Platelet Count as a Marker of Disease Severity in Pregnancy-Induced Hypertension: A Cross-Sectional Study

Background and objective Pregnancy-induced hypertension (PIH) is a major contributor to maternal and perinatal morbidity and mortality. Platelet count has been proposed as a simple hematological marker of disease severity. This study aimed to evaluate platelet count as a marker of PIH severity and examine its correlation with mean arterial pressure (MAP). Methods This hospital-based cross-sectional analytical study included 220 pregnant women at more than 20 weeks of gestation: 110 normotensive controls and 110 PIH cases, comprising 48 with gestational hypertension (GHTN), 39 with preeclampsia (PE), and 23 with severe preeclampsia (SPE). Continuous variables were summarized as the median (interquartile range (IQR)) because of their non-normal distribution. Platelet counts were measured using an automated hematology analyzer. Blood pressure and MAP were recorded using standard methods. Group comparisons were performed using appropriate non-parametric tests. The association between platelet count and MAP was also assessed. Exploratory receiver operating characteristic (ROC) analysis was performed to assess the discriminatory performance of the platelet count. Results Median age of the participants was similar across groups (p = 0.956). Median gestational age was significantly lower in women with PE and SPE than in normotensive women (p = 0.002). Platelet count showed a stepwise decline across groups, from 3.3 (2.9-3.6) ×10⁵/µL in normotensive women to 2.2 (2.1-2.4) ×10⁵/µL in GHTN (1.7 (1.4-1.9) ×10⁵/µL in PE, and 1.2 (1.1-1.3) ×10⁵/µL in SPE; p < 0.0001; η² ≈ 0.70). MAP increased progressively with disease severity and showed a strong inverse correlation with platelet count (Spearman's ρ = -0.774, p < 0.001). Exploratory ROC analysis showed good discriminatory performance of platelet count for PIH versus normotensive pregnancy (area under the curve (AUC): 0.95; optimal cut-off: 2.5×10⁵/µL; sensitivity: 90.0%; specificity: 90.9%) and for SPE versus non-severe disease (AUC: 0.96; optimal cut-off: 1.7×10⁵/µL; sensitivity: 95.7%; specificity: 86.8%). Conclusions Platelet count decreased progressively with increasing severity of PIH and was strongly inversely associated with MAP. Exploratory ROC findings suggest that platelet count has potential diagnostic utility, but the results should be interpreted cautiously because of the cross-sectional, single-center design. Prospective multicenter validation is needed before platelet count can be recommended as a standalone clinical marker.