INTRODUCTION

Nearly one tenth of all maternal deaths in Africa and Asia and one-quarter in Latin America are associated with hypertensive diseases in pregnancy, a category that encompasses pre-eclampsia.1Pre-eclampsia(PE) is a disorder of pregnancy characterized by high blood pressure and a large amount of protein in the urineand it is one of the leading causes of maternal and perinatal morbidity and mortality worldwide.2

 

	Corresponding author Ekiye ayinbuomwan (Consultant chemical pathologist fmcpath) Department of chemical pathology, University of Benin/ University of Benin Teaching Hospital, Benin city, Edo state. Email: ekiyeayinbuomwan@gmail.com

 

 

 

 

 

 

 

 

 

In pre-eclampsia, the systolic blood pressure is≥140mmHg, diastolic ≥90 mmHg and there is proteinuria of at least 300 mg in 24hour urine sample collection. According to the World Health Organization (WHO), the incidence of preeclampsia ranges from 2-10% of pregnancies worldwide with 1.8 – 16.7% occurring in developing countries while developed countries have a rate of 0.4%.In Nigeria, preeclampsia affects 37,000 women annually with a prevalence rate of 5.6% to 7.6% of pregnancies in Southern Nigeria.3,4,5  Onset of symptoms occur in the late second or third trimester, most commonly after the 32nd week. Some women will experience pre-eclampsia as early as 20weeks, though this is rare and it may also occur in the immediate postpartum period.6Women with mild proteinuria generally have no symptoms. However, women with severe pre-eclampsia (blood pressure ≥160/110 mmHg, proteinuria>2.5g/24h) may have symptoms such as renal insufficiency, liver diseases, haematological and neurological disturbances.2

During pregnancy, there is increased lipolysis and mobilization of triglyceride from adipocytes. Increased production of VLDL in combination with impaired lipoprotein lipase activity leads to ineffective clearance of triglyceride-rich lipoproteins such as VLDL and VLDL-remnants which eventually result in increased triglyceride levels.7 Hepatic lipase is responsible for the increased synthesis of  TGs whereas the decreased activity of lipoprotein lipase is responsible for decreased catabolism at the adipose tissue level, the net effect of which is increased circulating TGs.8 There is also accumulation of LDL due to decreased activity of lipoprotein lipase and LDL, total cholesterol and triglyceride levels increase from the second trimester until the third trimester with increasedrisk of development of atherosclerosis.9,10

The prevalence of maternal obesity is rising in some antenatal clinics, in line with the prevalence of obesity in the general population with its attendant complications such as gestational diabetes mellitus (GDM), chronic hypertension and preeclampsia.11Obesity is considered a risk factor for preeclampsia and there are many  mechanisms that link  obesity with a higher risk of developing preeclampsia; such as increased level of proinflammatory cytokines and leptin.12,13It has been described that leptin reduces cytotrophoblast proliferation. One of the early alterations observed in preeclampsia is poor cytotrophoblast proliferation.12,14The increasing prevalence of maternal obesity worldwide is therefore a major challenge in the care of pregnant women from preconception to postpartum. In this study, we intend to assess the relationship between lipid profile and obesity in women with preeclampsia.

 

MATERIAL AND METHODS

The subjects were registered pre-eclamptic ante-natal clinic (ANC) patients of the Obstetrics and Gynaecology Department of Government Specialist Hospital, Benin City, Edo State, Nigeria. The control subjects were non-pre-eclamptic ANC patients and analbuminuric hypertensive pregnant patients of the same Department and within the same age range. Patients were considered hypertensive when blood pressure (BP)>140/90 mmHg.

Sample size was 196 calculated from the Cochran’s formula (Cochran, 1977).15 Before carrying out the study, ethical clearance was obtained from the research and Ethics Committee of the Ministry of Health, Benin City, Edo State, Nigeria. Verbal informed consent was obtained from all participants. Structured questionnaires were administered to the study groups and used to document their personal data, medical history, social, obstetric and family history. A physical examination was carried out to measure their blood pressure. Fresh Urine samples were collected into sterile bottles in the hospital under supervision. The urine was used for urinalysisusing dipstick to determine those with proteinuria. Blood samples were collected from the antecubutal veins following routine aseptic procedure using a 10ml syringe and dispensed into plain specimen bottles for lipid profile. Samples were centrifuged at 3,000 revolutions/min after allowing the sample to stand for 30 minutes to clot. The serum was harvested with clean pasteur pipettes and stored at 2 - 8oC and analyzed within 48hrs.Total cholesterol (TC) and triglyceride (TG) were analyzed using the enzymatic endpoint method described by Roeschlau et. al.16high density lipoprotein (HDL-C) was analysed using the precipitation method described by Roeschlau et. al16 while thelow density lipoprotein (LDL-C) was estimated from the Friedewald’s Equation.17

Data was collected and entered into a proforma and analyzed using Statistical package for social science (SPSS) version 16.0. The means and standard deviations of the age, BMI, gestational age and lipid profile were calculated. The Pearson correlation was used in calculating the correlations between any two variables. Univariate analysis were presented as frequencies while bivariate or multivariate analysis were presented as means and standard error of means. The level of statistical significance was set at a p-value of < 0.05 for all tests of statistical significance. Data presentation, tables and charts were done using Microsoft Office.

 

RESULTS

A total of 196 respondents consisting of 124 pre-eclamptics (PE), 36 normotensive pregnant women (NPW) and 36 analbuminuric hypertensive pregnant women (AHPW) participated in this study. Most of the PE (44%) and Normotensive pregnant women (41.7%) were in the age bracket of 31-35 years while most of the analbuminuric hypertensive pregnant women (40%) were in the age range of 36-40 years (Fig 1). Amongst the PE 39(31.5%) were mild while 85 (68.5%) had severe PE based on a BP> 160/110mmHg(Fig.2).

The results revealed a significant(P<0.05) higher BMI in PE(33.35±0.75Kg/m2) when compared with NPW(26.57±0.66Kg/m2) and AHPW (24.84±1.26Kg/m2. Majority 71 (57.30%) of PE were overweight and obese (30{24.2%}) while most of the NPW 18(50%) and AHPW 23 (63.9%) were of normal weight. The mean indexsystolic and diastolic blood pressures were found to be significantly (p< 0.05) higher in PE (160.24±9.34mmHg and 108.56±8.02mmHg) than in NPW (106.00±11.23mmHg and 63.38±4.32mmHg) and AHPW (141.38±14.21mmHg and 98.21±4.94mmHg).  (Table 1&2)

The mean TC,TG and LDL-C were significantly (P<0.05) increased in PE (228.44±3.39mg/dl,154.73±3.96mg/dl and 146.17±2.85mg/dl) and AHPW (192.13±21.21mg/dl, 134.51±12.62mg/dl and 141.23±10.25mg/dl) when compared with NPW(179.53±5.97mg/dl, 122.92±5.52mg/dl and 116.83±5.48mg/dl) However mean HDL-C was significantly (p < 0.05) lower in PE (38.54±0.61mg/dl) and AHPW(35.63±8.05mg/dl than in NPW (45.61±1.32mg/dl). (Table 3)

TC and TG were significantly (P<0.05) increased inthe 2ndtrimester inPE (205.76 ± 5.23 mg/dl, and 176.03 ± 6.20 mg/dl,) and AHPW (190.57 ±11.23mg/dl and 165.65±9.44mg/dl) than in NPW (159.44±9.15mg/dl and 113.63±9.16mg/dl)and also in the 3rdtimester(PE: 211.13±4.63mg/dl and 193.43±4.97mg/dl, AHPW: 202.82±10.13mg/dl and 180.94±11.75mg/dl, NPW: 173.82±8.02mg/dl and 130.35±6.12mg/dl). There was also a significant (p < 0.05) increase in TG in the 3rd than in the 2nd trimesters within the PE and AHPW. LDL-C was significantly (P<0.05) higher in PE(145.86±3.76mg/dl and 157.56±4.29mg/dl) and AHPW(130.38±11.42mg/dl and 141.06±10.93mg/dl) than NPW(105.74±0.81mg/dl and 113.40±7.50mg/dl) in the 2nd and 3rd trimester while HDL-C was significantly (P<0.05) lower in PE(38.44±0.91mg/dl) and AHPW(33.98±7.55mg/dl) than NPW(45.67±1.17mg/dl) in the 3rd trimester. (Table 4)

Mean serum LDL-C and TG were significantly (P<0.05) higher in severe (155.61±5.10mg/dl and 160.72±5.20mg/dl) than in mild (142.79±3.43mg/dl and 147.39±5.60mg/dl) PE. LDL-C and TC levels were found to be non-significantly (P<0.05)higher amongst the Obese (150.51±6.55mg/dl and 214.46±7.25mg/dl) and overweight (145.73±3.29mg/dl and 208.69±4.26mg/dl) than in the normal weight (141.96±7.81mg/dl and 203.26±8.69). In the pre-eclamptics, plasma HDL was found to be non-significantly (P<0.05) higher in the normal weight (37.05 1.43mg/dl) than in the overweight (35.46±0.78mg/dl) and Obese (33.85±1.31mg/dl) while mean plasma TG was found to be relatively the same amongst the three groups of pre-eclamptics. (Table 5 & 6)

DISCUSSION

Preeclampsia is one of the most common medical complications during pregnancy with unknown etiology. It is however, characterized by vasoconstriction, metabolic changes, endothelial dysfunction and activation of the coagulation cascade in conjunction with an inflammatory response.18 In Nigeria, PE has a prevalence rate of 5.6% and it is associated with maternal and fetal morbidity and mortality worldwide.19,20

We observed a significantly higher concentration of triglyceride in PE than in the NPW and AHPW which was also reported by Enquobahrie et al21, Cekmen et al22 and Phalak and Tilak23 in their studies of lipid profile in preeclampsia in India. Normal pregnancy results in physiologic hyperlipidemia with an increase in triglyceride and cholesterol due to hyperestrogenemia which induces hepatic biosynthesis of lipids.7,24Insulin resistance  during pregnancy, leads to increased influx of fatty acids to the liver promoting the synthesis of VLDL with increased TG concentration.25 There is also an increase in hepatic lipase activity which increases the synthesis of TG in the liver with associated decrease in the activity of lipoprotein lipase leading to decreased catabolism of adipose tissue. The net effect is an increase in serum TG level.8 In preeclampsia, there is an additional alteration in blood lipids reflecting disordered lipid and lipoprotein metabolism. The release of free fatty acids and apolipoprotein-CIII from triglycerides promote oxidative stress and proatherogenic responses in macrophages and endothelial cells.26 VLDL remains in the plasma for a longer time due to a decreased activity of lipoprotein lipase leading to an increase in blood LDL-C and this is associated with development of atherosclerosis. A significant increase in LDL-C was seen in PE and AHPW when compared with NPW in this study. Studies by Gratacos et al and Cassandra et alsupport this finding.27,28Also, significantly increased serum total cholesterol in PE than in AHPW and NPW was observed in our study. Abnormal lipid metabolism is not a mere manifestation but is also involved in the pathogenesis of PE and hypercholesterolemia promotes the formation of free radicals which are also implicated in the pathogenesis of preeclampsia.29,30

A significantly decreased HDL-C was observed in PE and AHPW than in NPW. HDL-C was lower in the 3rd than in the 2nd trimester in PE and AHPW while the level remained the same in both trimesters in NPW. HDL-C also decreased with severity in PE. This finding is in accordance with studies by Adiga et aland Phalak and Tilak.29,23 According to Cekmenet al, low HDL-C in PE is due to insulin resistance while Bozkurt et al stated that there is a direct correlation between adipose tissue lipoprotein lipase activity and plasma HDL-C and this may be responsible for the observed low levels of HDL-C.22,25 Anuradha and Durga also reported significant increases in LDL-C and TC and no significant difference in HDL-C was observed between mild and severe PE.31Vidyabati et al observed that the clinical manifestations of PE preceeded dyslipidemia particularly, hypertriglyceridemia and elevated LDL.32 This indicates that hypertriglyceridemia and high LDL-C may contribute to the aetiologic and pathophysiologic mechanisms responsible for PE.

The association between lipid profile and BMI was not significant, suggesting that maternal lipid levels were independent of overweight or obesity status, similar to findings by Daniel et al.33However, we found that more of the preeclamptic women were obesewhen compared to the NPW and the AHPW.  Similarly, numerous studies have shown a strong correlation between an increased BMI and the risk of developing preeclampsia.34,35

 

CONCLUSION

Abnormal lipid metabolism particularly high triglyceride and LDL-C and obesity may contribute to oxidative stress and therefore the etiology of PE. Hence, weight control and lipid testing followed by appropriate management pre-conception and during pregnancy would improve the care of women with preeclampsia.

RECOMMENDATIONS

Routine estimation of serum lipids can be useful as a simple screening test to detect dyslipidemia in PE in order to reduce the incidence of complications. Despite the fact that weight loss is not recommended during pregnancy, weight loss should be recommended in women with obesity or overweight that are planning to get pregnant.

 

Source of support : nil

Conflict of interest : nil

 

REFERENCES

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4. Olaoye T, Oyerinde OO, Elebuji OJ, Ologun O. Knowledge, perspective and management of preeclampsia among health care providers in a maternity hospital. Int J MCH AIDS 2019;8:80-88.
5. Adeosun OG, Charles-Davies MA, Ogundahunsi OA, Ogunlewe J. Maternal and neonatal outcomeof preeclampsia in African black women. South West Nigeria. Greener J MedSci2015;7:45-51.
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8. Rubina A. and Tabassum, M. Pre-eclampsia and lipid profile. Pakistan Journal of Medical Sciences 2007;23(5): 751 – 754.
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11. Abraham T, Romani AMP. The Relationship between Obesity and Pre-Eclampsia: Incidental Risks and Identification of Potential Biomarkers for Pre-Eclampsis. Cells 2022;11(9):1548.
12. Spradley FT, Palei AC, Granger JP. Immune Mechanisms Linking Obesity and Preeclampsia.Biomolecules 2015;5:3142 – 3176.
13. Hendler I, Blackwell SC, Mehta SH, Whitty JE, Russell E, Sorokin Y, Cotton DB. The levels of Leptin, adiponectin, and resist in in normal weight, overweight, and obese pregnant women with and without preeclampsia. Am J Obst et Gynecol. 2005;193(3 Pt 2):979 – 983.
14. Liu H, Wu Y, Qiao F. et al. Effect of leptin on cytotrophoblast proliferation and invasion. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 2009;29:631 – 636.
15. Cochran W.G. Sampling Techniques. (3rd ed.), John Wiley and Sons 1997.  New York.
16. Rosechlau P, Bernt E. and Gruber, J.W. Determination of cholesterol in serum. Chemical Klino stat in Biochemistry 1974;12(5): 226
17. Friedwald WT, Levy RI. and Fredrickson DS. Estimation of the concentration of low density lipoprotein cholesterol without use of the preparative ultracentrifuge. Clinical Chemistry 1972; 18(16): 499 – 502.
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19. Onyiriuka AO. and Okolo, AA.Perinatal outcome in patients with pre-eclampsia in Benin City, Nigeria. Tropical Journal of Obstetrics and Gynecology 2004;21(2):148 – 152.
20. Centre for Maternal and Child Enquiries (CMACE).“Saving mothers lives: Reviewing Maternal Deaths to Make Motherhood Safer”, 2006 – 2008.  The Eight Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. Biological Journal of Obstetrics and Gynecology2011;118: 68 – 72.
21. Enquobahrrie DA, Williams MA, Butler CL, Frederick IO, Miller RS, Luthy DA. Maternal plasma lipid concentration in early pregnancy and risk of pre-eclampsia. American Journal of Hypertension 2004;17(7): 574 – 81.
22. Cekmen, MB,Erbagei AB, Balat A, Duman C, Moral H, Ergen, K., Ozden M. et al. Plasma lipid and lipoprotein concentration in pregnancy induced hypertension. Clinical Biochemistry;2003;36(7): 575 – 578.
23. Phalak P. and Tilak M. Study of Lipid Profile in Pre-eclampsia. Indian Journal of Basic and Applied Medical Research2012;5(2):  405 – 409.
24. Nasioudis D, Doulaveris G, Kanninen TT. Dyslipidemia in pregnancy and maternal–fetal outcome. Minerva Ginecol. 2019;71(2): 155 – 162.
25. Bozkurt L, Gobl CS, Hormayer AT. The impact of preconceptional obesity on trajectories of maternal lipids during gestation. Sci Rep. 2016;20(6):29971.
26. Botham KM, Moore EH, Pascale D, Bejita F. The induction of macrophage foam cell formation by chylomicronremnants. BiochemSoc Trans. 2007;35(3):454 – 458.
27. Gratacos E, Casals E, Gomez O, Llurba E, Mercader I, Cararach V, Cabero, L. Increased susceptibility to low density lipoprotein oxidation in women with a history of pre-eclampsia. British Journal of Obstetrics and Gynecology 2003; 110(4): 400 – 404.
28. Cassandra NS, Caitlin JS, Audrey FS, Jennifer GR, Kelli KR. Maternal Hyperlipidemia and the Risk of Preeclampsia: a Meta-Analysis. Am J Epidemiol. 2014; 180(4): 346 – 358.
29. Gohil JT, Patel PK, Gupta P. Estimation of lipid profile in subjects of pre-eclampsia. Indian Journal of Obstetrics and Gynecology. 2011;61(4):399 – 403.
30. Adiga U,D’souzar V, Kamath A, Mangalore N. Antioxidant activity and lipid peroxidation in pre-eclampsia. Journal of Clinical Medical Association 2007;70(10): 435 – 438.
31. Anuradha R., Durga T. Estimation of lipid profile among preeclampsia women by comparing with normal pregnancy. International Journal of Contemporary Medical Research 2016;3(7):1958 – 1961.
32. Vidyabati RK,Hijam D, Singh NK. Singh WG. Serum BhCG and lipid profile in early second trimester as predictors of pregnancy induced hypertension. Indian Journal of Obstetrics and Gynecology 2010;60(1):44 – 50.
33. Daniel E, Michael F, Tina L, Grammata K, Ingo R, Guelen Y, Wolfgang E. et al. Association between maternal triglycerides and disturbed glucosa metabolism in pregnancy. Acta Diabetol 2021;58(4):459-465.
34. Fernańdez Alba JJ, Mesa Páez C, Vilar Sánchez Ā, Soto Pazos E, González Mucias MDC, Serrano Negro E. et al. Overweight and obesity at risk factors for hypertensives tatesofpregnancy: a retrospective cohortstudy. Nutr. Hosp. 2018;35: 874 – 880.
35. HutcheonJA, Stephansson O, Cnattingius S, Bodnar LM, Wikström AK, Johansson K. Pregnancy Weight Gain Before Diagnosis and Risk of Preeclampsia: A Population –Based Cohort Study in Nulliparous Women. Hypertension. 2018;72(2):433-441.

 

 

 

 

 

Fig 1:AGE GROUP DISTRIBUTION OF SUBJECTS

 

Values in parenthesis represent percentage distribution, while the bars on top of the histogram represent standard error.

KEY:

PE        Preeclampsia

NPW    Normotensive pregnant women

AHPW  Analbuminuric hypertensive pregnant women

Fig2: SEVERITY OF PRE-ECLAMPSIA

TABLE 1.          CLINICAL AND ANTHROPOMETRIC CHARACTERISTICS OF PE, NPW AND AHPW

Clinical/Anthropometric parameter	PE	NPW	AHPW
Booking SBP (mmHg)	136.03 ±23.01a	103.05 ± 12.60b	140.00 ± 25.52ac
Booking DBP (mmHg)	85.08 ± 1.46a	62.77 ± 7.01b	80.00 ± 5.16ac
Index SBP (mmHg)	160.24 ± 9.34a	106.00 ± 11.23b	141.38 ± 14.21cd
Index DBP (mmHg)	108.56 ± 8.02a	63.38 ± 4.32b	98.21 ± 4.94cd
BMI (kg/m2)	33.35 ± 0.75a	26.57 ± 0.66b	24.84 ± 1.26cb

Values are represented as Mean ± SEM

Values in the same row with different alphabets differ significantly (p<0.05)

Key:

 

SBP                  Systolic blood pressure          

DBP                 Diastolic blood pressure

BMI                 Body mass index                    

PE                    Pre-eclampsia

NPW    Normotensive pregnant women

AHPW  Analbuminuric hypertensive pregnant women

 

TABLE 2.          DISTRIBUTION OF PE, NPW AND AHPW SUBJECTS BASED ON BMI

BMI(kg/m2)	PE (n = 124)	NPW (n = 36)	AHPW (n = 36)
Normal weight  (18-24.9)	23 (18.50)	18 (50.00)	23 (63.90)
Overweight(25-29.9)	71 (57.30)	9 (25.00)	6 (16.70)
Obese                 (>30)	30 (24.20)	9 (25.00)	7 (19.40)
Total	124	36	36

Values in parenthesis represent percentages

Key:

BMI   Body mass index                                    PE        Pre-eclampsia

NPW    Normotensive pregnant women         AHPW  Analbuminuric hypertensive pregnant women

 

TABLE 3. LIPID PROFILE STATUS IN PE, NPW AND AHPW, SUBJECTS.

Analyte	PE (n = 124)	NPW (n = 36)	AHPW                  (n = 36)
Serum TC (mg/dl)	228.44 ± 3.39a	179.53 ± 5.97b	192.13 ± 21.21ac
Serum TG (mg/dl)	154.73 ± 3.96a	122.92 ± 5.52b	134.51 ± 12.62cb
Serum LDL-C (mg/dl) Serum HDL-C(mg/dl)	146.17 ± 2.85a 38.54 ±0.61a	116.83 ± 5.48b 45.61±1.32b	141.23 ± 10.25ac 35.63 ±8.05ac

Values are represented as mean ± SEM

 

Values in the same row with different alphabets differ significantly (p<0.05).

  keys: TC Total cholesterol, TG Triglyceride, LDL-C Low density lipoprotein cholesterol

HDL-C  High density lipoprotein cholesterol,   PE Pre-eclampsia,

NPW    Normotensive pregnant Women

AHPW   Analbuminuric hypertensive pregnant women

 

 

TABLE 4. LIPID PROFILEIN VARIOUS TRIMESTERS IN PE, NPW AND AHPW.          

Analytes	Trimester	PE n = 124	NPW n = 36	AHPW                   n  = 36
Serum TC (mg/dl)	2nd	205.76±5.23a	159.44±9.15b	190.57±11.23 cd
	3rd p-Value	211.13±4.36a 0.19	173.82±8.025b 0.03	202.82±10.13ac 0.07
Serum TG   (mg/ml)	2nd	176.03±6.20a	113.63±9.16b	165.65±9.44ac
	3rd p-Value	193.43±4.97a 0.04	130.35±6.12b 0.14	180.94±11.75cd 0.04
Serum LDL-C   (mg/dl)	2nd	145.86±3.76a	105.74±0.81a	130.38±11.42ac
	3rd p-Value	157.56±4.29a 0.52	113.40±7.50b 0.77	141.06±10.93ac 0.53
Serum HDL  (mg/dl)	2nd	42.65±2.79a	45.80±2.15b	43.07±8.33ac
	3rd p-Value	38.44±0.91a 0.62	45.67±1.17b 0.64	33.98±7.55cd 0.02

Values are represented as mean ± SEM

 

Values in the same row with different alphabets differ significantly (p < 0.05)

TC        Total cholesterol                                                      TG Triglyceride

LDL-C   Low density lipoprotein cholesterol               HDL –CHigh density cholesterol

NPW      Normotensive pregnant women

AHPWAnalbuminuric hypertensive pregnant women     PE   Pre-eclampsia

 

TABLE 5. LIPID PROFILE IN PE SUBJECTS AT DIFFERENT PHASES OF PE

Analyte	Mild (n=39)	Pre-eclamptics	Severe (n=85)
Serum TC  (mg/dl)	209.94 ±5.02a		207.27 ± 4.42a
Serum LDL-C (mg/dl)	142.79± 3.43a		155.61 ± 5.10b
Serum HDL-C (mg/dl) Serum TG (mg/dl)	38.28 ± 1.06a 147.39 ±5.60a		35.450 ± 0.73a 160.72±5.20b

Values are represented as mean ± SEM

Values in the same row with different alphabets differ significantly (p < 0.05)

TC                    Total cholesterol

TG                    Triglyceride

LDL-C               Low density lipoprotein cholesterol

HDL-C               High density cholesterol

PE                    Pre-eclampsia

NPW                Normotensive pregnant women

AHPW              Analbuminuric hypertensive pregnant women

 

TABLE 6. RELATIONSHIP BETWEEN BMI AND LIPID PROFILE IN PE

Analyte	Normal weight      N=23	BMI Overweight N=71	Obese                          N=30
Serum TC (mg/dl)	203.26 ± 8.69a	208.69±4.26a	214 ± 7.25a
Serum TG (mg/dl)	157.08 ±9.41a	157.00±4.99a	157.08 ± 9.4 a
Serum LDL-C(mg/dl) Serum HDL-C (mg/dl)	141.96 7.81a 37.05 ±1.43a	145.73±3.29a 35.46±0.78a	150.51± 6.55a 33.85±1.31a

Values are represented as mean ± SEM

Values in the same row with different alphabets differ significantly (p < 0.05)

TC        Total cholesterol

TG        Triglyceride

LDL-C   Low density lipoprotein cholesterol

HDL-C  High density cholesterol

PE        Pre-eclampsia

NPW    Normotensive pregnant women

AHPW  Analbuminuric hypertensive pregnant women