Hypertensive disorders of pregnancy (HDP) remain a major cause of maternal and perinatal morbidity and mortality worldwide. These disorders encompass a spectrum of clinical conditions-gestational hypertension, preeclampsia, eclampsia, chronic hypertension, and preeclampsia superimposed on chronic hypertension-each carrying varying degrees of risk for the mother and fetus. Among them, preeclampsia is particularly notorious for its unpredictable onset and potentially catastrophic complications, including placental abruption, disseminated intravascular coagulation, hepatic rupture, and maternal or fetal death. Globally, the incidence of preeclampsia ranges between 2% and 8% of pregnancies, while hypertensive disorders collectively account for up to 18% of maternal deaths in developing countries. In India, HDP contributes significantly to the maternal mortality ratio, underscoring the persistent gaps in antenatal screening, risk stratification, and preventive strategies.[1] Recent decades have witnessed a paradigm shift in the understanding of preeclampsia and other hypertensive disorders of pregnancy-from being regarded merely as disorders of abnormal blood pressure regulation to being recognized as multisystem endothelial dysfunction syndromes. The pathogenesis is multifactorial, involving abnormal placentation, systemic inflammation, oxidative stress, and immunologic maladaptation between maternal and fetal tissues. Central to these processes is endothelial dysfunction, which leads to vasoconstriction, increased vascular permeability, and coagulation abnormalities. However, growing evidence now implicates micronutrient imbalances, particularly vitamin D deficiency, as a potentially modifiable factor influencing both the development and severity of hypertensive disorders during pregnancy.[2] Vitamin D, a secosteroid hormone traditionally associated with calcium and phosphorus homeostasis, plays several extra-skeletal roles that are particularly relevant in pregnancy. The vitamin exists in two major forms-ergocalciferol (D₂) from plant sources and cholecalciferol (D₃) synthesized endogenously in the skin upon exposure to ultraviolet B radiation. After hydroxylation in the liver and kidneys, it becomes 1,25-dihydroxyvitamin D [1,25(OH)₂D], the biologically active metabolite. During pregnancy, maternal vitamin D metabolism undergoes significant alterations: plasma concentrations of the active metabolite increase by two to threefold, reflecting the heightened demands of both the growing fetus and the placenta.[3] The placenta itself expresses vitamin D receptors (VDRs) and key hydroxylating enzymes such as 1-α-hydroxylase, suggesting an autocrine and paracrine role of vitamin D in regulating placental implantation, angiogenesis, and immune tolerance. Adequate vitamin D is essential for decidualization, modulation of T-helper cell balance, and suppression of pro-inflammatory cytokines-all critical events in establishing a healthy maternal-fetal interface. Conversely, deficiency in vitamin D has been linked to impaired trophoblastic invasion, abnormal vascular remodeling, and heightened inflammatory responses-all of which are central to the pathogenesis of preeclampsia and related hypertensive disorders.[4] Aim To assess the association between maternal serum vitamin D levels and pregnancy outcomes in women with hypertensive disorders of pregnancy. Objectives 1. To estimate the serum vitamin D levels among pregnant women diagnosed with hypertensive disorders of pregnancy. 2. To evaluate the relationship between maternal vitamin D status and the severity of hypertensive disorders of pregnancy. 3. To determine the association between maternal vitamin D levels and adverse maternal and neonatal outcomes.

Source of Data Data were obtained from antenatal women diagnosed with hypertensive disorders of pregnancy attending the Department of Obstetrics and Gynecology. Both outpatient and inpatient records were reviewed, and serum samples were collected after obtaining informed consent. Study Design This study was a hospital-based cross-sectional analytical study. Study Location The study was conducted at the Department of Obstetrics and Gynecology, at tertiary care hospital. Study Duration The study was carried out over a period of 18 months (April 2023 to October 2024). Sample Size A total of 200 pregnant women diagnosed with hypertensive disorders of pregnancy were included. Inclusion Criteria • Pregnant women aged 18-40 years diagnosed with gestational hypertension, preeclampsia, or eclampsia as per ACOG guidelines. • Singleton pregnancies beyond 20 weeks of gestation. • Women who provided informed written consent. Exclusion Criteria • Women with chronic renal disease, hepatic dysfunction, thyroid disorders, or diabetes mellitus. • Women already receiving vitamin D supplementation or calcium with vitamin D combination therapy. • Multiple pregnancies or pregnancies with congenital anomalies. • Patients unwilling to participate. Procedure and Methodology Eligible participants were enrolled after fulfilling inclusion and exclusion criteria. Detailed clinical history was taken, including age, parity, gestational age, dietary habits, sun exposure, and socioeconomic status. Blood pressure measurements and obstetric examinations were conducted. The diagnosis and classification of hypertensive disorders were made as per American College of Obstetricians and Gynecologists (ACOG, 2020) guidelines. Venous blood samples (5 mL) were drawn under aseptic precautions. Serum was separated by centrifugation and stored at -20°C until analysis. Relevant biochemical investigations including serum calcium, liver and renal function tests, and urine protein estimation were also performed. Sample Processing Serum vitamin D levels were measured using a quantitative enzyme-linked immunosorbent assay (ELISA) method. The assay determined serum 25-hydroxyvitamin D [25(OH)D] concentration-the best indicator of vitamin D status. Based on established cutoffs: • Deficient: <20 ng/mL • Insufficient: 20-30 ng/mL • Sufficient: >30 ng/mL Quality control procedures were maintained using internal and external calibration standards. Data Collection All patient data were recorded in a structured proforma including demographic details, obstetric history, blood pressure readings, laboratory parameters, and maternal-fetal outcomes such as mode of delivery, birth weight, APGAR score, preterm birth, intrauterine growth restriction, and NICU admission. Each case was followed up till delivery. Statistical Methods Data were entered into Microsoft Excel and analyzed using SPSS version 26.0. Continuous variables were expressed as mean ± standard deviation (SD) and compared using Student’s t-test or ANOVA as appropriate. Categorical variables were expressed as proportions and analyzed using Chi-square or Fisher’s exact test. Correlation between serum vitamin D levels and clinical parameters was assessed using Pearson’s or Spearman’s correlation coefficient. Logistic regression analysis was performed to identify independent predictors of adverse pregnancy outcomes. A p-value <0.05 was considered statistically significant.

Table 1: Association between maternal serum 25(OH)D (ng/mL) and pregnancy outcomes in women with HDP (N = 200) Variable Category / Metric n (%) or Mean ± SD Test of significance Effect size (95% CI) p-value Serum 25(OH)D Overall mean 19.8 ± 7.6 - Mean (95% CI): 18.7 to 20.9 - Composite adverse outcome* Present (n=96) 17.8 ± 6.8 Welch t(≈184)=3.37 Mean diff -3.6 (-5.6 to -1.5) 0.0009 Absent (n=104) 21.4 ± 7.8 - - - Birthweight (kg) Pearson r with 25(OH)D - r-test r = 0.26 (0.12 to 0.39) 0.0004 Gestational age at delivery (weeks) Pearson r with 25(OH)D - r-test r = 0.22 (0.08 to 0.35) 0.0021 SBP at diagnosis (mmHg) Pearson r with 25(OH)D - r-test r = -0.19 (-0.32 to -0.04) 0.0068 Any NICU admission Yes vs No 25(OH)D: 18.1 ± 6.9 vs 20.6 ± 7.7 Welch t(≈143)=2.28 Mean diff -2.5 (-4.7 to -0.3) 0.024 Logistic regression (composite adverse outcome) per 10 ng/mL ↑ in 25(OH)D - Wald χ²=9.47 OR 0.62 (0.46 to 0.84) 0.0021 Adjusted logistic regression† per 10 ng/mL ↑ in 25(OH)D - Wald χ²=7.06 aOR 0.66 (0.49 to 0.90) 0.0079 *Composite adverse outcome = preterm <37 w, LBW <2.5 kg, IUGR, NICU admission, HELLP/eclampsia, or stillbirth. †Adjusted for maternal age, BMI, parity, and trimester at sampling. Table 1 demonstrates the overall association between maternal serum 25(OH)D levels and key pregnancy outcomes among 200 women diagnosed with hypertensive disorders of pregnancy (HDP). The mean vitamin D concentration in the study cohort was 19.8 ± 7.6 ng/mL, with a 95% confidence interval (CI) of 18.7-20.9 ng/mL, indicating widespread insufficiency. Women who experienced composite adverse outcomes (preterm delivery, low birth weight, intrauterine growth restriction, NICU admission, HELLP/eclampsia, or stillbirth) had significantly lower vitamin D levels (17.8 ± 6.8 ng/mL) than those without complications (21.4 ± 7.8 ng/mL, p = 0.0009). Positive correlations were observed between serum vitamin D and birthweight (r = 0.26, 95% CI 0.12-0.39, p = 0.0004) as well as gestational age at delivery (r = 0.22, 95% CI 0.08-0.35, p = 0.0021), suggesting that higher vitamin D levels favored better fetal growth and longer gestation. Conversely, a negative correlation was seen with systolic blood pressure (SBP) at diagnosis (r = -0.19, p = 0.0068), supporting the role of vitamin D in vascular modulation. Women whose babies required NICU admission had lower mean vitamin D levels (18.1 ± 6.9 ng/mL) compared with those without NICU admissions (20.6 ± 7.7 ng/mL, p = 0.024). Logistic regression revealed that for every 10 ng/mL rise in vitamin D, the odds of adverse outcome decreased by 38% (OR 0.62, 95% CI 0.46-0.84, p = 0.0021); after adjusting for age, BMI, parity, and trimester, the association remained significant (aOR 0.66, p = 0.0079). Table 2: Serum vitamin D levels among pregnant women with HDP (distribution and determinants) (N = 200) Variable Category n (%) or Mean ± SD Test of significance Effect size (95% CI) p-value 25(OH)D (ng/mL) Overall 19.8 ± 7.6 - Mean (95% CI): 18.7 to 20.9 - Vitamin D status Deficient <20 117 (58.5%) One-sample prop. CI p̂ 0.585 (0.512 to 0.655) - Insufficient 20-29 56 (28.0%) - - - Sufficient ≥30 27 (13.5%) - - - Trimester at sampling Second (n=121) 20.9 ± 7.4 Welch t(≈178)=2.65 Mean diff +2.9 (0.76 to 5.10) 0.009 Third (n=79) 18.0 ± 7.6 - - - Daily sun exposure <30 min (n=132) 18.6 ± 7.3 Welch t(≈175)=3.17 Mean diff +3.6 (1.4 to 5.8)‡ 0.0019 ≥30 min (n=68) 22.2 ± 7.6 - - - BMI category 18.5-24.9 (n=61) 22.6 ± 7.1 One-way ANOVA F(2,197)=7.84 η² = 0.074 0.0006 25.0-29.9 (n=89) 19.4 ± 7.2 Pairwise (Obese vs Normal) -5.3 (-7.9 to -2.7) <0.001 ≥30.0 (n=50) 17.3 ± 7.8 Pairwise (Overwt vs Normal) -3.2 (-5.8 to -0.6) 0.016 ‡Difference shown as ≥30 min minus <30 min. Table 2 explores the distribution and determinants of serum vitamin D levels among the 200 participants. The mean serum 25(OH)D concentration was 19.8 ± 7.6 ng/mL, confirming a generally deficient state. More than half of the women (58.5%) were vitamin D deficient (<20 ng/mL), while 28.0% were insufficient (20-29 ng/mL), and only 13.5% had sufficient levels (≥30 ng/mL). Women assessed in the second trimester had significantly higher mean levels (20.9 ± 7.4 ng/mL) than those in the third trimester (18.0 ± 7.6 ng/mL, p = 0.009), suggesting progressive depletion as pregnancy advanced. Daily sun exposure emerged as a strong determinant: participants with exposure ≥30 minutes had higher mean vitamin D (22.2 ± 7.6 ng/mL) than those with <30 minutes (18.6 ± 7.3 ng/mL, p = 0.0019). Analysis by body mass index (BMI) showed an inverse relationship between adiposity and vitamin D status (ANOVA F(2,197)=7.84, p < 0.001). Normal-weight women (22.6 ± 7.1 ng/mL) had significantly higher levels than overweight (19.4 ± 7.2 ng/mL, p = 0.016) and obese women (17.3 ± 7.8 ng/mL, p < 0.001). Table 3: Relationship between maternal vitamin D status and severity of hypertensive disorder (N = 200) Vitamin D status Gestational HTN (n=62) Mild preeclampsia (n=84) Severe PE/Eclampsia (n=54) Row total Deficient (<20), n=117 26 (22.2%) 47 (40.2%) 44 (37.6%) 117 Insufficient (20-29), n=56 22 (39.3%) 26 (46.4%) 8 (14.3%) 56 Sufficient (≥30), n=27 14 (51.9%) 11 (40.7%) 2 (7.4%) 27 Omnibus association: χ²(4)=14.10, Cramér’s V = 0.188 (95% CI 0.07-0.31), p=0.007 Trend (deficient → sufficient): Cochran-Armitage Z = -3.05, p=0.002 (lower vitamin D → higher severity) Risk of severe PE/Eclampsia: Deficient vs Sufficient → RR 5.08 (1.31-19.7), p=0.019; Deficient vs Insufficient → RR 2.63 (1.30-5.32), p=0.005. Table 3 depicts the relationship between maternal vitamin D status and the severity of hypertensive disorders of pregnancy. Among the 117 vitamin D-deficient women, 37.6% had severe preeclampsia or eclampsia, while only 7.4% of those with sufficient vitamin D presented with severe forms. In contrast, mild preeclampsia predominated among women with insufficient levels (46.4%), whereas gestational hypertension was more common in those with adequate vitamin D (51.9%). The overall association between vitamin D status and disease severity was statistically significant (χ²(4)=14.10, p = 0.007; Cramér’s V = 0.188, 95% CI 0.07-0.31). A significant linear trend (Z = -3.05, p = 0.002) demonstrated a dose-response pattern-lower vitamin D corresponded with increasing severity of HDP. Women with deficiency were five times more likely to develop severe preeclampsia/eclampsia compared to those with sufficient vitamin D (RR 5.08, 95% CI 1.31-19.7, p = 0.019), and more than twice as likely as those with insufficiency (RR 2.63, p = 0.005). These findings reinforce vitamin D deficiency as an independent correlate of disease severity, suggesting its potential involvement in endothelial dysfunction and placental maladaptation underlying hypertensive disorders. Table 4: Maternal and neonatal outcomes across vitamin D categories (N = 200) Outcome Deficient (<20) n=117 Insufficient (20-29) n=56 Sufficient (≥30) n=27 Test of significance Effect size (95% CI) p-value Preterm delivery <37 w 43 (36.8%) 15 (26.8%) 4 (14.8%) χ²(2)=6.93 RR Def vs Suf: 2.49 (0.98-6.35) 0.031 Low birth weight <2.5 kg 39 (33.3%) 13 (23.2%) 3 (11.1%) χ²(2)=7.87 RR Def vs Suf: 3.00 (0.99-9.11) 0.019 IUGR diagnosed 28 (23.9%) 9 (16.1%) 2 (7.4%) χ²(2)=6.02 RR Def vs Suf: 3.24 (0.80-13.1) 0.049 Any NICU admission 32 (27.4%) 10 (17.9%) 2 (7.4%) χ²(2)=7.22 RR Def vs Suf: 3.71 (0.93-14.8) 0.027 Cesarean delivery 68 (58.1%) 27 (48.2%) 10 (37.0%) χ²(2)=6.10 RR Def vs Suf: 1.57 (0.93-2.64) 0.047 HELLP/Eclampsia composite 21 (17.9%) 6 (10.7%) 1 (3.7%) χ²(2)=6.23 RR Def vs Suf: 4.86 (0.67-35.0) 0.044 Composite adverse outcome* 63 (53.8%) 22 (39.3%) 11 (40.7%) χ²(2)=4.51 RR Def vs Suf: 1.32 (0.78-2.25) 0.034 Table 4 examines maternal and neonatal outcomes across vitamin D categories. The adverse outcomes were markedly more frequent among vitamin D-deficient women compared to those with sufficient levels. Preterm delivery occurred in 36.8% of deficient mothers, versus only 14.8% among the sufficient group (p = 0.031; RR 2.49, 95% CI 0.98-6.35). Similarly, low birth weight (<2.5 kg) was seen in one-third (33.3%) of the deficient group compared with 11.1% in the sufficient group (p = 0.019). Incidences of intrauterine growth restriction (IUGR) (23.9% vs 7.4%), NICU admissions (27.4% vs 7.4%), and cesarean deliveries (58.1% vs 37.0%) were all significantly higher in women with low vitamin D. Severe maternal complications such as HELLP syndrome or eclampsia were also more common in the deficient category (17.9% vs 3.7%, p = 0.044). The composite adverse outcome rate was 53.8% in deficient women compared to 40.7% in those with sufficient vitamin D (p = 0.034).

Association between Vitamin D and Pregnancy Outcomes (Table 1): In the current study, the mean serum 25(OH)D level among HDP cases was 19.8 ± 7.6 ng/mL, confirming widespread deficiency. Women with composite adverse outcomes (such as preterm birth, low birth weight, IUGR, HELLP syndrome, or NICU admission) had significantly lower vitamin D levels (17.8 ± 6.8 ng/mL) compared to those without complications (21.4 ± 7.8 ng/mL, p = 0.0009). A positive correlation was observed between serum vitamin D and both birth weight (r = 0.26) and gestational age at delivery (r = 0.22), while an inverse relationship was noted with systolic blood pressure (r = -0.19). These findings emphasize the protective role of vitamin D in improving placental function, prolonging gestation, and enhancing fetal growth. Comparable observations were made by Gilani S et al. (2020)[5], who reported a fivefold higher risk of preeclampsia among women with vitamin D levels <15 ng/mL. Similarly, Cui C et al. (2024)[6] demonstrated that each 10 ng/mL increase in vitamin D significantly reduced the odds of preeclampsia and preterm birth, aligning with the present study’s logistic regression finding (aOR = 0.66; 95% CI: 0.49-0.90; p = 0.0079). Furthermore, Olapeju B et al. (2020)[7] established a linear inverse association between maternal vitamin D concentration and blood pressure, supporting the observed negative correlation with SBP in our study. The significant relationship between low vitamin D and NICU admission (p = 0.024) also mirrors findings by Suárez-Varela MM et al. (2022)[8], who found that neonatal complications, including respiratory distress and growth restriction, were more frequent among vitamin D-deficient mothers. Hence, our data reinforce that vitamin D insufficiency not only predisposes to HDP but also worsens pregnancy outcomes, likely through endothelial dysfunction and placental hypoperfusion. Distribution and Determinants of Vitamin D Levels (Table 2): More than half of the women in this study (58.5%) were vitamin D deficient, while 28.0% were insufficient and only 13.5% had sufficient levels. The mean 25(OH)D level (19.8 ng/mL) aligns with reports from Indian studies, where deficiency among pregnant women ranges from 60% to 90% due to limited sunlight exposure, vegetarian diets, and higher skin melanin. Rayes B et al. (2023)[9] in rural North India reported mean vitamin D levels of 18.9 ng/mL and a deficiency prevalence of 84%, consistent with our findings. Women assessed during the second trimester had significantly higher vitamin D (20.9 ± 7.4 ng/mL) compared to those in the third trimester (18.0 ± 7.6 ng/mL, p = 0.009), indicating progressive depletion as pregnancy advances-possibly due to fetal calcium demands and limited supplementation. Similar trimester-wise decline was reported by Zhao R et al. (2022)[10]. Daily sunlight exposure and BMI also showed strong associations. Women with <30 minutes of sun exposure had significantly lower levels (18.6 ± 7.3 ng/mL) than those with ≥30 minutes (22.2 ± 7.6 ng/mL, p = 0.0019), corroborating findings by Lee SB et al. (2023)[11] that inadequate sunlight is the most significant predictor of deficiency even in tropical climates. Higher BMI was inversely related to vitamin D, with obese women showing the lowest levels (17.3 ± 7.8 ng/mL). This is consistent with Dahma G et al. (2022)[12], who described sequestration of vitamin D in adipose tissue, reducing bioavailability. Thus, environmental and metabolic factors play crucial roles in determining maternal vitamin D status during pregnancy. Vitamin D Status and Severity of Hypertensive Disorders (Table 3): The study found a graded association between declining vitamin D levels and increasing HDP severity. Among vitamin D-deficient women, 37.6% developed severe preeclampsia/eclampsia, while only 7.4% of those with sufficient vitamin D experienced severe disease (p = 0.007). The relative risk of severe disease was five times higher in deficient women compared to those sufficient (RR = 5.08, p = 0.019). This trend is consistent with Fondjo LA et al. (2021)[13], who both observed a significant association between hypovitaminosis D and the severity of preeclampsia. Similarly, Vestergaard AL et al. (2023)[14] reported that women with vitamin D <20 ng/mL were twice as likely to develop severe HDP. The observed dose-response relationship in our cohort (Z = -3.05, p = 0.002) further substantiates the hypothesis that vitamin D deficiency contributes to endothelial dysfunction, altered immune regulation, and increased vascular resistance, all of which underlie severe preeclampsia. Mechanistically, this association is supported by vitamin D’s known role in regulating the renin-angiotensin-aldosterone system (RAAS) and anti-inflammatory pathways. Reduced vitamin D leads to increased renin expression, vasoconstriction, and hypertension-explaining the observed inverse relationship between vitamin D and SBP. Maternal and Neonatal Outcomes across Vitamin D Categories (Table 4): Adverse maternal and neonatal outcomes were significantly more prevalent among vitamin D-deficient women. The rates of preterm delivery (36.8%), low birth weight (33.3%), IUGR (23.9%), and NICU admission (27.4%) were all notably higher in deficient women compared to those with sufficient vitamin D (14.8%, 11.1%, 7.4%, and 7.4%, respectively). These findings are consistent with Chen GD et al. (2020)[15], who reported similar trends linking low maternal vitamin D to fetal growth restriction and preterm labor. The higher incidence of HELLP syndrome and eclampsia (17.9% vs 3.7%) among deficient women reflects the role of vitamin D in endothelial stability and immune modulation. The composite adverse outcome was observed in 53.8% of deficient women versus 40.7% in sufficient ones (p = 0.034). Similar observations were made by Chien MC et al. (2024)[16], who found that vitamin D-deficient women had a higher risk of cesarean delivery and neonatal morbidity.

The present cross-sectional study demonstrates a strong and consistent association between maternal vitamin D deficiency and both the severity and adverse outcomes of hypertensive disorders of pregnancy (HDP). More than half of the study participants were vitamin D deficient, and low serum 25(OH)D concentrations were significantly correlated with higher systolic blood pressure, earlier gestational age at delivery, lower birth weight, and increased incidence of composite maternal and neonatal complications such as preterm birth, intrauterine growth restriction, NICU admissions, and HELLP/eclampsia syndromes. A clear dose-response trend was observed, wherein women with sufficient vitamin D levels experienced fewer and less severe manifestations of HDP. These findings reinforce the biological plausibility that vitamin D deficiency contributes to endothelial dysfunction, abnormal placentation, and heightened inflammatory responses underlying hypertensive disorders in pregnancy. The study underscores the potential benefit of routine screening and optimization of vitamin D status during antenatal care, especially in women at high risk for HDP, as a cost-effective strategy to improve maternal and perinatal outcomes.

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