Nulliparous pregnant women in their third trimester (25-36 weeks of gestation), attending Obstetrics and Gynecology Department, Chhatrapati Shivaji Subharti Hospital were enrolled and divided into study group (Pre-eclamptic) and control group (Normotensive with no proteinuria). Each group had 50 subjects. Clearance was obtained from the (IEC) and informed consent was obtained from every subject.

Patients with Diabetes Mellitus, Gestational Diabetes, Chronic hypertension (hypertension arising before 20 weeks gestation), Coronary artery disease, Hepatitis B infections, Human immunodeficiency virus (HIV) infection, Chronic obstructive pulmonary disease (COPD), Complicated and/or multiple pregnancies, women consuming antihypertensive medication, aspirin and / or corticosteroids, Undiagnosed patients and patients positive for urinary protein with urinary tract infection were not included in the study.

General information(s), detailed history, complete general and systemic examination and routine investigations were done in all subjects.

Sample was collected from the antecubital vein, aseptically through venipuncture. Hemolysed samples were discarded. Either the blood sample was immediately processed or stored in a fridge at 2-8°C. In some events the serum was separated, labeled and stored at -70°C. These samples were thawed prior to analysis.

PE was diagnosed as a blood pressure level ≥ 140/90 mm of Hg; confirmed by at least two blood pressure measurements six hours apart and proteinuria ≥2+ by dipstick in “clean-catch-midstream” random sample of urine, collected at the time of enrollment.

Lipid profile including TC, TG, HDL-c, LDL-c, VLDL-c and Serum uric acid levels were investigated in all the subjects.

The serum was processed in Vitros-250 auto analyser using readymade dry chemistry kits procured from Ortho-Clinical Diagnostics, Johnson & Johnson, USA. Internal and external quality controls were followed as per NABL accreditation program. Levi-Jenning Plot was fed in Vitros 250 auto analyser and strictly followed. Samples giving readings above or below two SD were reprocessed / discarded.

All the data recorded was compiled and statistically analysed by using Mean, Standard deviation and Students t-test.

The present study was conducted on 100 nulliparous pregnant women in their third trimester between the ages 18 to 35 years; 50 were patients of PE in study group and 50 normotensive non-pre-eclamptic women in control group. PE was diagnosed on the basis of history, clinical examination, blood pressure findings and presence of proteinuria. Subjects were distributed as; between 18-26 and 27-35 years.

In the study group 43 (86%) were in the age group 18-26 years and 7 (14%) were between 27-35 years of age while in the control group distribution of subject was 46 (92%) and 4 (8%) respectively.

Results and observations are given in [Table/Fig-1,2,3,4,5and6].

Definition of PE has changed with time. The initial international classification and definition of the hypertensive disorders of pregnancy compiled by Davey et al., defined it to be having a diastolic blood pressure of 90 mm Hg on two occasions, or 110 mm Hg on a single occasion [9].

In PE the glomerular barrier is certainly altered and there is an increased excretion of protein including albumin. When total protein excreted (TPE) exceeds 1 g/24 hours or 1+ by dipstick, tubular protein reabsorption will be saturated and individual proteins excretion rates will be related to their molecular weights (Davison) [10].

We selected nullipara women for the present study as nulliparity is not only have high risk of PE but is the most common maternal risk factor which can easily be assessed just by the history. Duckitt et al., concluded in their study that nulliparity is not only the most common maternal risk factor but it has been shown to almost triple the risk of PE [11].

It was found that TC, LDL-c and VLDL-c levels in the study group as a whole and in the patients between 18-26 years were statistically significant at p<0.01 level of significance; while HDL-c levels were found raised in all the three subgroups in patients of PE compared to normotensive pregnant women and were found to be statistically significant only in patients between 27-35 years.

It was also observed that TG and uric acid levels were found raised in all the three subgroups in patients of PE as compared to normotensive pregnant women and that these levels in all the three study groups were statistically significant.

Wladimiroff et al., [12] and Cleusen et al., [13] obtained similar findings for lipid profile in pre-eclamtic and normotensive pregnancies.

Increased levels of TG with reduced HDL-C have been observed in our study. Enquobahrie et al., [14] and Gractacose et al., [15]; in their respective studies concluded that hypertriglyceridemia is probably a consequence of competition between chylomicrons and very low-density lipoprotein (VLDL) cholesterol for the lipoprotein lipase.

The principle modulator of this hypertriglyceridemia is oestrogen as pregnancy is associated with hyperoestrogenaemia. Oestrogen induces hepatic biosynthesis of endogenous TG which is carried by VLDL [16]. This process may be modulated by hyper insulinism found in pregnancy [17]. Serum TG concentration increases much more significantly in pre-eclamptic pregnancy. Our study also corroborated with the findings of Equobohrie et al., [14] and Cekmen et al., [18].

The above mentioned interactions along with increased endothelial TG accumulation may result in endothelial cell dysfunction [19]. Increased TG found in pregnancy induced hypertension including PE, 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 generation of small dense LDL [20].

In the present study, serum VLDL-c level was also significantly higher (p < 0.01) in the third trimester of pre-eclamptic pregnancy which is probably due to hypertriglyceridemia leading to enhanced entry of VLDL that carries endogenous TG into circulation. VLDL levels were also found increased in pre-eclamptic in the studies conducted by Kokio et al., and Teichmann et al., this is probably due to increased VLDL lipoproteins which accumulate over the maternal vascular endothelium, particularly those of uterine and renal vessels. The VLDL–c level as reported by some researchers might increases upto 2.5 folds at term over the pre-pregnancy level [21,22].

A significant higher level of LDL-c level, as was found in the present study, was also reported by Grratacos et al. and wakatsuki et al., in third trimester of pre-eclamptic pregnancy, may be attributed to hyperestrogenacmia [23].

Lipid metabolism is altered during pregnancy and is characterised by normal or even low cholesterol during early pregnancy and hypertriglyceridaemia in late pregnancy. The anabolic phase of early pregnancy produces metabolic changes that encourage lipogenesis and fat storage in preparation for the catabolic phase of late pregnancy in which there is rapid fetal growth. The insulin resistance of pregnancy increases lipolyis in adipose tissue, leading to an enhanced flux of fatty acids to the liver. This promotes the synthesis of VLDLs and as a result, increased TG concentrations. In addition, insulin resistance reduces the activity of lipoprotein lipase an insulin dependent enzyme that is responsible for VLDL clearance from plasma. Therefore, VLDL remains in the plasma for longer and ultimately leads to accumulation of low density lipoprotein (LDL) [24].

In the past, uric acid was only considered as being the cause of gout; however, it is now increasingly thought of as a factor that can alter endothelial cell function. Hence, interest has been renewed in uric acid as a possible initiator of the maternal response in PE, rather than it being just a ‘bystander’ marker of the disorder. Over the past 10–20 years, a number of biochemical markers have been proposed to predict which women will develop preeclampsia. These markers include human chorionic gonadotropin, α-fetoprotein, urinary calcium, antiphospholipid antibodies, urinary kallikrein and homocysteine. In the past 5–10 years, additional factors, such as soluble endoglin, P1GF and cellular fibronectin have also been proposed as biomarkers for PE [25].These markers were identified based on the pathophysiological abnormalities associated with PE, including placental dysfunction, endothelial and coagulation activation and systemic inflammation. However, data regarding the reliability of these markers as predictors of the development of PE have been inconsistent, as most markers lack the specificity and sensitivity needed for routine clinical use [26].

It was observed from the present study that uric acid levels were not only found raised in all the three subgroups in patients of PE as compared to normotensive pregnant women but they were highly significant also. Lilliana Susanana et al., have made similar observations of higher levels of uric acid in serum of patients of PE which were statistically significant in their study which compared these levels in essential hypertensives, normal and pre-eclamptic women during pregnancy in their third trimester [27].

Serum uric acid is one of the parameters used in early diagnosis of preeclampsia. An elevated level of uric acid reflects the degree of placental cell destruction as well as severity of preeclampsia [28].This may lead to decrease in the renal tubular excretion. Altered renal handling of urate clearance may be due to renal dysfunction and increased xanthine oxidase activity. Thus hyperuricemia in PE is primarily due to decreased renal clearance and increased tubular reabsorption of uric acid, because of the reduction in glomerular filtration rate [29,30].

AC Martin et al., concluded that increased uric acid concentrations may be part of the pathogenesis of the clinical syndrome rather than a marker of PE. Alternatively, production of uric acid might increase in pre-eclamptic women as part of an appropriate response to inflammation. The known role of uric acid as a scavenger of oxygen free radicals supports this theory [31].

Uric acid has important role in vascular damage and oxidative stress. Hyperuricemia may also reflect impaired endothelial integrity and contribute to the pathogenesis of PE. Hence, early estimation of serum uric acid might reduce systemic complications and maternal deaths due to PE [28].

1. Sample should be drawn serially at definite intervals in third trimester and tested for lipid profile and uric acid levels.

2. A group including normal healthy non-pregnant women in same age should also be included in the study and their levels of lipid profile and uric acid be compared with the existing two groups.

Total cholesterol, LDL-c, VLDL-c, TG and uric acid levels were raised in pre-eclamptic and statistically significant; while HDL-c levels were raised in these patients but statistically non-significant, it can be concluded that there exists an association in lipid profile and uric acid with pre-eclamptic therefore dyslipidemia and raised uric acid levels are the features of pre-eclamptic in nullipara pregnant women in their third trimester.