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IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 20
Original Research Article
EVALUATION OF SERUM LEVELS OF FASTING LIPID PROFILE
IN PRE-ECLAMPTIC WOMEN
Wuraola Serah Nnaemeka1
, Olisekodiaka2
, MJ, Onuegbu2
, AJ, Ezeugwunne1
, IP,
Maduka, IG1
, Suru, SM1
and Johnkennedy Nnodim3
1. Department of Human Biochemistry, College of Health Sciences, Nnamdi Azikiwe University,
Nnewi, Nigeria.
2. Department of Chemical Pathology, College of Health Sciences, Nnamdi Azikiwe University, Nnewi,
Nigeria.
3. Department of Medical Laboratory Science, Imo State University Owerri, Nigeria.
Corresponding author: Wuraola Serah Nnaemeka , Technologist; Nnamdi Azikiwe University, Nnewi,
Nigeria.
Publication history: Received on 31/08/2017 Published on 25/09/2017
Article ID:IRO JMAS 107
Copyright © 2017 Wuraola Serah Nnaemekaet al. This is an open access article distributed under the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract:
Objectives: This study was designed to evaluate the role of lipid profile alteration in the development of pre-eclampsia.
Methodology: A total of 35 pre-eclamptic subjects (20-40weeks gestation age) aged between 18-40years participated in this
study. For comparative assessment 34 aged matched healthy pregnant women with same gestational age was used as control.
Serum lipid profile (total cholesterol, triglyceride, HDL-C, LDL-C, and VLDL-C) of the subjects respectively were
monitored.Result: The serum TG concentration increased significantly (0.95±0.53 to 0.77± 0.33 p<0.05).Conclusion: Lipid
metabolism plays a vital role in the pathophysiology of pre-eclampsia. Increased TG levels and triglyceride clearance and
high blood pressure are associated with the development of pre-eclampsia.
Keywords: Pre-eclampsia(PE), High Density Lipoprotein-Cholesterol (HDL-C), Low Density Lipoprotein cholesterol
(LDL-C), Very Low Density Lipoprotein-Cholesterol (LDL-C), Triglycerides (TG), Total Cholesterol (TC).
INTRODUCTION
Complications of pre-eclampsia remain a major cause of maternal morbidity and mortality especially in
developing countries (1). Pre-eclampsia is characterized by hypertension,proteinuria,and oedema(2).
Pre-eclampsia most commonly occurs during the last trimester of pregnancy. The risk of developing
pre-eclampsia appears to be greater in women who have family history of essential hypertension and
there may also be a relationship between risk of pre-eclampsia and the metabolic syndrome (2). Pre-
eclampsia is a medical condition which affects virtually all maternal organ systems (5). Despite
considerable research, the cause or causes of pre-eclampsia remain unclear and there are no clinically
useful screening tests to identify women in whom it will develop (4).Early pregnancy dyslipidaemia is
associated with an increased risk of PE(5). Women with a history of PE have significant differences in
lipid parameters and an increased susceptibility to lipoprotein oxidation when compared with women
who had normal pregnancy . Disorders of lipoprotein metabolism are reported to be a major cause of
hypertension and proteinuria in PE (6), (2). This present study was designed to ascertain/investigate the
alteration in lipid profile in normal and pre-eclamptic women.
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IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 21
MATERIALS AND METHODS
The study was approved by the Nnamdi Azikiwe University Teaching Hospital(NAUTH) ethics
committee. A total of 69 participants were selected from the ante-natal clinic and pre-natal wards
(obstetrics and gynaecology) of NAUTH Nnewi, Anambra State Nigeria. These subjects were divided
into two groups
(a)35 pre-eclamptic subjects (pre-eclampsia was defined as the occurrence after 20 weeks of gestation, a
diastolic Bp> 90mmHg systolic Bp> 140mmHg more than two occasions at least 4hours apart, and
proteinuria of 0.3g/l or more in a 24hour urine collection period) (mean age 28.29±5.3)
(b) 34 Normotensive pregnant women as controls of matching age (mean age 26.29±4.9). None was
known to have chronic hypertension or any renal /other metabolic disease.
Fasting blood specimens were collected from all control and pre-eclamptic subjects. Blood was always
collected before onset of labor. Serum was separated for analysis.
Serum total cholesterol (mmol/l): Serum total cholesterol was determined after enzymatic hydrolysis
and oxidation, indicator quinoneimine is formed from hydrogen peroxide and 4-aminoantipyrine in the
presence of phenol and peroxidase. (7)
Triglycerides (mmol/l): Triglycerides were determined after enzymatic hydrolysis with lipases. The
indicator was a quinoneimine formed from hydrogen peroxide, 4-amino-phenazone and 4-chlorophenol
under the catalytic influence of preoxidase.
HDL-cholesterol (mmol/l): Cholesterol in chylomicron, very low density lipoproteins, and low density
lipoproteins are precipitated by adding phosphotungistic acid and magnesium ions to form the sample.
Centrifugation leaves only the HDL in the supernatant while the cholesterol content was determined
enzymatically. (7) Body Mass Index was calculated by dividing body weight (kg) by square of height
(meters).
LDL-cholesterol (mmol/l) and VLDL-cholesterol (mmol/l): were determined using friedewald’s and
colleagues formulae (1972).
LDL-C=TC-(VLDL+HDL) and VLDL-C=TG/2.
Statistical Analysis: Mean and standard deviation were calculated for both pre-eclaptic and control
groups. Level of significance between control and pre-eclamptic were analyzed using student’s t test.
Data are presented as mean± standard deviation. Pvalue <0.01 was considered statically significant.
RESULTS.
TABLE 1: ANTHROPOMETRIC AND BLOOD PRESSURE DATA (MEAN±SD) OF PRE-
ECLAMPTIC AND NORMOTENSIVE SUBJECTS.
PARAMETERS PRE-ECLAMPSIA
n=35
CONTROL
n=34
t-TEST P-Value
AGE(Yr) 28.29±5.8 26.29±4.9 1.54 0.127
SBP(mmHg) 158.3±3.8 117.94±6.4 31.86 <0.001*
DBP(mmHg) 106.0±8.1 80.29±7.4 13.75 <0.001*
BMI(Kgm2
) 27.23±3.9 26.62±3.8 0.66 0.514
PULSE
PRESSURE(mmHg)
52.29±8.77 37.65±9.39 6.69 <0.001*
MEAN ARTERIAL
PRESSURE(mmHg)
123.43±5.63 92.84±5.51 22.79 <0.001*
*P < 0.01 significant as compared to normal and control.
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IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 22
TABLE 2: LIPID PROFILE DATA(MEAN±SD) OF PRE-ECLAMPTIC AND
NORMOTENSIVE SUBJECTS.
PARAMETERS PREECLAMPSIA
n=35
CONTROL
n=34
t-Test P-Value
TG (mmol/l) 0.95±0.53 0.77±0.33 1.64 0.03*
TC (mmol/l) 4.81±1.44 5.04±1.35 -0.71 0.48
HDL-C (mmol/l) 1.48 ±0.42 1.56± 0.33 -0.80 0.26
LDL-C (mmol/l) 2.42± 1.27 2.68± 1.20 -0.86 0.64
VLDL-C
(mmol/l)
0.40± 0.21 0.35± 0.15 1.25 0.11
* P< 0.05 significant as compared to normal and control.
Mean Triglyceride (0.95±0.53 vs 0.77±0.33) levels are significantly higher in the pre-eclamptic group
compare to the control group (P< 0.05) as shown in table 2 while mean HDL-C (1.48 ±0.42 vs 1.56±
0.33), Total cholesterol (4.81±1.44 vs 5.04±1.35), LDL-C (2.42± 1.27 vs 2.68± 1.20) and VLDL-C
(0.40± 0.21 vs 0.35± 0.15) levels were not statistically different between pre-eclamptic and normal
subjects as shown in table 2.
DISCUSSION.
In this study we investigated the role and relationship between lipid profile and the incidence of pre-
eclampsia.There was a positive correlation between pre-eclampsia and lipid parameters as shown in
table 2.
We observed higher levels of triglycerides during pre-eclampsia which provide evidence of abnormal
lipid metabolism. Pre-eclampsia is characteristically associated with hypertriglyceridemia. Higher levels
of triglycerides with high blood pressure have been observed in our study as shown in table 1 and 2.
These types of higher results also have been reported in other studies in pre-eclamptic women (5, 6, 8-
11).
During the course of normal pregnancy, plasma triglyceride and cholesterol concentrations rise and as
pregnancy progresses both become normal. Hormonal variations during pregnancy affect lipid
metabolism. The endogenous female sex hormones have significant effect on serum lipids (11). During
pregnancy there is an increase in the hepatic lipase activity and decrease in lipoprotein lipase activity.
Hepatic lipase isresponsible for the increased synthesis of the triglycerides at the hepatic level, whereas
the decreased activity of lipoprotein lipase is responsible for the decreased catabolism at the adipose
tissue level, the net effect of which will be an increase in circulating triglycerides and the second step
uptake of the remnant chylomicrons by the liver is delayed so it leads to accumulation of triglycerides in
serum as observed during the present studyshown in table 2.
Another hypothesis is that hypertriglyceridemia is probably as a result of the competition between
chylomicrons and VLDL-C for lipoprotein lipase. Classically chylomicron clearance occurs in two
sequential steps (1) triglycerides hydrolysis by lipoprotein lipase (2) uptake of the remnant by the liver.
Delay in the second step leads to accumulation of remnants in plasma and is generally thought to
represent the atherogenic risk of hypertriglyceridemia. The conclusion of another study also showed
that there exists a consistent positive relationship between elevated maternal TG and the risk of pre-
eclampsia. (12)
Summaringly, the findings reported in this article implies that women who developed pre-eclampsia had
altered lipid profile due to abnormal lipid metabolism. Elevated triglyceride levels, delayed triglycerides
clearance and high blood pressure are the reasons for the development of pre-eclampsia. This
association maybe significant in understanding the pathophysiology process of pre-eclampsia and may
help in developing strategies for early detection, better prevention, treatment and management.
www.earthjournals.in
IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 23
REFERENCES.
1. Vanderjagt DJ, Patel RJ, Nafaty EJ, Melah GS, Crossey MJ, Glew RH.(2004) High density lipoprotein
andhomocysteine levels correlate inversely in pre-eclamptic women in northern Nigeria. Acta Obstet Gyneacol
Scand 83(6):536-542.
2. Packer CS.(2005) Biochemical markers and physiological parameters as indices for identifying patients at risk of
developing pre-eclampsia J Hypertens 23(1) 45-46.
3. Tariq M, Rehmani H, Tayyab M, Kammal F, Yasmeen N, Sultan F. (2000) Clinico pathological study of pre-
eclampsia. Biomedica 16:60-65.
4. Caren G, Solomon, Seely EW. (2004) Pre-eclampsia searching for cause. New Eng J Med 350(7):641-642.
5. Enquobahrie DA, Williams MA,Butler CL, Fredrick IO, Miller RS, Luthy DA. (2004) maternal plasma lipid
concentration in early pregnancy and risk of pre-eclampsia.Am J Hypertens 17(7):574-581.
6. Gractacose E, Casals E, Gomez O,Llurba E, Mercader I, Carach V.(2003) Increased Susceptibility to low density
lipoprotein oxidation in women with a history of pre-eclampsia. Br J Obstet Gynaecol 110(4):400-404.
7. Study Group, European Atherosclerosis Society. (1987) Strategies for the prevention of coronary heart disease: A
policy statement of European Atherosclerosis society. Euro Heart J 1987:8:77-88.
8. Winkler K, Wetzka B, Hoffmann MM, Friedrich I, Kinner M, Baumstark MW (2003) Triglyceride rich
lipoproteins are associated with hypertension in pre-eclampsia J Clin Endor Metab 88(3):162-1166.
9. Toescu V, Nuttall SI, Martin U, Nightingale P, Kendal MJ, Brydon P, et al.(2004) Changes in plasma lipids and
markers of oxidative stress in normal pregnancy and pregnancy complicated by diabetes.Clin Sci 106(1):93-98.
10. Ray JG, Diamond P, Singh G, Bell CM. (2006) Brief Overview of maternal triglycerides as a risk factor for pre-
eclampsia. Br J Obstet Gynaecol 113(4):379-386.
11. Patrizia B, Giancarlo T, Franca E, Loreta P, Salvatore D,Mario M (1999) Lipoprotein metabolism during normal
pregnancy. Am J Obstet Gynaecol 181(2):430-434.
12. Rubina A, Tabassum M.(2006) Pak J Med Sci 23(5): 751-754.

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Iroijmas107

  • 1. www.earthjournals.in IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 20 Original Research Article EVALUATION OF SERUM LEVELS OF FASTING LIPID PROFILE IN PRE-ECLAMPTIC WOMEN Wuraola Serah Nnaemeka1 , Olisekodiaka2 , MJ, Onuegbu2 , AJ, Ezeugwunne1 , IP, Maduka, IG1 , Suru, SM1 and Johnkennedy Nnodim3 1. Department of Human Biochemistry, College of Health Sciences, Nnamdi Azikiwe University, Nnewi, Nigeria. 2. Department of Chemical Pathology, College of Health Sciences, Nnamdi Azikiwe University, Nnewi, Nigeria. 3. Department of Medical Laboratory Science, Imo State University Owerri, Nigeria. Corresponding author: Wuraola Serah Nnaemeka , Technologist; Nnamdi Azikiwe University, Nnewi, Nigeria. Publication history: Received on 31/08/2017 Published on 25/09/2017 Article ID:IRO JMAS 107 Copyright © 2017 Wuraola Serah Nnaemekaet al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract: Objectives: This study was designed to evaluate the role of lipid profile alteration in the development of pre-eclampsia. Methodology: A total of 35 pre-eclamptic subjects (20-40weeks gestation age) aged between 18-40years participated in this study. For comparative assessment 34 aged matched healthy pregnant women with same gestational age was used as control. Serum lipid profile (total cholesterol, triglyceride, HDL-C, LDL-C, and VLDL-C) of the subjects respectively were monitored.Result: The serum TG concentration increased significantly (0.95±0.53 to 0.77± 0.33 p<0.05).Conclusion: Lipid metabolism plays a vital role in the pathophysiology of pre-eclampsia. Increased TG levels and triglyceride clearance and high blood pressure are associated with the development of pre-eclampsia. Keywords: Pre-eclampsia(PE), High Density Lipoprotein-Cholesterol (HDL-C), Low Density Lipoprotein cholesterol (LDL-C), Very Low Density Lipoprotein-Cholesterol (LDL-C), Triglycerides (TG), Total Cholesterol (TC). INTRODUCTION Complications of pre-eclampsia remain a major cause of maternal morbidity and mortality especially in developing countries (1). Pre-eclampsia is characterized by hypertension,proteinuria,and oedema(2). Pre-eclampsia most commonly occurs during the last trimester of pregnancy. The risk of developing pre-eclampsia appears to be greater in women who have family history of essential hypertension and there may also be a relationship between risk of pre-eclampsia and the metabolic syndrome (2). Pre- eclampsia is a medical condition which affects virtually all maternal organ systems (5). Despite considerable research, the cause or causes of pre-eclampsia remain unclear and there are no clinically useful screening tests to identify women in whom it will develop (4).Early pregnancy dyslipidaemia is associated with an increased risk of PE(5). Women with a history of PE have significant differences in lipid parameters and an increased susceptibility to lipoprotein oxidation when compared with women who had normal pregnancy . Disorders of lipoprotein metabolism are reported to be a major cause of hypertension and proteinuria in PE (6), (2). This present study was designed to ascertain/investigate the alteration in lipid profile in normal and pre-eclamptic women.
  • 2. www.earthjournals.in IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 21 MATERIALS AND METHODS The study was approved by the Nnamdi Azikiwe University Teaching Hospital(NAUTH) ethics committee. A total of 69 participants were selected from the ante-natal clinic and pre-natal wards (obstetrics and gynaecology) of NAUTH Nnewi, Anambra State Nigeria. These subjects were divided into two groups (a)35 pre-eclamptic subjects (pre-eclampsia was defined as the occurrence after 20 weeks of gestation, a diastolic Bp> 90mmHg systolic Bp> 140mmHg more than two occasions at least 4hours apart, and proteinuria of 0.3g/l or more in a 24hour urine collection period) (mean age 28.29±5.3) (b) 34 Normotensive pregnant women as controls of matching age (mean age 26.29±4.9). None was known to have chronic hypertension or any renal /other metabolic disease. Fasting blood specimens were collected from all control and pre-eclamptic subjects. Blood was always collected before onset of labor. Serum was separated for analysis. Serum total cholesterol (mmol/l): Serum total cholesterol was determined after enzymatic hydrolysis and oxidation, indicator quinoneimine is formed from hydrogen peroxide and 4-aminoantipyrine in the presence of phenol and peroxidase. (7) Triglycerides (mmol/l): Triglycerides were determined after enzymatic hydrolysis with lipases. The indicator was a quinoneimine formed from hydrogen peroxide, 4-amino-phenazone and 4-chlorophenol under the catalytic influence of preoxidase. HDL-cholesterol (mmol/l): Cholesterol in chylomicron, very low density lipoproteins, and low density lipoproteins are precipitated by adding phosphotungistic acid and magnesium ions to form the sample. Centrifugation leaves only the HDL in the supernatant while the cholesterol content was determined enzymatically. (7) Body Mass Index was calculated by dividing body weight (kg) by square of height (meters). LDL-cholesterol (mmol/l) and VLDL-cholesterol (mmol/l): were determined using friedewald’s and colleagues formulae (1972). LDL-C=TC-(VLDL+HDL) and VLDL-C=TG/2. Statistical Analysis: Mean and standard deviation were calculated for both pre-eclaptic and control groups. Level of significance between control and pre-eclamptic were analyzed using student’s t test. Data are presented as mean± standard deviation. Pvalue <0.01 was considered statically significant. RESULTS. TABLE 1: ANTHROPOMETRIC AND BLOOD PRESSURE DATA (MEAN±SD) OF PRE- ECLAMPTIC AND NORMOTENSIVE SUBJECTS. PARAMETERS PRE-ECLAMPSIA n=35 CONTROL n=34 t-TEST P-Value AGE(Yr) 28.29±5.8 26.29±4.9 1.54 0.127 SBP(mmHg) 158.3±3.8 117.94±6.4 31.86 <0.001* DBP(mmHg) 106.0±8.1 80.29±7.4 13.75 <0.001* BMI(Kgm2 ) 27.23±3.9 26.62±3.8 0.66 0.514 PULSE PRESSURE(mmHg) 52.29±8.77 37.65±9.39 6.69 <0.001* MEAN ARTERIAL PRESSURE(mmHg) 123.43±5.63 92.84±5.51 22.79 <0.001* *P < 0.01 significant as compared to normal and control.
  • 3. www.earthjournals.in IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 22 TABLE 2: LIPID PROFILE DATA(MEAN±SD) OF PRE-ECLAMPTIC AND NORMOTENSIVE SUBJECTS. PARAMETERS PREECLAMPSIA n=35 CONTROL n=34 t-Test P-Value TG (mmol/l) 0.95±0.53 0.77±0.33 1.64 0.03* TC (mmol/l) 4.81±1.44 5.04±1.35 -0.71 0.48 HDL-C (mmol/l) 1.48 ±0.42 1.56± 0.33 -0.80 0.26 LDL-C (mmol/l) 2.42± 1.27 2.68± 1.20 -0.86 0.64 VLDL-C (mmol/l) 0.40± 0.21 0.35± 0.15 1.25 0.11 * P< 0.05 significant as compared to normal and control. Mean Triglyceride (0.95±0.53 vs 0.77±0.33) levels are significantly higher in the pre-eclamptic group compare to the control group (P< 0.05) as shown in table 2 while mean HDL-C (1.48 ±0.42 vs 1.56± 0.33), Total cholesterol (4.81±1.44 vs 5.04±1.35), LDL-C (2.42± 1.27 vs 2.68± 1.20) and VLDL-C (0.40± 0.21 vs 0.35± 0.15) levels were not statistically different between pre-eclamptic and normal subjects as shown in table 2. DISCUSSION. In this study we investigated the role and relationship between lipid profile and the incidence of pre- eclampsia.There was a positive correlation between pre-eclampsia and lipid parameters as shown in table 2. We observed higher levels of triglycerides during pre-eclampsia which provide evidence of abnormal lipid metabolism. Pre-eclampsia is characteristically associated with hypertriglyceridemia. Higher levels of triglycerides with high blood pressure have been observed in our study as shown in table 1 and 2. These types of higher results also have been reported in other studies in pre-eclamptic women (5, 6, 8- 11). During the course of normal pregnancy, plasma triglyceride and cholesterol concentrations rise and as pregnancy progresses both become normal. Hormonal variations during pregnancy affect lipid metabolism. The endogenous female sex hormones have significant effect on serum lipids (11). During pregnancy there is an increase in the hepatic lipase activity and decrease in lipoprotein lipase activity. Hepatic lipase isresponsible for the increased synthesis of the triglycerides at the hepatic level, whereas the decreased activity of lipoprotein lipase is responsible for the decreased catabolism at the adipose tissue level, the net effect of which will be an increase in circulating triglycerides and the second step uptake of the remnant chylomicrons by the liver is delayed so it leads to accumulation of triglycerides in serum as observed during the present studyshown in table 2. Another hypothesis is that hypertriglyceridemia is probably as a result of the competition between chylomicrons and VLDL-C for lipoprotein lipase. Classically chylomicron clearance occurs in two sequential steps (1) triglycerides hydrolysis by lipoprotein lipase (2) uptake of the remnant by the liver. Delay in the second step leads to accumulation of remnants in plasma and is generally thought to represent the atherogenic risk of hypertriglyceridemia. The conclusion of another study also showed that there exists a consistent positive relationship between elevated maternal TG and the risk of pre- eclampsia. (12) Summaringly, the findings reported in this article implies that women who developed pre-eclampsia had altered lipid profile due to abnormal lipid metabolism. Elevated triglyceride levels, delayed triglycerides clearance and high blood pressure are the reasons for the development of pre-eclampsia. This association maybe significant in understanding the pathophysiology process of pre-eclampsia and may help in developing strategies for early detection, better prevention, treatment and management.
  • 4. www.earthjournals.in IRO INTER. J. MED. APPLIED SCI./ Vol.1 /Issue 1/2018 Page 23 REFERENCES. 1. Vanderjagt DJ, Patel RJ, Nafaty EJ, Melah GS, Crossey MJ, Glew RH.(2004) High density lipoprotein andhomocysteine levels correlate inversely in pre-eclamptic women in northern Nigeria. Acta Obstet Gyneacol Scand 83(6):536-542. 2. Packer CS.(2005) Biochemical markers and physiological parameters as indices for identifying patients at risk of developing pre-eclampsia J Hypertens 23(1) 45-46. 3. Tariq M, Rehmani H, Tayyab M, Kammal F, Yasmeen N, Sultan F. (2000) Clinico pathological study of pre- eclampsia. Biomedica 16:60-65. 4. Caren G, Solomon, Seely EW. (2004) Pre-eclampsia searching for cause. New Eng J Med 350(7):641-642. 5. Enquobahrie DA, Williams MA,Butler CL, Fredrick IO, Miller RS, Luthy DA. (2004) maternal plasma lipid concentration in early pregnancy and risk of pre-eclampsia.Am J Hypertens 17(7):574-581. 6. Gractacose E, Casals E, Gomez O,Llurba E, Mercader I, Carach V.(2003) Increased Susceptibility to low density lipoprotein oxidation in women with a history of pre-eclampsia. Br J Obstet Gynaecol 110(4):400-404. 7. Study Group, European Atherosclerosis Society. (1987) Strategies for the prevention of coronary heart disease: A policy statement of European Atherosclerosis society. Euro Heart J 1987:8:77-88. 8. Winkler K, Wetzka B, Hoffmann MM, Friedrich I, Kinner M, Baumstark MW (2003) Triglyceride rich lipoproteins are associated with hypertension in pre-eclampsia J Clin Endor Metab 88(3):162-1166. 9. Toescu V, Nuttall SI, Martin U, Nightingale P, Kendal MJ, Brydon P, et al.(2004) Changes in plasma lipids and markers of oxidative stress in normal pregnancy and pregnancy complicated by diabetes.Clin Sci 106(1):93-98. 10. Ray JG, Diamond P, Singh G, Bell CM. (2006) Brief Overview of maternal triglycerides as a risk factor for pre- eclampsia. Br J Obstet Gynaecol 113(4):379-386. 11. Patrizia B, Giancarlo T, Franca E, Loreta P, Salvatore D,Mario M (1999) Lipoprotein metabolism during normal pregnancy. Am J Obstet Gynaecol 181(2):430-434. 12. Rubina A, Tabassum M.(2006) Pak J Med Sci 23(5): 751-754.