Pregnancy-Induced Hypertension

Ichiro Yasuhi, MD,

2 oseph W Hogan, SCD3,
3 acob Canick, PHD2,
4 Maryellen B Sosa, RN and
5 Marshall W Carpenter, MD
Author AIIiliations
1.
1
Departments of Obstetrics and Gynecology
2.
2
Pathology, and
3.
3
Center for Statistical Sciences, Brown University School of Medicine, Providence,
Rhode Island

Next Section
-stract
OB1ECTIVETo test the hypothesis that elevated midpregnancy serum insulin (IRI) and C-
peptide (CP) concentrations are associated with later development oI pregnancy-induced
hypertension (PIH), independent oI prepregnancy obesity and midpregnancy blood pressure
RESERCH DESIGN ND METHODSIn this prospective study, a cohort oI normotensive
women, ages _ years, perIormed a 50-g glucose challenge test at 2430 weeks` gestational
age Blood samples were collected aIter an overnight Iast and h aIter glucose ingestion Serum
IRI and CP concentrations were measured in each sample Maternal height, blood pressure, and
proteinuria were measured at the time oI glucose challenge testing and aIter 36 weeks`
gestational age
RESULTSOI 320 subjects enrolled, 44 women (3) had subsequent PIH Crude odds
ratios (ORs) Ior development oI PIH associated with each U rise in log Iasting IRI, log Iasting
CP, and glucose-induced increase in CP (expressed as log |postprandial CP/Iasting CP|) were 20
(95 CI 333), (CI 22), and 23 (CI 49), respectively AIter controlling Ior
prepregnancy BMI, gestational age, and midpregnancy mean arterial pressure, adjusted ORs
corresponding to log Iasting IRI and CP Ior the development oI PIH were 3 (95 CI 023)
and (CI 2), respectively, and, aIter adjustment Ior Iasting CP, the adjusted OR oI the
glucose-induced rise in log CP was 3 (CI 593)
CONCLUSIONSMid-pregnancy Iasting and postoral glucose CP levels are associated with
subsequent development oI PIH, independent oI maternal obesity and midpregnancy baseline
blood pressure These Iindings may reIlect an ampliIied -cell response to glycemic stimulus,
similar to that Iound in states oI insulin resistance, that appears to be independently associated
with PIH
O CP, C-peptide
O IRI, immunoreactive insulin
O MAP, mean arterial pressure
O OR, odds ratio
O PIH, pregnancy-induced hypertension
Insulin resistance and related hyperinsulinemia are associated with essential hypertension in
nonpregnant individuals () Hyperinsulinemia is also linked with obesity, glucose intolerance,
hypertension, atherosclerotic cardiovascular disease, and dyslipidemia, labeled the 'insulin
resistance syndrome (,2) Insulin resistance is characterized by decreased sensitivity oI glucose
uptake to insulin The resulting compensatory hyperinsulinemia (3), reIlected in elevated Iasting
and postprandial insulin and C-peptide (CP) concentrations, has been associated with insulin
resistance (4)
Physiological insulin resistance is noted during late pregnancy, and patients with gestational
diabetes show more insulin resistance compared with pregnant control subjects with normal
glucose tolerance () Pregnancy-induced hypertension (PIH), identiIied in 0 oI pregnancies
(9), is associated with an increased incidence oI perinatal morbidity and mortality (0) Its
incidence is higher in gravidas with glucose intolerance () PIH may predict an increased risk
Ior hypertension (2) and cardiovascular disease (3) in later liIe
PIH and/or pre-eclampsia have been associated with hyperinsulinemia in both cross-sectional
study designs (4) and cohort studies (5,6), although one study () did not support this
association More recent studies have identiIied insulin resistance in women with PIH () and
pre-eclampsia (9) using the hyperinsulinemic-euglycemic clamp method
On the other hand, maternal obesity and midpregnancy blood pressure are both associated with
maternal hyperinsulinemia and development oI PIH No studies have addressed the possible
conIounding eIIect oI maternal obesity and midpregnancy blood pressure on the association
between maternal hyperinsulinism and PIH
We hypothesized that 1) Iasting hyperinsulinemia (elevated immunoreactive insulin |IRI| or CP
concentrations) at 2430 weeks` gestational age is associated with a higher probability oI
subsequent development oI PIH, and 2) the association is independent oI obesity and mid-
pregnancy blood pressure
Previous SectionNext Section
RESERCH DESIGN ND METHODS
We enlisted gravidas ages _ years and at 2430 weeks` gestation Irom a universal screening
program Ior gestational diabetes Women who had prepregnancy hypertension, prepregnancy
diabetes or prior gestational diabetes, chronic renal disease, thyroid disease, drug abuse, or
multiIetal pregnancy were excluded Subjects whose systolic blood pressure was _40 mmHg or
diastolic pressure was _90 mmHg beIore or at the time oI midpregnancy glucose challenge were
also excluded Subjects gave written inIormed consent as per the Women & InIants` Hospital
Institutional Review Board
Between 24 and 30 weeks` gestation, subjects visited the clinic aIter an overnight Iast oI 02
h AIter subjects rested Ior 5 min in the sitting position, the investigator (IY) measured their
blood pressure manually, using an appropriate size cuII and anaerobic sphygmomanometer
according to the procedures recommended by the American Heart Association (20) Subjects`
blood pressures were measured twice, 5 min apart, and the mean oI the two measurements was
used as the blood pressure observation
Height, prepregnancy body weight, and current body weight were documented Each subject`s
prepregnancy BMI was calculated Irom the report oI her prepregnancy weight and our
measurement oI height (kg/m
2
) We chose prepregnancy rather than midpregnancy BMI as a
measure oI adiposity because oI the uncertain association oI this variable with adiposity in the
context oI gestational changes Analysis oI the substitution oI prepregnancy BMI Ior mid-
pregnancy BMI showed no eIIect on the association oI IRI and CP (Iasting and postprandial
increase) with PIH
Blood samples were drawn Irom the antecubital vein The Iirst sample was collected in the
Iasting state and the second h aIter subjects drank a 50-ml aqueous solution oI 50 g oI
glucose Samples Ior plasma glucose assay were collected in noncoated tubes containing 0 mg
oI potassium oxalate and 25 mg oI sodium Iluoride These were iced immediately, centriIuged,
and assayed within 2 h by the ultraviolet-hexokinase method (Synchron Systems, Beckman
Instruments, Fullerton, CA) Samples Ior serum IRI and CP were collected in silicone-coated
tubes, iced immediately, centriIuged, and stored at 0C until analysis Both serum IRI and CP
concentrations were determined by competitive radioimmunoassays (Diagnostic Systems Lab,
Webster, TX)
Beginning at 36 weeks` gestation, blood pressure was measured weekly, aIter subjects rested in
the sitting position Ior _5 min PIH was deIined as having systolic blood pressure _40 mmHg
or diastolic blood pressure _90 mmHg beIore the onset oI labor, based on at least two
assessments ~6 h apart Pre-eclampsia was deIined as PIH in patients with proteinuria (deIined
as either 300 mg oI urinary protein in 24 h or 2 on Ames Dipstix Irom at least two random
urine specimens collected ~6 h apart)
Sample size was determined as Iollows In the nonhyperinsulinemic group, deIined as Iasting IRI
_5th percentile, we assumed that 5 oI women would eventually develop PIH We also
assumed that variables such as prepregnancy BMI, mean arterial pressure (MAP), and estimated
gestational age at entry would conIound the relationship between hyperinsulinemia and
development oI PIH; roughly, the increase in sample size needed to overcome conIounding
eIIects was inversely proportional to r
2
, where r is the multiple correlation coeIIicient
relating hyperinsulinemic status to the conIounders Under a 5 type I error rate (u), assuming
no conIounding eIIects, we calculated that 29 subjects were needed to detect, with 0 oI
power, a relative increase oI three in the odds oI PIH Ior subjects with hyperinsulinemia We
assumed r 025, giving a target sample size oI 3
For analytic purposes, we used natural log transIormations oI endocrine variables To examine
the pairwise associations among variables, we calculated pairwise correlations Iirst and then
made adjustment Ior conIounding variables using a multiple regression model We used logistic
regression analysis to test the association between each predictive variable and the development
oI PIH When we tested the association oI the postprandial rise in insulin and CP with PIH, we
adjusted Ior Iasting values oI those variables We also modeled probability oI PIH as a Iunction
oI the independent variables (prepregnancy BMI, gestational age, and MAP at entry) using
logistic regression For our hypothesis tests, two-sided signiIicance levels at P 005 were
accepted
Previous SectionNext Section
RESULTS
OI 35 participants, 65 were excluded Irom analysis because oI preterm delivery beIore 36
weeks` gestation (n 4), pre-existing hypertension (n 3), inappropriate blood sampling
either at the Iasting state or aIter -h glucose challenge (n 3), incomplete medical records (n
9), delivery in another place (n ), inappropriate gestational age at glucose challenge testing (n
5), twin gestation (n 2), and suspected endocrinopathy (n 2) Analysis was based on the
remaining 320 subjects Maternal demographic data are summarized in Table Subjects` racial
backgrounds were as Iollows: 39 Hispanic, 3 white, 9 AIrican American, and 4 other
ethnic backgrounds, which was consistent with the overall racial distribution among patients at
the Women and InIants` Hospital Antenatal Clinic The distribution oI values oI each metabolic
variable in the 320 subjects is summarized in Table 2 Only one subject was determined to have a
signiIicantly elevated Iasting glucose concentration (2 mg/dl) She was treated with insulin
and had no hypertension during pregnancy The mean Iasting glucose concentration among the
other 0 subjects with gestational diabetes was mg/dl (range 6902), and only one oI them
later developed PIH
Table 3 documents the correlation coeIIicients among Iour endocrine variables (log Iasting IRI,
log Iasting CP, and the absolute postglucose challenge rise in log IRI and log CP) and MAP at
the time oI glucose challenge testing Log Iasting IRI was signiIicantly associated with the other
three endocrine variables and the glucose challenge MAP Log Iasting CP was also signiIicantly
associated with MAP
Table 4 summarizes regression coeIIicients describing the relationship between MAP at 2430
weeks` gestation and each oI the Iour endocrine variables We Iit one model Ior each measure oI
insulin secretion while controlling in each model Ior prepregnancy BMI and estimated
gestational age at entry Each regression coeIIicient reIlects the mean diIIerence in MAP at entry,
corresponding to a -U diIIerence in the log value oI each endocrine variable AIter controlling
Ior prepregnancy BMI and gestational age, only log Iasting IRI was signiIicantly associated with
midpregnancy MAP
OI the 320 subjects, 44 (3) developed PIH, including 9 who developed pre-eclampsia
(2) All endocrine variables were signiIicantly associated with later development oI PIH For
each unit rise in the log value oI an endocrine variable, the crude odds ratios (ORs) were as
Iollows: log Iasting IRI, OR 20 (95 CI 333); log postprandial IRI/Iasting IRI, OR
(CI 069); log Iasting CP, OR (CI 22); and log postprandial CP/Iasting CP, OR
23 (CI 49)
We then Iit logistic regression models to estimate the eIIects oI the insulin secretion measures
aIter adjusting Ior prepregnancy BMI, gestational age, and midterm MAP Because substitution
oI either systolic or diastolic blood pressure, or their combination, Ior MAP did not change the
association between CP and PIH, and because midpregnancy MAP had a slightly higher
association with PIH than the other blood pressure variables, we chose to use MAP in the
regression model Table 5 summarizes the Iitted models, and reports adjusted ORs with 95 CI
Ior each measure oI insulin secretion In this analysis, we Iound that both log Iasting CP and
change in log CP (Irom the Iasting to the postprandial states) had a signiIicant positive
association with subsequent development oI PIH A log-unit diIIerence in midpregnancy CP was
associated with a 0 increase in the odds oI PIH (OR |2|), and a -U glucose-
stimulated increase in log CP corresponded to a nearly IourIold increase in the odds oI PIH (OR
3 |CI 596|) IRI was positively associated with the development oI PIH (Ior log-unit
increase, OR 3 |02|), but the eIIect was not statistically signiIicant
Excluding subjects with gestational diabetes Irom the multiple logistic regression analysis did
not change CP ORs Ior PIH (Iasting CP OR oI PIH |95 CI 2|; postprandial
increase in CP 36 |492|) The Iasting and postprandial glucose concentrations among
subjects developing subsequent PIH were 2 and 2 mg/dl, respectively; values among
subjects who did not develop subsequent PIH were 9 and 09 2 mg/dl, respectively
Previous SectionNext Section
CONCLUSIONS
Fasting and postprandial hyperinsulinemia have been known to be associated with chronic
hypertension in nonpregnant individuals (2) This observation may reIlect an association
between insulin resistance (determined by the hyperinsulinemic-euglycemic glucose clamp
method) and essential hypertension (,22)
Obesity may conIound the association between hypertension and insulin resistance () Some
investigations have Iound an association oI Iasting and postprandial insulin concentration with
hypertension independent oI obesity (2) Others, however, have Iound that the association
between insulin concentration and blood pressure disappeared when the eIIects oI age and
obesity were taken into account (23)
Pregnancy provides an opportunity to examine the association between increased -cell secretion
and developing high blood pressure in subjects with no history oI hypertension Cross-sectional
studies oI third trimester Iasting (4), postprandial hyperinsulinemia (24), and insulin resistance
() have identiIied those conditions as being associated with new onset hypertension in late
pregnancy
Cohort studies during pregnancy have been inconclusive regarding the eIIect oI maternal obesity
on the association between hyperinsulinemia and subsequent PIH Midgestation Iasting
hyperinsulinemia has been Iound to predict subsequent development oI pre-eclampsia
(proteinuria and hypertension) in AIrican-American gravidas (5) and PIH in a apanese cohort
at risk Ior gestational diabetes (6) Both cohort studies Iound this association to be independent
oI prepregnancy BMI and gestational age In contrast, others have Iound that hyperinsulinemia at
262 weeks` gestation was not predictive oI PIH aIter controlling Ior BMI, race, and age ()
Consequently, we sought to examine possible conIounding oI maternal obesity and
midpregnancy blood pressure on the association oI insulin and CP with subsequent hypertension
Data Irom the present study suggest that ampliIied midpregnancy -cell secretory activity (as
reIlected in Iasting and postprandial CP concentrations) is associated with subsequent
development oI PIH, and that this association is independent oI obesity and midpregnancy blood
pressure
Whether this CP and later PIH association can be ascribed to altered insulin metabolism or to
insulin resistance is unclear A negative correlation exists between insulin sensitivity and insulin
secretion Glucose disappearance aIter intravenous insulin inIusion (the insulin tolerance test) is
an indirect measure oI insulin sensitivity and has been Iound to be associated with Iasting
peripheral insulin and CP concentrations in obese, euglycemic subjects (6) and among subjects in
a study oI stroke risk Iactors in apan (5) Kahn et al (25) identiIied a hyperbolic negative
correlation between insulin secretion and sensitivity in nondiabetic subjects using Bergman`s
minimal model technique Insulin sensitivity, as determined by the hyperinsulinemic-euglycemic
clamp technique, has also been shown to be negatively associated with Iasting insulin and CP
concentrations () These observations suggest that the association oI Iasting and postprandial
CP concentrations with later PIH Iound in this study, independent oI obesity, may maniIest the
underlying association between insulin resistance and the development oI new-onset
hypertension in late pregnancy
We Iound that the apparent association oI midpregnancy Iasting insulin concentration with later
development oI PIH disappeared aIter conIounding by midpregnancy blood pressure was
accounted Ior The discrepant association oI PIH with CP but not with Iasting insulin may reIlect
the variability oI hepatic clearance oI insulin among subjects Time-related changes in peripheral
CP concentrations have been correlated with and used to calculate insulin release (26) However,
insulin extraction by the liver may be aIIected by body Iat and its distribution (2) and may
contribute to conIounding by maternal obesity oI the insulin-PIH association The insulin-PIH
association may also be conIounded by an underlying subclinical hypertension, resulting, in our
study, in higher midpregnancy blood pressure among those with higher Iasting insulin
concentrations
In summary, our data document that high midpregnancy Iasting and postprandial CP
concentrations are associated with subsequent development oI new-onset PIH, and that this
association is independent oI obesity and midpregnancy blood pressure These Iindings may
reIlect an ampliIied -cell response to a glycemic stimulus, similar to that Iound in states oI
insulin resistance, that appears to be independently associated with PIH
hLLp//caredlabeLes[ournalsorg/conLenL/24/4/743full
9 ls more common durlng a womans flrsL pregnancy and ln women whose moLhers or slsLers had 9
1he rlsk of 9 ls hlgher ln women carrylng mulLlple bables ln Leenage moLhers and ln women older
Lhan 40 years of age CLher women aL rlsk lnclude Lhose who had hlgh blood pressure or kldney dlsease
before Lhey became pregnanL 1he cause of 9 lsnL known
hLLp//famllydocLororg/famllydocLor/en/dlseasescondlLlons/pregnancylnducedhyperLenslon/causes
rlskfacLorshLml

ge
II you are in your 30's or 40's, you will be considered to be an 'older' mother This may mean that
you are more prone to complications such as gestational diabetes, pre-eclampsia and pregnancy
induced hypertension so you will be monitored regularly
Age is considered a 'risk Iactor' in pregnancy and you are considered to be an older mother iI you
are pregnant in your 30s and 40s as you will be more prone to certain complications oI
pregnancy such as:
O gestational diabetes

O pre-eclampsia

O Pregnancy induced hypertension

UnIortunately, many older women also have an increased risk oI miscarrying and stillbirth,
though this is minimal and many 'older' mothers continue through their pregnancy without any
problems

Pregnancy later on in liIe also carries an increased risk oI certain chromosomal disorders such as
Down's syndrome so many older women are oIIered the Nuchal translucency scan along with the
alpha-Ietoprotein blood test Some women may also be oIIered an amniocentesis to determine iI
their child has a chromosomal abnormality You do not have to have any oI these tests, it's up to
you iI you want them or not

To put things in perspective, beIore the age oI 30 the risk oI having a Down's syndrome baby is
about one in ,000, by the age oI 40 this has increased to a one in 00 chance Though this may
seem very high, it still only means that iI you had 00 children, one oI them would have Down's!

On the positive side many older women are oIten more prepared Ior motherhood, both
emotionally and Iinancially More and more women are waiting until at least their mid-thirties
beIore starting a Iamily and are happy that their increased Iinancial security and selI-conIidence
have made it worth the wait
hLLp//wwwyourdlscoverycom/homeandhealLh/arLlcle[sp?secLlon_ld4Lheme_ld6subLheme_ld7
1arLlcle_ld34slLeuk


Preeclampsia and eclampsia are complications oI pregnancy In preeclampsia, the woman has
dangerously high blood pressure, swelling, and protein in the urine II allowed to progress, this
syndrome will lead to eclampsia
High blood pressure in pregnancy (ypertension) is a very serious complication It puts both the
mother and the Ietus at risk Ior a number oI problems Hypertension can exist in several diIIerent
Iorms One oI these is the preeclampsia-eclampsia continuum (also called pregnancy-induced
hypertension or PIH) In this type oI hypertension, high blood pressure is Iirst noted sometime
aIter week 20 oI pregnancy and is accompanied by protein in the urine and swelling Chronic
hypertension is another Iorm oI hypertension It usuallyexists beIore pregnancy or may develop
beIore week 20 oI pregnancy Chronic hypertension with superimposed preeclampsia is another
Iorm oI chronic hypertension This syndrome occurs when a woman with pre-existing chronic
hypertension begins to have protein in the urine aIter week 20 oI pregnancy Late hypertension is
another Iorm oI high blood pressure It usually occurs aIter week20 oI pregnancy and is
unaccompanied by protein in the urine and does not progress the way preeclampsia-eclampsia
does
Preeclampsia is most common among women who have never given birth The disease is most
common in mothers under the age oI 20, or over the age oI 35 AIrican-American women have
higher rates oI preeclampsia than do Caucasian womenOther risk Iactors include poverty,
multiple pregnancies (twins, triplets, etc), pre-existing chronic hypertension, kidney disease,
diabetes, excess amniotic Iluid, and a condition oI the Ietus called nonimmune hydrops The
tendency to develop preeclampsia appears to run in Iamilies The daughters and sisters oI women
who have had preeclampsia are more likely to develop the condition
Experts are still trying to understand the exact causes oI preeclampsia and eclampsia It is
generally accepted that preeclampsia and eclampsia are problematic because these conditions
cause blood vessels to leak The eIIects are seen throughout the body When blood vessels leak
they allow Iluid to Ilow outinto the tissues oI the body The result is swelling in the hands, Ieet,
legs, arms, and Iace While many pregnant women experience swelling in their Ieet, and
sometimes in their hands, swelling oI the upper limbs and Iace is a sign oI a more serious
problem As Iluid is retained in these tissues, the woman may experience signiIicant weight gain
(two or more pounds per week)
Blood vessels also sometimes leak in the brain They can cause severe damagewithin the brain,
resulting in seizures or coma II the blood vessels in theeyes begin to leak the woman may
experience problems seeing, and may have blurry vision or may see spots Also, the retina may
become detached When bloodvessels in the lungs leak Iluid may leak into the tissues oI the
lungs, resulting in shortness oI breath
Leaky vessels within the liver may cause it to swell The liver may be involved in a serious
complication oI preeclampsia, called the HELLP syndrome In this syndrome, red blood cells are
abnormally destroyed, chemicals called liver enzymes are abnormally high, and cells involved in
the clotting oI blood (platelets) are low The small capillaries within the kidneys can leak
Normally, the Iiltration system within the kidney is too Iine to allow protein (which is relatively
large) to leave the bloodstream and enter the urine In preeclampsia, however, the leaky
capillaries allow protein to be dumped into the urine The development oI protein in the urine is
very serious, and oIten results in a low birth weight baby
In preeclampsia, the volume oI circulating blood is lower than normal becauseIluid is leaking
into other parts oI the body The heart tries to make up Ior this by pumping a larger quantity oI
blood with each contraction Blood vessels usually expand in diameter (dilate) in this situation to
decrease the work load on the heart In preeclampsia, however, the blood vessels are abnormally
constricted, causing the heart to work even harder to pump against the small diameters oI the
vessels This causes an increase in blood pressure
The most serious consequences oI preeclampsia and eclampsia include brain damage in the
mother due to brain swelling and oxygen deprivation during seizures Mothers can also suIIer
Irom blindness, kidney Iailure, liver rupture, andplacental abruption Babies born to preeclamptic
mothers are oIten smaller than normal, which makes them more susceptible to complications
during labor,delivery, and in early inIancy Babies oI preeclamptic mothers are also at risk oI
being born prematurely
Diagnosing preeclampsia may be accomplished by noting painless swelling oI the arms, legs,
and/or Iace, in addition to abnormal weight gain The patient'sblood pressure is taken during
every doctor's visit during pregnancy An increase oI 30 mm Hg in the systolic pressure, or 5
mm Hg in the diastolic pressure, or a blood pressure reading greater than 40/90 mm Hg is
considered indicative oI preeclampsia A simple laboratory test in the doctor's oIIice canindicate
the presence oI protein in a urine sample (a dipstick test)
With mild preeclampsia, treatment may be limited to bed rest, with careIul daily monitoring oI
weight, blood pressure, and urine protein via dipstick This careIul monitoring will be required
throughout pregnancy, labor, delivery,and even Ior 2-4 days aIter the baby has been born II the
diastolic pressuredoes not rise over 00 mm Hg prior to delivery, and no other symptoms
develop, the woman can continue pregnancy until the Ietus is mature enough to be delivered
saIely Ultrasound tests can be perIormed to monitor the health and development oI the Ietus
II the diastolic blood pressure continues to rise over 00 mm Hg, or iI othersymptoms like
headache, vision problems, abdominal pain, or blood abnormalities develop, then the patient may
require medications to prevent seizures Magnesium sulIate is commonly given through a needle
in a vein (intravenous, orIV) Medications that lower blood pressure (antihypertensive drugs) are
reserved Ior patients with very high diastolic pressures (over 0 mm Hg), because lowering the
blood pressure will decrease the amount oI blood reaching theIetus This places the Ietus at risk
Ior oxygen deprivation II preeclampsiaappears to be progressing toward true eclampsia, then
medications may be given in order to start labor Babies can usually be delivered vaginally AIter
the baby is delivered, the woman's blood pressure and other vital signs will usually begin to
return to normal quickly
The prognosis in preeeclampsia and eclampsia depends on how careIully a patient is monitored
Very careIul, consistent monitoring allows quick decisions to be made, and improves the
woman's prognosis Still, the most common causesoI death in pregnant women are related to
high blood pressure
About 33 oI all patients with preeclampsia will have the condition again with later
pregnancies Eclampsia occurs in about out oI every 200 women withpreeclampsia II not
treated, eclampsia is almost always Iatal
More inIormation on how preeclampsia and eclampsia develop is needed beIore
recommendations can be made on how to prevent these conditions Research is being done with
patients in high risk groups to see iI calcium supplementation,aspirin, or Iish oil supplementation
may help prevent preeclampsia Most importantly, it is clear that careIul monitoring during
pregnancy is necessary to diagnose preeclampsia early

http://wwwIaqsorg/health/topics/34/Pregnancy-induced-hypertensionhtml