Study of Serum Lipid Profile and Magnesium in Normal Pregnancy and in Pre-Eclampsia: A Case Control Study
The aim was to evaluate changes in serum magnesium and lipid profile in pre-eclamptics, their correlation with each other and roles of these changes in its Pathophysiology. Serum magnesium levels were determined by Calmagite method and total lipid profile by enzymatic calorimetric method in healthy non pregnant women (Group-1), primigravidas with normal pregnancy (Group-2) and primigravidas with pre-eclampsia (Group-3). Results of Group-2 were compared with Group-1 and results of Group-3 were compared with Group-2. Compared with normal pregnancy, in pre-eclampsia the level of TG (Triglycerides) (p<0.0001) and VLDL-C (Very Low Density Lipoprotein Cholesterol) (p<0.0001), LDL-C (Low Density Lipoprotein Cholesterol) (p<0.012) were significantly increased and HDL-C (High Density Lipoprotein Cholesterol) (p<0.0001) and Mg++ (p<0.001) levels were decreased significantly. In normotensive pregnant women TG (p<0.0001) and VLDL-C (p<0.0001) and HDL-C (p<0.0001) levels were high and LDL-C (p<0.0001) level was low compared to healthy non pregnant women. No significant change could be observed in serum Mg++ in Group-2 as compared to Group-1 (p<0.2636). No significant change could be observed in total cholesterol level in any group. In addition serum TG correlated negatively(r = -0.47) with serum Magnesium in Pre-eclampsia. The inverse correlation between serum Mg++ and serum triglycerides in pre-eclampsia may suggest the role of magnesium in the pathogenesis of pre-eclampsia along with dyslipidemia. During pregnancy, detection of hypomagnesaemia and dyslipidemia early will prevent its metabolic complication and in established pre-eclamptic women it will help in better management of the disease.
January 17, 2011; Accepted: February 21, 2011;
Published: May 07, 2011
Hypertension, defined by a blood pressure (BP) of 140/90 mmHg or more, affects
up to 8-10% of pregnancies (Iribhogbe et al., 2011).
It includes a spectrum of conditions namely, Pre-eclampsia, Eclampsia, Pre-eclampsia
superimposed on chronic hypertension, chronic hypertension and gestational hypertension.
Unlike other hypertensive disorders in pregnancy, pre-eclampsia is a multisystem
disease. Its distinctive feature being the sudden onset of proteinuria (≥300
mg/24 h urine) (Roberts and Redman, 1993). Being a hypertensive
complication of pregnancy, it is associated with significant morbidity and mortality
for mother and baby (Walker, 2000; Brown
and Buddle, 1996). Eclampsia is a convulsive form of Pre-eclampsia that
affects 0.1% of all pregnancies. Chronic hypertension is diagnosed with BP readings
equal to or greater than 140/90 mmHg prior to pregnancy or before the 20th week
of gestation. It represents a major risk factor for pre-eclampsia, which affects
25% of these women, in contrast to 5% of women without preexisting hypertension
and otherwise normal pregnancies. Gestational hypertension refers to hypertension
occurring for the first time during the second half of pregnancy in the absence
of proteinuria. It includes women with pre-eclampsia who have not yet developed
proteinuria, those with hypertension only, and a subset of patients in whom
BP remains elevated after delivery, leading to the diagnosis of chronic hypertension.
Although the first two forms of gestational hypertension typically abate with
the termination of pregnancy, the third form may lead to chronic hypertension,
which is diagnosed when gestational hypertension persists beyond 12 weeks postpartum.
Although hypertension and proteinuria are the simple clinical criteria for
diagnosis of pre-eclampsia the pathophysiological mechanisms that lead to the
disorder are by all evidence very diverse (Ness and Roberts,
1996; Mushambi and Halligan, 1996). Pre-eclampsia
develops in a particular woman following an unfortunate combination of maternal
(trophoblast-independent) risk factors and an excessive maternal response to
the trophoblast/trophoblast-derived factors. The maternal risk factors include
disorders associated with endothelial dysfunction such as chronic hypertension,
diabetes, kidney disease and dyslipidemia. Some studies say that there is no
correlation between serum lipids in normal pregnancy and Pre-eclampsia (Ness
and Roberts, 1996; Redman et al., 1999; Punthumapol
and Kittichotpanich, 2008a).
Magnesium is the 4th most abundant cation in the body and is present in more
than 300 enzymatic systems where it is crucial for ATP metabolism (Byrd
and Roy, 2003). Magnesium may influence blood pressure by modulating vascular
tone and structure through its effects on myriad biochemical reactions that
control vascular contraction/dilation, growth/apoptosis, differentiation and
inflammation. Magnesium acts as a calcium channel antagonist. It stimulates
production of vasodilator prostacyclins and nitric oxide and alters vascular
responses to vasoconstrictor agents. Its deficiency can also play a role in
hypertension of pregnancy (Yogi et al., 2011).
Regarding Mg there are lots of contrast studies. Some studies do not support
the hypothesis that low serum magnesium is a risk factor for developing hypertension
and vascular dysfunction, whereas very few findings support the hypothesis that
hypomagnesaemia is one of possible etiologies of pre-eclampsia (Khan
et al., 2010; Sukonpan and Phupong, 2005;
Punthumapol and Kittichotpanich, 2008b).
While maternal obesity, diabetes mellitus and chronic hypertension are each
probable risk factors for Pre-eclampsia, less is known about the relationship
between other conditions such as dyslipidemia, hypomagnesaemia and the risk
of pre-eclampsia (O Brien et al., 2003;
Bryson et al., 2003; Ros et al., 1998;
Rey and Couturier, 1994).
So the aim of present study was to evaluate the risk of pre-eclampsia in association with maternal lipids and to find out whether hypomagnesaemia is associated with hypertension of pregnancy. We also found out whether there was any correlation between hypomagnesaemia and dyslipidemia.
MATERIALS AND METHODS
Three groups of women were recruited for the study. First group (G1) comprised
25 healthy non-pregnant women taken as controls. Second group (G2) comprised
of 20 age and gestational age matched normotensive pregnant women and third
group (G3) consisted of 20 pre-eclamptic women who were selected after admission
to Obstetrics and Gynecology department, J.L.N. Government Medical College,
Ajmer. This research was conducted from 21 June 2010 to 10 November 2010. Pre-eclampsia
was defined as development of blood pressure >140/90 mm Hg after 20 weeks
gestation and proteinuria of ≥300 mg as confirmed by 24 h urine collection
in women with no known history of hypertension, renal disease, endocrine abnormalities
and had single pregnancy and had no family history of lipid or carbohydrate
disorders (Lampinen et al., 2008).
The Pre-eclamptic women had an average blood pressure at admission of 157±4/103±2 mm Hg as measured by standard mercury sphygmomanometer and urinary protein averaged 1.8±0.3 g day-1.
Normotensive non-pregnant and normotensive pregnant women were carefully matched for age with the pre-eclamptic group and had average blood pressure of 116±2/71±2 mm Hg. The women included in the study were 25 to 35 years old. Women with concomitant disease such as diabetes or a history of gestational diabetes, chronic hypertension, and kidney disease or coagulation disorders were excluded. All pregnant women were in the third trimester of pregnancy.
All women gave informed consent to participate in the study, which was approved by the locally appointed ethics committee.
Blood samples were collected from anticubital vein by aseptic techniques following
a fast of 12 h for the analysis of lipids (total cholesterol, low density lipoproteins,
high-density lipoproteins, and triglycerides) and magnesium. Serum Total Cholesterol
was measured by using CHOD-PAP method (Allain et al.,
). Serum triglyceride was measured by using GPO-POD enzymatic colorimetric
method (Bucolo and David, 1973
). Serum HDL-Cholesterol
was measured by using Phosphotungestic acid method (Assmann
et al., 1983
). VLDL-C and LDL-C were calculated according to Friedwald
W.T.s equation. Serum magnesium level was measured by using Calmagite method
The values of laboratory parameters are presented as the Mean±SD. A
Students unpaired t-test was used for cross sectional comparisons of continuous
variables between the 2 groups. The association between lipid parameters and
magnesium level was analyzed by means correlation test. The correlation coefficient
was obtained by the method of least squares. To determine correlation between
quantitative variables, Pearson's coefficient of determination was used. For
this purpose, Pearson Correlation (v1.0.3) in Free Statistics Software (v1.1.23-r6)
was used (Wessa, 2008). The results were considered statistically
significant when the probability of the null hypothesis was less than at least
5% (p<0.05). The main statistical comparisons were performed between healthy
non-pregnant and healthy pregnant women, between healthy pregnant women and
Women with an uncomplicated course of pregnancy were investigated during routine
check-ups in the third trimester of pregnancy. The gestational age at blood
sampling in Pre-eclamptic women (Group 3) was (33±0.8 week).
|| Comparison of biochemical parameters in Healthy non pregnant
women and Normotensive pregnant women
|Values are as Mean±SD. ***Significant at p<0.001,
**Significant at p<0.01, *Significant at p<0.0, (a: Significant, p<0.001),
(c: Not significant, p>0.05)
|| Comparison of biochemical parameters in Normotensive pregnant
women and Pre-eclamptic women
|Values are as Mean±SD. ***Significant at p<0.001,
**Significant at p<0.01, *Significant at p<0.05, (a: Significant,
p<0.001) (b: Significant, p< 0.05)
|| Pearsons coefficient of determination between serum
Mg++ and lipid profile parameters in Pre-eclamptic women
|*Significant at p<0.05
This matches the gestational age (32±1 week) of normotensive pregnant
women (Group 2). In this study we compared the level of various serum lipid
parameters and serum magnesium of normotensive pregnant women with the lipid
parameters and serum magnesium of healthy non-pregnant women. We also compared
the Pre-eclamptic women with normotensive pregnant women for the same parameters.
Mean fasting total cholesterol level in Group 1 (Healthy non pregnant women) was 211.88±11.00 and in Group 2 (Normotensive pregnant women) it was 218.1±16.45. No significant alteration in total cholesterol level could be observed in Group 2 compared to Group 1 (Table 1).
Mean serum Triglyceride (TG) concentration was significantly increased (p<0.0001)
in Group 2 (Normotensive pregnant women, 215.3±27.32) compared with Group
1 (Healthy non pregnant women, 117.28±12.13), the mean value being raised
almost two folds. Mean serum VLDL-C level also rose significantly (p<0.0001)
in normal pregnancy (43.06±5.46) in comparison to healthy non-pregnant
||Scatter plot showing single values of serum Mg++
in healthy non pregnant women (n = 25) normotensive pregnant women (n =
20) and Pre-eclamptic women (n = 20)
We observed significant decrease in LDL-C (p<0.0001) in normotensive pregnant
women (115.56±12.02) compared to healthy non pregnant women (140.46±14.79).
In this study we found that the mean value of HDL-C was about 25% higher in
the third trimester of normal pregnancy (59.47±8.54) over the non pregnant
healthy women (47.96±9.25) and the alteration was statistically significant
(p<0.0001). No significant fall (p<0.2636) in serum Mg++ level
was found in normal pregnancy in comparison to healthy non pregnant women (Table
Mean fasting total cholesterol level in Group 2 (Normotensive pregnant women) was 218.1±16.45 and in Group 3 (Pre-eclamptic women) it was 236.8±35.32. No significant alteration in total cholesterol level could be observed in Group 3 compared to Group 2. Significant increase in mean serum TG concentration (p<0.0001) was found in Group 3 (Pre-eclamptic women, 275.7±38.35) in comparison to group 2 (normotensive pregnant women, 215.3±27.32). Significant increase in LDL-C (p<0.012) was observed in Pre-eclamptic women (135.71±32.20) compared to normotensive pregnant women (115.56±12.02). Significant decrease in HDL-C level (p<0.0001) was observed in Pre-eclamptic women (45.95±8.03) compared to the normotensive pregnant women (59.47±8.54).There was a significant fall (p<0.001) in serum Mg++level in Pre-eclamptic women (1.55±0.80) compared to the normotensive pregnant women (2.42±0.80) (Table 2).
Figure 1 shows the single values of serum Mg++ in healthy non pregnant women (n = 25) normotensive pregnant women (n = 20) and Pre-eclamptic women (n = 20).
The evaluation of correlation of serum Mg level with various lipid parameters in Pre-eclamptic women using linear correlation evaluation methods, showed converse linear statistically significant correlation between serum Mg level and TG level and VLDL levels (r = -0.47) (Fig. 2). No significant correlation could be observed between serum Mg level and other lipid parameters (Table 3).
||Graphical presentation of negative correlation between serum
magnesium and serum TG in Pre-eclamptic women
In present study we could not find any significant increase in total cholesterol
level in any of the groups. These findings are similar to some previous studies
(Sattar et al., 1997; Jayanta
et al., 2006). Sahu et al. (2009) observed
significant rise in the fasting triglycerides, total cholesterol and LDL-C levels
in PIH (p<0.0001) compared to pregnant women in their third trimester of
pregnancy. Osadolor et al. (2005) also observed
that there were significant increases in serum T-CHOL, (p<0.05), TG (p<0.01)
and LDL-C (p<0.05) in hypertensives relative to normotensive controls.
As described above, in present study significant increase in TG was observed
in both normotensive pregnant women and Pre-eclamptic women. Many other studies
showed the same results (Jayanta et al., 2006;
Chiang et al., 1995; Howlader et al.,
2007). But Turpin et al. (2008) in their study
found that serum Triglycerides level decreases in preeclampsia compared to normotensive
pregnant women. Significant modulators of lipoproteins during pregnancy include
insulin, oestrogen, lipoprotein lipase (LPL) (Silliman et
al., 1994). In some studies lowering of lipoprotein lipase (LPL) was
shown to increase serum TG level in normal pregnancy (Herrera
et al., 1988). Other studies have shown that the principle modulator
of this hypertriglyceridemia is oestrogen as pregnancy is associated with hyperoestrogenaemia.
Oestrogen inhibits the hepatic lipid oxidation so the net effect is increased
delivery of free fatty acids into hepatic biosynthesis of endogenous triglycerides
which is carried by VLDL (Jayanta et al., 2006;
Silliman et al., 1994; Alvarez
et al., 1996). However, hypertriglyceridemia in pre-eclampsia is
probably not due to hyperoestrogenaemia as the levels of oestrogen decrease
Some studies have concluded that hypertriglyceridemia may be modulated by hyperinsulinism
found in pregnancy (Adegoke et al., 2003). Insulin
resistance and resultant hyperinsulinemia are characteristic of normal pregnancy
and are maximal in the third trimester. This is probably mediated by several
hormonal changes, including elevations in levels of human placental lactogen;
progesterone, cortisol, and estradiol (Barbieri, 1999).
Many of markers, which correlate with insulin resistance likewise, vary over
the course of pregnancy. For example, levels of triglycerides, small dense LDL
particles, and free fatty acids increase as normal pregnancy and associated
insulin resistance progress (Belo et al., 2002).
In pregnancies complicated by hypertension, there appears to be an exaggeration
of insulin resistance and associated metabolic changes. In a report, Pre-eclamptic
women were more insulin resistant than normotensive controls, so in pre-eclampsia
TG level further increases due to the exaggeration of insulin resistance (Kaaja
et al., 1999). Increased TG, found in Pre-eclampsia, is likely to
be deposited in predisposed vessels, such as the uterine spiral arteries and
contributes to the endothelial dysfunction, both directly and indirectly through
increased generation of small, dense LDL (Sattar et al.,
1997). It was indicated that small dense LDL had a greater capacity to stimulate
thromboxane synthesis by endothelial cells thereby causing vasoconstriction
(Weisser et al., 1993). Small dense LDL are also
more susceptible to oxidative modifications forming peroxides which inhibit
EDRF (Endothelium Derived Relaxation Factor) and also leads to foam cell formation
of deciduas (Krauss, 1997; Pierucci
et al., 1996). Study by Uboh et al. (2008)
supports this hypothesis as they observed increased levels of free radical products
of lipid peroxidation (Malondialdehyde) in pre-eclamptic condition compared
to normotensive pregnant women and healthy non pregnant women. Oxidized LDL
also impairs endothelial function by expression of adhesion molecules, inhibition
of endothelial prostacyclin synthesis, increased endothelin production and release
and increased platelet aggregability (Vogel, 1999).
In present study we found that LDL-C level decreases in normal pregnancy which
can be explained by increased oestrogen levels in pregnancy. In pre-eclampsia
LDL-C level increased compared to normal pregnancy which can be due to decreased
level of oestrogen in pre-eclampsia (Bradley and Crook, 1995).
A significant increase in LDL-C in third trimester of gestational hypertensive
disorders was also reported in many studies (Gratacos et
al., 2003; Wakatsuki et al., 2000).
VLDL-C level increased in present study in both normal pregnancy and pre-eclampsia.
Same was reported in other studies. Another study concluded that VLDL-C level
might rise up to 2.5 folds at term over the pre-pregnancy level. It is due to
hypertriglyceridemia leading to enhanced entry of VLDL that carries endogenous
triglyceride into the blood circulation (Herrera et al.,
1988; Teichmann et al., 1988). We also found
that HDL-C level increases in normal pregnancy compared to non-pregnant women
and in pre-eclamptic women HDL-C levels decreases compared to normotensive pregnant
women. Other studies also reported lesser quantities of serum alpha lipoprotein
fraction in women with pre-eclampsia in the third trimester of pregnancy (Sattar
et al., 1997; Enquobahrie et al., 2004).
Whereas Turpin et al. (2008) in their study found
that serum HDL-C level increases in preeclampsia compared to normotensive pregnant
According to some studies oestrogen is responsible for induction of TG and
HDL and suppression of serum LDL (Krauss, 1997). So
in normotensive pregnant women the increase in HDL-C and decrease in LDL-C can
be explained by hyperoestrogenemia. In Pre-eclampsia the oestrogen level decreases
so reduced HDL-C and raised LDL-C levels may be due to hypoestrogenemia. This
reduced HDL-C level may also contribute to the reduced prostacyclin level seen
in pre-eclampsia (Kaaja et al., 1995). Lower
serum HDL-C level may also reduce antioxidative protection for other lipoproteins
(Mackness and Durrington, 1995).
In the present study, we were unable to find any differences in serum Mg++
in normotensive pregnant women compared with healthy non-pregnant women but
we found decreased serum Mg++ level in pre-eclamptic women compared
to both normotensive pregnant women and healthy non-pregnant women. In some
studies the serum magnesium in PIH decreased significantly (p<0.01) and the
decrease of magnesium concentration may be one of the important factors responsible
for the pathophysiological changes of PIH (Qi et al.,
1997; Borekci et al., 2009). But in some
studies there was no difference in serum magnesium among normal pregnancy and
Pre-eclampsia (Punthumapol and Kittichotpanich, 2008a;
Kumru et al., 2003).
According to one study, in normal pregnancy hemodilution effect of oestrogen
and increased demand of fetus decreases the serum magnesium level and in pre-eclampsia
urinary excretion of magnesium also increases so the level decreases further
(Kesteloot, 1984). Magnesium deficiency causes hemodynamic
abnormalities such as arterial wall thickening, abnormal vascular tone and endothelial
dysfunction which are due to alteration in the biology of cellular and non cellular
components of arterial wall. There may be a causal relationship between hypomagnesaemia
and pre-eclampsia since magnesium is involved in blood pressure regulation through
an intracellular inhibition of NO synthase in endothelial cells (Sanders
et al., 1999). In magnesium deficiency, the production of ATP and
ATP dependent sodium / potassium and calcium pump are also impaired, providing
another hypothesis to unify the clinical thinking about pre-eclampsia (Newman
and Amarasingham, 1993).
Previous studies mainly focused on separate study of lipid profile and magnesium
in pre-eclampsia. There are no studies on correlation of lipid profile and magnesium
in pregnancy induced hypertension. In a study, statistically significant inverse
correlation was observed between intralymphocyte free Mgi and plasma
triglycerides in essential hypertensive subjects (r = -0.521, P = 0.002) (Pietro
et al., 1996). This study focused on ionized Mgi in hypertensive
subjects rather than total Mg in hypertensive pregnant women, thus preventing
direct comparison with our data.
In present study we found statistically significant inverse correlation between
serum Mg and triglycerides in pre-eclamptic women (r = -0.47) who also had elevated
levels of LDL-C, TG, VLDL-C and low HDL-C. So we suggest that a low serum Mg
level might in some way be linked to dyslipidaemia thus explaining the pathogenesis
of pre-eclampsia. The relationship between total magnesium and plasma lipids,
although imperfectly understood, has been known for some time (Pietro
et al., 1996; Rayssiguier, 1986).
Due to insufficient data, we cannot account for the association between serum triglycerides and serum Mg++.
In a study, ischemic heart disease patients were treated with oral magnesium
for 3 months. Interestingly plasma triglycerides decreased in them (Rasmussen
et al., 1989).
In another study, hyperlipidemic patients of Frederickson types IV and IIb were supplemented with oral physiological magnesium in addition to the usual dietary measures.
It was found to reduce serum triglycerides (values, Mean±SD, decreased
from 198.17±47.01 to 163.20±40.55 mg dL-1, p<0.05)
(Kisters et al., 1993). Furthermore, an important
feature of hyperlipidemia associated with magnesium deficiency in experimental
animal models is the accumulation of triglyceride-rich lipoproteins (Altura
et al., 1990).
So we can hypothesize that intake of magnesium supplementation in pregnancy can improve the lipid status and decrease the risk of developing pre-eclampsia. In pre-eclampsia oral intake of magnesium supplementation can decrease the level of pathological lipids (mainly TG) and their role in the pathogenesis of pre-eclampsia. But further studies are needed to prove this hypothesis. If proven it will really be helpful to lower the incidents of this disease and early detection of these parameters is going to aid in better management of pre-eclampsia.
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