Hypertens Res. 2026 Feb 17. doi: 10.1038/s41440-026-02571-2. Online ahead of print.
ABSTRACT
Emerging evidence links maternal immune dysregulation to hypertensive disorders of pregnancy (HDP), yet gestational immune alterations preceding symptom onset remain unclear. This study aimed to evaluate the associations between first-trimester immune biomarkers and incident HDP risk across clinical subtypes. This retrospective cohort study enrolled pregnant women aged ≥18 years undergoing first-trimester antenatal screening at a tertiary hospital from March to November 2023. First-trimester peripheral immune markers-neutrophils, monocytes, lymphocytes, and platelets-were measured, with derived indices including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), and aggregate index of systemic inflammation (AISI). Outcomes included HDP, gestational hypertension (GHTN), and preeclampsia confirmed via electronic medical records. Multivariable logistic regression models were performed to evaluate the relationship between peripheral immune markers and outcomes. Among the 2739 pregnant women who met inclusion criteria, 195 developed HDP, including 96 GHTN and 99 preeclampsia. Multivariable logistic regression demonstrated that first-trimester neutrophils, monocytes, platelets, lymphocytes, SII, and AISI were independently and positively associated with HDP risk in a linear dose-response manner (all FDR P < 0.05), with platelets exhibiting the strongest association (OR T3 vs. T1: 2.20; per log-SD: OR = 1.55). Distinct biomarker profiles were identified between GHTN and preeclampsia: GHTN exhibited associations with neutrophils, platelets, SII, and AISI, while preeclampsia correlated with monocytes, platelets, lymphocytes, SII, and AISI (all FDR P < 0.05). Elevated first-trimester immune markers correlate with HDP, particularly platelet-related indices. Divergent immune signatures between GHTN and preeclampsia suggest subtype-specific pathophysiological mechanisms.
PMID:41699290 | DOI:10.1038/s41440-026-02571-2
