Hypertensive disorders of pregnancy, particularly pregnancy-induced hypertension (PIH), remain a significant cause of maternal and perinatal morbidity and mortality despite extensive research. PIH occurs in approximately 3–5% of pregnancies worldwide and contributes significantly to adverse outcomes, including preeclampsia, which affects 8–10% of pregnancies in India. The incidence is higher in primigravidae (10%) than in multigravidae (5%), suggesting that obstetric history plays a crucial role in the risk of developing PIH (1,2). Preeclampsia is a pregnancy-specific syndrome that affects multiple organ systems and is associated with abnormal vascular responses to placentation. This leads to increased systemic vascular resistance (SVR), platelet aggregation, activation of the coagulation system, and endothelial dysfunction, ultimately affecting the renal, hepatic, central nervous, and coagulation systems. The consequences of preeclampsia range from mild to life-threatening, with severe maternal complications such as convulsions, abruptio placentae, acute renal failure (ARF), cerebrovascular events, liver hemorrhage, and disseminated intravascular coagulation (DIC) (3,4). Similarly, infants born to preeclamptic mothers face a higher risk of preterm birth, growth retardation, thrombocytopenia, delayed adaptation, and other neonatal complications (4).

Despite advancements in technology and clinical research, the exact pathogenesis and prevention of PIH remain unclear, limiting the availability of rational preventive or therapeutic interventions. Early identification and individualization of cases are essential for improving outcomes, yet there is a lack of formulated guidelines for the management of PIH, particularly in low-resource settings. Maternal dyslipidemia in the early second trimester (12–24 weeks) has emerged as a potential non-invasive predictor of PIH (2,3). Abnormal lipid profiles, including elevated levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL), as well as altered TC/HDL and LDL/HDL ratios, have been associated with an increased risk of developing PIH (5).

Identifying and monitoring dyslipidemia in early pregnancy may enable timely preventive and therapeutic measures, potentially reducing maternal and perinatal complications. Therefore, studies evaluating lipid profiles as predictors of PIH are valuable in enhancing clinical outcomes and guiding appropriate management strategies. The present study aims to estimate serum lipid profile levels between 12–24 weeks of pregnancy and assess the predictive value of dyslipidemia in the development of pregnancy-induced hypertension in antenatal women. It also aims to study pregnancy outcomes and correlate maternal and neonatal outcomes with serum lipid levels in cases of pregnancy-induced hypertension.

This hospital-based prospective cohort study analyzed the predictive value of serum lipids in the early second trimester for the development of pregnancy-induced hypertension (PIH) in 400 antenatal women. Conducted over two years in the Department of Obstetrics and Gynecology at a rural tertiary care hospital, the study was approved by the Institutional Ethics Committee. Antenatal women aged 18–30 years with singleton pregnancies and normal blood pressure in the first trimester were included, while those with chronic hypertension, diabetes mellitus, congenital anomalies, or multiple gestations were excluded.

Clinical and demographic data were collected, and a thorough examination was performed, including blood pressure measurement and gestational age confirmation using the last menstrual period and ultrasound. Routine investigations and serum lipid profiles (TC, TG, HDL-C, LDL-C, and VLDL-C) were conducted between 12–24 weeks of gestation. Ultrasonography was performed in different trimesters to assess fetal well-being, and women were followed until delivery and postpartum for 7 days. PIH diagnosis followed NHBPEP criteria, and outcomes were recorded. Statistical analysis was conducted using IBM SPSS Statistics for Windows, Version 26.0 (IBM Corp., Armonk, NY, USA), with a p-value of <0.05 considered statistically significant.

The present study aimed to evaluate the predictive value of dyslipidemia in the second trimester (12–24 weeks) for the development of pregnancy-induced hypertension (PIH). A total of 400 antenatal women were enrolled and followed up until delivery and for 7 days postpartum to monitor the occurrence of PIH and assess pregnancy and labor complications. The relative risk of developing PIH due to dyslipidemia was documented, and maternal and perinatal outcomes in women with PIH were analyzed and compared with those in normotensive women.

Table 1 compares the systolic and diastolic blood pressure between women with pregnancy-induced hypertension (PIH) and normotensive women at the time of booking (12–24 weeks) and at delivery. At booking, the mean systolic blood pressure was significantly higher in the PIH group (112.85 ± 9.17 mmHg) compared to the normotensive group (108.71 ± 9.73 mmHg) with a p-value of 0.0007. Similarly, at delivery, the mean systolic blood pressure was markedly higher in the PIH group (143.93 ± 12.01 mmHg) compared to the normotensive group (119.46 ± 10.18 mmHg), with a highly significant p-value of <0.001. The mean diastolic blood pressure at booking was slightly higher in the PIH group (73.83 ± 6.55 mmHg) compared to the normotensive group (71.69 ± 10.94 mmHg), though this difference was not statistically significant (p = 0.0963). However, at delivery, the mean diastolic blood pressure was significantly higher in the PIH group (94.53 ± 9.06 mmHg) compared to the normotensive group (76.74 ± 7.47 mmHg), with a p-value of <0.001. These findings indicate that blood pressure levels, particularly at delivery, were significantly higher in women with PIH compared to normotensive women.

Table 2 shows a comparison of the serum lipid profile between women with pregnancy-induced hypertension (PIH) and normotensive women. Total cholesterol (210.13 ± 50.74 mg/dL vs. 178.09 ± 47.10 mg/dL), triglycerides (160.23 ± 67.39 mg/dL vs. 135.99 ± 66.07 mg/dL), low-density lipoprotein (134.21 ± 47.34 mg/dL vs. 105.13 ± 42.27 mg/dL), and very low-density lipoprotein (31.90 ± 13.45 mg/dL vs. 27.56 ± 15.12 mg/dL) were significantly higher in the PIH group (p < 0.05). Additionally, the TC/HDL and LDL/HDL ratios were elevated in the PIH group (p < 0.001). HDL levels were slightly lower in the PIH group, but the difference was not statistically significant (p = 0.2308). These results indicate that dyslipidemia is associated with an increased risk of developing PIH.

Table 3 presents the distribution of women according to antepartum, intrapartum, and postpartum complications. Antepartum complications included accidental hemorrhage, which occurred in 1 (1.25%) woman with pregnancy-induced hypertension (PIH) and 1 (2.5%) normotensive woman. Placenta accreta was observed in 1 (1.25%) PIH case, while none occurred in the normotensive group. Intrapartum complications included disseminated intravascular coagulation (DIC), which occurred in 2 (2.50%) PIH cases and none in the normotensive group. Postpartum complications included atonic postpartum hemorrhage, which was noted in 3 (3.75%) PIH cases and 1 (2.5%) normotensive case, while acute renal failure occurred in 2 (2.50%) PIH cases and none in the normotensive group. The majority of women had no complications, with 71 (88.75%) in the PIH group and 318 (99.37%) in the normotensive group. Overall, complications were more frequent in the PIH group compared to normotensive women.

Table 4 shows the distribution of fetal outcomes in women with pregnancy-induced hypertension (PIH) and normotensive women. NICU admissions due to complications such as hyperbilirubinemia, intrauterine growth restriction (IUGR), asphyxia, and low birth weight were significantly higher in the PIH group (22 cases, 27.5%) compared to the normotensive group (21 cases, 6.5%), accounting for 10.75% of all cases. Anomalous babies were noted in 1 (0.31%) normotensive case, while none were reported in the PIH group. Intrauterine death (IUD) occurred in 2 (2.5%) cases in the PIH group and none in the normotensive group. A normal fetal outcome was observed in 56 (70%) PIH cases and 298 (93.13%) normotensive cases, representing 88.50% of all cases. Overall, adverse fetal outcomes, including NICU admissions and IUD, were more frequent in the PIH group compared to normotensive women.

Hypertensive disorders of pregnancy, including pregnancy-induced hypertension (PIH), are among the most common complications during pregnancy, affecting up to 8% of all gestations (3). Along with hemorrhage and infection, PIH forms a deadly triad that significantly contributes to maternal morbidity and mortality. Despite ongoing research, the exact mechanism of PIH remains unclear, and standardized predictive models are lacking, making its management challenging and often controversial. The reduction of maternal and perinatal morbidity and mortality due to PIH is a global priority, and understanding its risk factors, including dyslipidemia, may provide a valuable approach for early prediction and management. Abnormal lipid metabolism in early pregnancy has been implicated as a contributing factor in the development of PIH, with altered lipid synthesis leading to a decrease in the prostacyclin-to-thromboxane (PGI2:TXA2) ratio, resulting in impaired trophoblast invasion and increased vascular resistance (6).

The present study found the frequency of PIH to be 20%, which is consistent with previous studies by Vidyabati et al. (7) (17.68%), U Singh et al(8). (21.48%), Yadav Kiran et al(9). (17.5%), and Revankar et al(10). (23.63%). However, the frequency was lower than that reported by Ephraim et al (11). (54.54%) and Siddiqui IA et al (12). (33.33%). The lipid profile findings in this study revealed that total cholesterol, triglycerides, LDL, and VLDL levels were significantly higher in women with PIH compared to normotensive women, while HDL levels were slightly lower but not statistically significant. These findings are comparable with those of Yadav Kiran et al(9). and Revankar et al(10)., whereas studies by Vidyabati et a(7)l. and U Singh et al(8). reported higher serum lipid levels. This reinforces the association between dyslipidemia and the development of PIH, highlighting the role of lipid abnormalities in predicting adverse pregnancy outcomes.

Maternal complications in this study were observed in 9 (11.25%) women with PIH, including antepartum (accidental hemorrhage), intrapartum (DIC), and postpartum (atonic postpartum hemorrhage and acute renal failure) complications, compared to 2 (5%) complications in normotensive women. These findings align with the study by Tanja et al.(13), where PIH was reported in 4.9% of cases and preeclampsia in 3.7%. Revankar et al.(10) also reported similar outcomes, with 7.69% of cases developing eclampsia and 22.5% of women experiencing preeclampsia-related complications.

Adverse fetal outcomes were also more frequent in the PIH group, with 24 (30%) cases showing complications such as NICU admissions due to hyperbilirubinemia, intrauterine growth restriction, asphyxia, and low birth weight, compared to 22 (6.81%) cases in normotensive women. Preterm deliveries were noted in 12 (15%) cases, and 44 (55%) neonates had low birth weight in the PIH group. These findings are consistent with the study by Tanja et al.(13), which reported a 5.3% incidence of preterm births and 9.3% of small-for-gestational-age infants. The higher frequency of maternal and fetal complications in women with PIH highlights the need for early identification of at-risk women through lipid profile screening and timely intervention to improve pregnancy outcomes.

Pregnancy-induced hypertension (PIH) remains a poorly understood condition despite its significant impact on maternal and fetal outcomes. The study concludes that dyslipidemia is a strong predictor of PIH, with high levels of TC, TG, LDL, and VLDL increasing the risk. Early screening, timely intervention, and balanced obstetric care can help reduce maternal and perinatal complications.

Conflict of Interest: The authors declare no conflict of interest.

Source of Funding: This research received no external funding.

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