Preeclampsia (PE) is a pregnancy-specific hypertensive disorder characterized by the new onset of hypertension after 20 weeks of gestation in a previously normotensive woman, accompanied by proteinuria and/or maternal organ dysfunction [1]. It complicates approximately 2–8% of pregnancies and remains a leading cause of maternal and perinatal morbidity and mortality worldwide, accounting for significant health-care costs [1–5]. In the absence of timely prophylaxis, PE may progress to eclampsia, characterized by tonic–clonic seizures, which substantially increases maternal mortality, especially in resource-limited settings [6]. The clinical spectrum of PE is diverse, ranging from mild hypertension to severe multisystem involvement. It may cause maternal complications such as renal, hepatic, pulmonary, neurologic, and hematologic dysfunctions [7,8], while adverse fetal outcomes include oligohydramnios, intrauterine growth restriction (IUGR), preterm birth, placental abruption, and perinatal death [9,10]. Pathophysiologically, PE is widely regarded as a two-stage disorder: abnormal trophoblastic invasion and failure of spiral artery remodeling initiate placental hypoperfusion and hypoxia [11]. Subsequent oxidative stress induces the release of pro-inflammatory cytokines, anti-angiogenic factors, exosomes, and cell-free fetal DNA into the maternal circulation, which in turn trigger endothelial dysfunction and increased vascular permeability [12,13]. Given this cascade, numerous biomarkers have been explored in recent decades for their potential utility in predicting PE, even as early as the first trimester [14]. Early identification of high-risk patients enables timely prophylaxis, such as low-dose aspirin, and improves maternal-fetal outcomes [15]. Studies indicate that hyperactivation of inflammatory cells, along with dysregulated lymphocyte and neutrophil responses, drive endothelial dysfunction through the release of pro-inflammatory mediators [16,17]. This phenomenon is often described as “low-grade inflammation,” wherein mild increases in immune cell counts and circulating pro-inflammatory proteins are observed in the absence of overt inflammatory disease [4]. Systemic inflammatory response (SIR) markers obtained from routine complete blood counts (CBC)—such as red cell distribution width (RDW), plateletcrit (PCT), mean platelet volume (MPV), platelet distribution width (PDW), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte ratio (NLR)—have been increasingly recognized as potential predictive indices in both inflammatory diseases and complicated pregnancies [11,18]. However, existing studies have reported conflicting results regarding their association with PE, highlighting the need for further investigation. In this context, the present study was undertaken to evaluate NLR and PLR, along with platelet count, RDW, and PCT, in women with preeclampsia compared to gestationally matched normotensive controls. By analyzing these hematological parameters, we aim to determine their clinical significance as simple, inexpensive, and non-invasive markers in predicting preeclampsia and its complications.

Study Design and Setting This cross-sectional study was conducted over a period of 18 months, from January 2021 to July 2022, in the Department of Obstetrics and Gynecology at Rajarajeswari Medical College and Hospital (RRMCH), Bengaluru, India. Ethical clearance was obtained from the Institutional Ethics Committee prior to commencement of the study. Study Population Pregnant women aged 18–40 years with a gestational age of more than 20 weeks, presenting with preeclampsia, and attending the outpatient or inpatient services of the department were recruited. Participants were selected using purposive sampling until the required sample size was achieved. Written informed consent was obtained from all study participants prior to enrollment. Inclusion Criteria 1. Women aged 18–40 years. 2. Pregnant women beyond 20 weeks of gestation diagnosed with preeclampsia. 3. Primigravida. Exclusion Criteria 1. Women with ruptured membranes. 2. Presence of anemia, fever, or infections. 3. HELLP syndrome or multiple gestation. 4. Eclampsia. 5. Coexisting comorbidities such as diabetes mellitus, hypothyroidism, chronic hypertension, collagen vascular disease, renal disease, ischemic heart disease, or rheumatic disease. 6. Patients receiving anti-inflammatory drugs or anticoagulants. Data Collection and Laboratory Analysis Sociodemographic and clinical details were collected using a pretested, semi-structured questionnaire administered through face-to-face interviews. Following enrollment, 2 mL of peripheral venous blood was collected in EDTA vials. Samples were processed within one hour of collection in the Department of Hematology using an automated hematology analyzer (Sysmex XN-1000, Transasia, 6-part differential, based on the Coulter principle). Complete blood count (CBC) parameters were obtained for each participant. Neutrophil-to-lymphocyte ratio (NLR) was calculated as the absolute neutrophil count divided by the lymphocyte count. Platelet-to-lymphocyte ratio (PLR) was calculated as the platelet count divided by the lymphocyte count. All values were derived from the same blood sample. Sample Size Estimation Based on hospital statistics, an average of two cases per month met the eligibility criteria. Over 18 months, the expected population size was N = 36. Using Yamane’s formula for sample size calculation: n=N/1+N (e2) Where n = sample size, N = population size, and e = margin of error (0.05 at 95% confidence level). n=36/1+36(0.052) =36/1.12≈33 The final sample size was fixed at 42 participants per group (preeclampsia and normotensive controls) to improve statistical power. Statistical Analysis Data were compiled using Microsoft Excel and analyzed with SPSS version 26.0 (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables as frequencies and percentages. Comparisons between two groups were performed using the Student’s t-test for continuous variables and the Chi-square test for categorical variables. A p-value <0.05 was considered statistically significant.

The age distribution of study participants is presented in Table 1. The majority of participants in both groups were between 21–30 years (85.7% in the normotensive group and 76.2% in the preeclampsia group). The mean age was significantly higher in the preeclampsia group (27.17 ± 4.29 years) compared to the normotensive group (24.79 ± 3.38 years, p <0.001). Table 1. Demographic characteristics of the study population Age (years) Normotensive n=42 (%) Preeclampsia n=42 (%) p-value ≤20 4 (9.5) 1 (2.4) 21–30 36 (85.7) 32 (76.2) 31–40 2 (4.8) 9 (21.4) Mean ± SD 24.79 ± 3.38 27.17 ± 4.29 0.000 bstetric profiles are summarized in Table 2. In the normotensive group, 66.7% were multigravida, whereas in the preeclampsia group, 52.4% were primigravida. Nulliparity was more common among preeclampsia cases (66.7%). A history of abortion was more frequent in the preeclampsia group (33.3% vs. 19.0%). However, the differences were not statistically significant (p >0.05). Table 2. Obstetric characteristics of study participants Variable Category Normotensive n=42 (%) Preeclampsia n=42 (%) p-value Gravidity Primi 14 (33.3) 20 (52.4) 0.182 Multi 28 (66.7) 22 (47.6) Parity 0 17 (40.5) 28 (66.7) 1 17 (40.5) 12 (28.6) ≥2 8 (19.0) 2 (4.8) Living children 0 17 (40.5) 28 (66.7) 1 21 (50.0) 13 (31.0) ≥2 4 (9.5) 1 (2.4) Abortions None 34 (81.0) 11 (26.2) 1 4 (9.5) 11 (26.2) 2 3 (7.1) 1 (2.4) 3 1 (2.4) 20 (47.6) Gestational outcomes are presented in Table 3. Most normotensive women (50.0%) and preeclampsia patients (45.2%) delivered at term. Preterm deliveries were higher among preeclampsia cases (54.8% vs. 50.0%). Table 3. Gestational age at delivery Gestational Age Normotensive n=42 (%) Preeclampsia n=42 (%) Very preterm 2 (4.8) 4 (9.5) Moderate preterm 7 (16.7) 7 (16.7) Late preterm 12 (28.6) 12 (28.6) Term 21 (50.0) 19 (45.2) The hematological parameters and clinical profiles are summarized in Table 4. Mean NLR was slightly higher in preeclampsia (4.81 ± 3.37) than normotensives (4.24 ± 1.97), though not statistically significant. PLR values were lower in preeclampsia (112.02 ± 60.30) than controls (119.37 ± 43.87). Platelet count was also lower in preeclampsia. No significant intergroup differences were noted in RDW. Table 4. Comparison of clinical and hematological parameters between groups Variable Normotensive (Mean ± SD) Preeclampsia (Mean ± SD) p-value Gestational age (weeks) 36.50 ± 3.28 35.69 ± 2.73 0.09 Neutrophil count (/cumm) 8801.43 ± 2708.30 9109.19 ± 3116.05 0.465 Lymphocyte count (/cumm) 2262.62 ± 661.15 4069.24 ± 12187.62 0.418 Platelet count (lakh) 2.48 ± 0.74 2.34 ± 0.79 0.234 NLR 4.24 ± 1.97 4.81 ± 3.37 0.976 PLR 119.37 ± 43.87 112.02 ± 60.30 0.280 RDW (fl) 45.67 ± 8.80 43.62 ± 4.42 0.522 Among preeclampsia patients, clinical and hematological indices were further compared between mild and severe cases (Table 5). Mean gestational age was lower in severe PE (34.14 ± 3.06 weeks) compared to mild cases (36.46 ± 2.21 weeks). PLR was significantly reduced in severe PE (84.50 ± 41.96) compared to mild cases (125.79 ± 63.91, p = 0.03). Table 5. Clinical characteristics in mild versus severe preeclampsia Variable Mild PE (Mean ± SD) Severe PE (Mean ± SD) p-value Gestational age (weeks) 36.46 ± 2.21 34.14 ± 3.06 0.010 BMI (kg/m²) 24.64 ± 4.36 25.36 ± 4.73 0.612 Neutrophil count (/cumm) 9205 ± 3106.51 8917.57 ± 3243.53 0.598 Lymphocyte count (/cumm) 2043.07 ± 761.73 8121.57 ± 20993.67 0.694 Platelet count (lakh) 2.42 ± 0.77 2.16 ± 0.82 0.455 NLR 5.39 ± 3.76 3.64 ± 2.06 0.737 PLR 125.79 ± 63.91 84.50 ± 41.96 0.03 RDW (fl) 43.79 ± 4.70 43.29 ± 3.93 0.732 Table 6 summarizes maternal and neonatal outcomes. Emergency LSCS was the predominant mode of delivery among preeclampsia patients (71.4%), compared to 7.1% in the normotensive group. Intrauterine growth restriction (IUGR) was significantly higher in preeclampsia (31.0% vs. 4.8%, p = 0.04). Neonatal NICU admissions were more frequent in preeclampsia (38.1%) compared to normotensives (21.4%), though the difference was not statistically significant (p = 0.09). Table 6. Maternal and neonatal outcomes Outcome Normotensive n=42 (%) Preeclampsia n=42 (%) p-value Mode of delivery Emergency hysterotomy 0 1 (2.4) Emergency LSCS 3 (7.1) 30 (71.4) Elective LSCS 17 (40.5) 0 FTND 14 (33.4) 8 (19.1) PTVD 8 (19.0) 3 (7.1) Intrauterine growth restriction (IUGR) 2 (4.8) 13 (31.0) 0.04 Neonatal outcome Mother side 33 (78.6) 26 (61.9) 0.09 NICU admission 9 (21.4) 16 (38.1)

Preeclampsia (PE) is a multisystem hypertensive disorder of pregnancy with an unclear etiology. Maternal circulating leukocytes are physiologically activated in pregnancy and further activated in PE, contributing to vascular dysfunction [19]. This study was designed to evaluate hematological indices of systemic inflammation—namely neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), platelet count, red cell distribution width (RDW), and plateletcrit (PCT)—in women with preeclampsia compared to gestationally matched normotensive controls. In our cohort, preeclampsia was predominantly observed among women aged 21–34 years. This is consistent with studies by Safirani et al. [20] and Sumampouw et al. [21], who reported a higher incidence of PE in this age range. Similar findings were noted by Jaleel et al. [22] and Kumar et al. [23]. The clustering of cases in this younger age group may reflect sociocultural patterns in India, where early marriage and childbearing are common [22]. In the present study, a higher proportion of preeclampsia patients were primigravida (52.4%), in contrast to findings in Ethiopian study [24], which reported predominance among multigravida women. Such discrepancies may be attributable to differences in study populations and regional demographics. We observed a lower platelet count in preeclampsia cases (2.34 ± 0.79 lakh/µL) compared to normotensive women (2.48 ± 0.74 lakh/µL), though the difference was statistically insignificant. Chauhan et al. [25] and Meshram et al. [26] demonstrated significantly reduced platelet counts in PE cases compared to controls, whereas our findings align more closely with studies reporting only a nonsignificant decline. Subgroup analysis revealed further decreases in platelet count among severe PE compared to mild cases, similar to results by Gupta et al. [27], who found significantly reduced platelet counts with disease progression. Although our study showed a downward trend, the difference did not reach statistical significance. NLR is an inexpensive, reproducible marker of subclinical inflammation [28,29]. In PE, hyperactivation of inflammatory cells and dysregulated immune responses promote the release of pro-inflammatory cytokines and autoantibodies, leading to endothelial dysfunction [30-32]. The dysregulation of T-helper 1 (TH1) and T-helper 2 (TH2) immune responses has also been implicated [33,34]. In our study, mean NLR was higher in the PE group (4.81 ± 3.37) compared to normotensives (4.24 ± 1.97), although the difference was not statistically significant. These findings are in agreement with Zheng et al. [35], whose meta-analysis concluded that while NLR has limited specificity, its sensitivity supports its role as a diagnostic adjunct for PE. Conversely, studies by Kurtoglu et al. [36], Serin et al. [37], and Mohammad et al. [38] demonstrated significantly elevated NLR values in PE. Similarly, Gogoi et al. [39] and Sachan et al. [40] in India reported higher NLR values in PE, with ROC analyses indicating diagnostic utility. Prasmusinto et al. [41] also showed significantly elevated NLR with high sensitivity and specificity. Thus, although our findings suggest a trend toward increased NLR, statistical significance was not achieved, possibly due to sample size limitations. PLR reflects cytokine-driven immune activity and has been associated with ischemia, end-organ damage, and PE [42]. Placental hypoxia and oxidative stress contribute to increased proinflammatory markers in PE [43-45]. In our cohort, PLR was lower in PE patients compared to controls, with a significant reduction in severe PE. This is consistent with Yücel et al. [45], who reported significantly reduced PLR in severe PE, though they did not observe significant differences in NLR. Conversely, Gezer et al. [46] and Kirbas et al. [47] reported that both high NLR and PLR during early pregnancy were independent predictors of PE, with PLR significantly elevated in severe PE. These conflicting findings suggest that PLR may behave differently across disease stages or populations, warranting further investigation. RDW, a marker of erythrocyte size variability, is hypothesized to increase in PE due to inflammation-mediated impairment of erythropoiesis [48]. Our study found higher RDW levels in PE patients compared to controls, though the difference was not statistically significant. Kurt et al. [49] and Yücel et al. [50] reported significantly elevated RDW in severe PE, while Abdullahi et al. [51] found no association. Yılmaz et al. [52] also observed higher RDW in PE, with values increasing in severe disease. Taken together, RDW may have potential as a severity marker, though variability across studies highlights the need for larger cohorts. In our study, most women with PE underwent emergency cesarean section (71.4%), compared with only 7.1% of normotensives. These findings parallel those of Sachan et al. [53], who reported higher operative intervention rates in hypertensive disorders of pregnancy. Furthermore, intrauterine growth restriction (IUGR) was significantly more common among PE patients (31.0%) compared with controls (4.8%), consistent with the pathophysiological effects of placental insufficiency. Neonatal outcomes were poorer in the PE group, with 38.1% requiring NICU admission compared to 21.4% in normotensives, though this difference was not statistically significant.

Preeclampsia remains a life-threatening pregnancy complication with significant implications for maternal and perinatal health, underscoring the need for early and reliable predictive markers. In this study, although neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were found to be marginally elevated in women with preeclampsia compared to normotensive controls, the differences did not reach statistical significance. Nevertheless, these hematological indices, derived from routine complete blood counts, offer promise as simple, rapid, cost-effective, and widely accessible screening tools, particularly in low-resource settings. Larger, multicenter studies with greater sample sizes are warranted to validate their diagnostic and prognostic utility and to establish standardized cut-off values that could enhance early detection and improve maternal and neonatal outcomes.

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