|Year : 2018 | Volume
| Issue : 2 | Page : 83-86
A comparative study of serum lipid profile of women with preeclampsia and normotensive pregnancy
Shreya Yadav, Manjusha Agrawal, Chela Hariharan, Deepika Dewani, Kavita Vadera, Nilay Krishna
Department of Obstetrics and Gynaecology, JNMC, DMIMS (Deemed to be University) Sawangi (Meghe), Wardha, Maharashtra, India
|Date of Web Publication||23-Nov-2018|
Dr. Shreya Yadav
Radhikabai Girls Hostel, DMIMS, Sawangi (Meghe), Wardha, Maharashtra
Source of Support: None, Conflict of Interest: None
Introduction: Preeclampsia is associated with substantial risks for the fetus and the mother. Women with preeclampsia have a significant difference in lipid parameters compared to normal pregnancy. The association of serum lipid profile with gestational proteinuric hypertension is highly suggested to reflect a new diagnostic tool. Materials and Methods: The present study is a prospective case–control comparative study done over a period of 2 years, i.e., from October 2015 to July 2017. The study takes into account 100 normotensive pregnant women (control group) and 100 pre-eclamptic women (study group) in their third trimester of pregnancy. Serum total cholesterol (TC), triglycerides (TGs), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-C (HDL-C), and very LDL-C (VLDL-C) were estimated in both groups. Aims: The study aims to analyze the lipid profile in normotensive pregnant patients, to analyze the lipid profile in pregnancy-induced hypertension patients, and to investigate the alteration in lipid profile in both groups. Results: There was a significant rise in serum TC, TGs, LDL-C, VLDL-C, and a significant decrease in HDL-C in the study group as compared to controls. Conclusion: Altered lipid profile also has a potential role in the genesis of endothelial dysfunction and expression of preeclampsia. Early detection of these lipid parameters may help pregnant patients by preventing maternal and fetal complications in preeclampsia and is going to aid in better management of preeclampsia.
Keywords: Dyslipidemia, high, lipid profile, low-density lipoprotein, preeclampsia, total cholesterol, triglyceride density lipoprotein, very low-density lipoprotein
|How to cite this article:|
Yadav S, Agrawal M, Hariharan C, Dewani D, Vadera K, Krishna N. A comparative study of serum lipid profile of women with preeclampsia and normotensive pregnancy. J Datta Meghe Inst Med Sci Univ 2018;13:83-6
|How to cite this URL:|
Yadav S, Agrawal M, Hariharan C, Dewani D, Vadera K, Krishna N. A comparative study of serum lipid profile of women with preeclampsia and normotensive pregnancy. J Datta Meghe Inst Med Sci Univ [serial online] 2018 [cited 2019 Aug 22];13:83-6. Available from: http://www.journaldmims.com/text.asp?2018/13/2/83/246015
| Introduction|| |
Preeclampsia is a common medical complication of pregnancy. In India, the incidence of preeclampsia is reported to be 8%–10% of all the pregnancies. It leads significantly to maternal and fetal mortality and morbidity. Preeclampsia is a multisystem disorder characterized by hypertension to the extent of 140/90 mmHg or more, proteinuria (≥300 mg/day) and edema induced by pregnancy after the 20th week. Without any intervention, it progresses to eclampsia, which is characterized by malignant hypertension and epileptiform convulsions requiring emergency cesarean section.
Association of alteration of serum lipid profile in essential hypertension is well documented. Abnormal lipid profile is strongly associated with atherosclerotic cardiovascular diseases and has a direct effect on endothelial dysfunction. Most important feature in toxemia of pregnancy is hypertension which is supposed to be due to the vasospastic phenomenon in the kidney, uterus, placenta, and brain. Altered lipid synthesis leads to decrease in PGI: TxA2 ratio which is also supposed to be an important way of pathogenesis in pregnancy-induced hypertension (PIH).
Hence, abnormal lipid metabolism seems important in the pathogenesis of PIH. Moreover, the association of serum lipid profile with gestational proteinuric hypertension is highly suggested to reflect some new diagnostic tools. Early pregnancy dyslipidemia is associated with an increased risk of preeclampsia. Moreover, the hormonal imbalance is a prime factor for the etiopathogenesis of PIH, and this endocrinal imbalance is well reflected in the alteration of serum lipid profile.
Thus, simple measurement of serum lipid parameters may be of good predictive value in toxemia of pregnancy, avoiding the costly endocrinal investigations [Table 1].
| Materials and Methods|| |
The present study was carried out in the Department of Obstetrics and Gynecology, Acharya Vinoba Bhave Rural Hospital, Sawangi Meghe, Wardha, in Maharashtra. Duration of the study was from October 2015 to July 2017 (2 years). It is a prospective case–control comparative study. A study comprised 100 normotensive pregnant women as controls and 100 preeclampsia cases as study groups attending antenatal outpatient department or getting admitted in their third trimester of pregnancy. Informed consent was taken from all individuals included in the study. The diagnosis of preeclampsia was based on the definition of the American College of Obstetrics and Gynecologists as follows: (1) systolic blood pressure >140 mmHg or a rise of at least 30 mmHg or (2) diastolic blood pressure >90 mmHg or a rise of at least 15 mmHg (manifested on two occasions at least 6 h apart) and (3) proteinuria of 300 mg or greater in 24-h urine collection or protein concentration of 1 g/L (on two occasions of at least 6 h apart).
Inclusion criteria for controls
Gravid women, normotensive pregnant patient in their third trimester (gestational age of >32 weeks), single live singleton pregnancy, cases without any other systemic or endocrine disorder, and body mass index (BMI) ≤25 were included in the study.
For cases – gravid women, preeclamptic pregnant patient in the third trimester (gestational age of >32 weeks), single, live singleton pregnancy, cases without any other systemic or endocrine disorder, and BMI ≤25 were included in the study.
Diabetes mellitus with or without treatment, obesity, severe anemia (hemoglobin <6 g%), or individuals suffering from any other systemic or endocrine disorder, BMI >25, patients with <32 weeks of gestation, and multiple pregnancy BMI >25 were excluded from the study.
Blood samples (5 ml) were collected by venipuncture and analyzed for serum triglycerides (TGs), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-C (LDL-C), and very LDL-C (VLDL-C) by the following methods.
The data collection was continuously recorded in a predefined format in spreadsheet (MS Excel 2007, Microsoft Inc., Redmond, Washington, USA). Statistical analysis was done using Chi-square test and Student's t-test at 95% confidence interval to correctly ascertain the clinical applicability of the present study.
Observation tables and groups of various parameters are tabulated as follows: serum TC [Table 2], serum HDL-C [Table 3], serum LDL-C [Table 4], serum VLDL-C [Table 5], and serum TC [Table 6].
|Table 2: Total cholesterol levels in normotensive and preeclamptic pregnant women expressed as (mg/dl)|
Click here to view
|Table 3: High-density lipoprotein cholesterol levels in normotensive and preeclamptic pregnant women expressed as (mg/dl)|
Click here to view
|Table 4: Low-density lipoprotein cholesterol levels in normotensive and preeclamptic pregnant women expressed as (mg/dl)|
Click here to view
|Table 5: Very low-density lipoprotein cholesterol levels in normotensive and preeclamptic pregnant women expressed as (mg/dl)|
Click here to view
|Table 6: Triglyceride levels in normotensive and preeclamptic pregnant women expressed as (mg/dl)|
Click here to view
| Results|| |
The results with regard to the changes in lipid profile in both group are represented in [Table 2],[Table 3],[Table 4],[Table 5],[Table 6].
- As shown in [Table 2]: TC level in both group as follows: control group (normotensive group) 149.94 ± 34.54 (mg%) and in the study group (preeclamptic group) 221.92 ± 34.54 (mg%). The study group (preeclamptic group) showed significant rise with P < 0.01
- From [Table 3]: HDL-C level was found to be 59.32 ± 13.01 (mg%) in the control group (normotensive) and in the study group (preeclamptic) 32.93 ± 5.79 (mg%). The HDL-C was found to be marginally lowered (P < 0.01) in the study group
- It is evident from [Table 4] that the mean LDL-C was found to be 59.92 ± 37.29 (mg%) in normotensive group and 137.10 ± 29.05 (mg%) in the study group (preeclamptic). The LDL showed a significant rise with P < 0.01
- [Table 5] reveals VLDL-C level as 30.70 ± 5.73 (mg%) in normotensive (control) group and 51.19 ± 13.12 (mg%) in study (preeclamptic) group. The increase in VLDL-C in preeclamptic group was found to be highly significant with P < 0.001
- The mean TGs was found to be 151.61 ± 28.23 (mg%) in control (normotensive) group and 255.68 ± 65.17 (mg%) in study (preeclamptic) group. The increase level of TG in preeclamptic group was found to be highly significant (P < 0.001) as compared to normotensive group is shown as in [Table 6].
| Discussion|| |
Preeclampsia still remains as one of the most serious complications of pregnancy and the pathophysiology of the disease is not clearly understood. The possible involvement of genetic and immune mechanism in the etiology of preeclampsia has been increasingly attracting attention. Damage from free radicals has been implicated in many pathological conditions, and the activity of free radicals may increase during pregnancy and preeclampsia.
In this study, we observed an association between maternal dyslipidemia, particularly hypertriglyceridemia and the subsequent risk of preeclampsia. Pregnant women who had preeclampsia had increased TC, LDL-C, VLDL-C, and decreased HDL-C concentrations as compared with pregnant women who were normotensive.
In the study conducted by Vani et al., it was seen that the association of TC, HDL, VLDL, and TG level among normal and PIH cases is statistically significant (P < 0.05). Similar findings were seen in the study conducted by Nagtilak. Elevated plasma lipid levels are believed to be the probable cause of endothelial cell dysfunction. In the endothelial cell, oxidative stress is stimulated by linoleic acid. During pregnancy, serum lipoprotein levels increase considerably and are two times higher in PIH. Alterations that take place during pregnancy include insulin resistance, hyperlipidemia, and upregulation of inflammatory markers.
The present study also showed rise in serum TGs which was statistically significant (P < 0.001) in study patients when compared to women with normotensive pregnancy. The major modulator of this hypertriglyceridemia is estrogen as pregnancy is linked with hyperestrogenemia. Hypertriglyceridemia may be linked to hypercoagulability.
The present study also showed that the study group had 44.48% lower value of HDL-C over patients of normotensive (control) pregnancy which is consistent with study done by Mishra et al. Statistically, the difference was highly significant (P < 0.001). Estrogen is responsible for induction of TGs and HDL and inhibition of serum LDL and estrogen level falls in PIH. Low levels of HDL in PIH are not only because of hypoestrogenemia but also are due to insulin resistance.
In the current study, serum VLDL levels were significantly (P < 0.001) high in the study group which may be due to hypertriglyceridemia leading to increased entry of VLDL that carries the endogenous TGs into the circulation. Similar results were seen in the study done by Vani et al.
| Conclusion|| |
On the basis of findings of the present study, thus, we can conclude that in the third trimester of pregnancy, preeclamptic women have altered levels of serum lipid profile when compared to normotensive pregnant women. Hence, early detection of these parameters is going to aid in better management of preeclampsia cases which is important to improve the maternal and fetal outcome.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Kamath SA. Hypertension in pregnancy. J Assoc Physicians India 2006;54:269-70.
Dutta DC. Hypertensive disorders in pregnancy. In: Konar H.L., editor. Textbook of Obstetrics. 5th
ed. Kolkata: New Central Book Agency; 2001. p. 234-55.
Packer CS. Biochemical markers and physiological parameters as indices for identifying patients at risk of developing pre-eclampsia. J Hypertens 2005;23:45-6.
Lindheimer MD, Cunningham FG, Roberts JM. Introduction, History, Controversies, and Definitions in Chesley's Hypertensive Disorders in Pregnancy. Amsterdam, Netherlands: Elsevier; 2009. p. 1-24.
Simmons LA, Gillin AG, Jeremy RW. Structural and functional changes in left ventricle during normotensive and preeclamptic pregnancy. Am J Physiol Heart Circ Physiol 2002;283:H1627-33.
Enquobahrie DA, Williams MA, Butler CL, Frederick IO, Miller RS, Luthy DA, et al.
Maternal plasma lipid concentrations in early pregnancy and risk of preeclampsia. Am J Hypertens 2004;17:574-81.
Yagi K. Assay for serum lipid peroxide level and its clinical significance. In: Lipid peroxides in biology andmedicine. New York: Academic Press, 1982:223-41.
Vani I, Gayathri A, Nagamani T, Sunieeta H. Lipid profile parameters in normal and preeclampsia complicating pregnancies – A prospective observational study. Am J Sci Med Res 2015;1:61-6.
Nagtilak S. The levels of serum lipid profile and free fatty acids in normotensive and preeclamptic pregnanat women in their third trimester pregnancy. Int J Basic Med Clin Res 2015;2:65-134.
Sattar N, Bendomir A, Berry C, Shepherd J, Greer IA, Packard CJ, et al.
Lipoprotein subfraction concentrations in preeclampsia: Pathogenic parallels to atherosclerosis. Obstet Gynecol 1997;89:403-8.
Kokia E, Barkai G, Reichman B, Segal P, Goldman B, Mashiach S, et al.
Maternal serum lipid profile in pregnancies complicated by hypertensive disorders. J Perinat Med 1990;18:473-8.
Mishra PK, Yadav MK, Yadav KP, Simlai S. Evaluation of Serum Uric Acid and Lipid Profile in Pre-eclamptic Women: A Hospital Based Study. J Med Sci and Clin Res 2016;4:11314-20.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]