indeed, few previous
studies reporting the incidence of preeclampsia have been
population-based. Most of these studies originated from
one or a few tertiary hospital(s) where women who have
preeclampsia or are at high risk of developing preeclamp-
sia are more likely to be referred. Other studies have been
limited to primiparous women, who are at greater risk.
Thus, the incidence of preeclampsia is often overstated.
Our data captured more than 80 percent of the births that
had occurred in northern and central Alberta since 1992
and 90 percent of those that had occurred after 1994. From
1991 to 1996, the incidence of preeclampsia ranged from
1.6 percent to 2.0 percent, with an average rate of 1.7 per-
cent. Finally, the overall incidence of hypertensive disor-
ders, including chronic hypertension in pregnancy, in
Alberta is 6.5 percent (table 1). This figure is comparable
to the recently updated estimate of 68 percent for hyper-
tensive disorders in pregnancy, including gestational
hypertension, preeclampsia, and chronic hypertension,
published by the National High Blood Pressure Education
Program Working Group on High Blood Pressure in
Pregnancy (20, 21).
Our data support the hypothesis that preeclampsia is a
heterogeneous disorder (13) and that it may appear in at
least two forms (8): restricted fetal growth preeclampsia and
normal fetal growth preeclampsia. Patients with restricted
fetal growth preeclampsia often deliver prior to term, and
among these patients preeclampsia may follow the
ischemic model. Patients with normal fetal growth
preeclampsia often deliver at term. It is less likely that the
pathogenesis of preeclampsia follows the ischemic model
in these patients. Future epidemiologic and basic scientific
studies of preeclampsia may be needed to study these two
subsets of preeclampsia separately. In particular, future stud-
ies are needed to examine whether there is a difference
between these two possible subtypes of preeclampsia in
terms of onset and severity.
ACKNOWLEDGMENTS
Dr. Xu Xiong was supported by the Canadian Institutes of
Health Research. Dr. William D. Fraser received salary sup-
port through a Chercheur National Award from the Fond de
Recherche en Sant du Qubec.
The authors thank Nancy Bott, coordinator of the
Northern and Central Alberta Outreach Program, for data
preparation.
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