American journal of clinical and experimental immunology · 2026
Association of early-pregnancy platelet-to-high-density lipoprotein cholesterol ratio with preeclampsia: a retrospective cohort study.
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Wang Feifei, Wang Andi, Jiang Dong, Lin Chunhua, Fu Wenyu, Qiao Longwei, Sun Jian
Аннотация
BACKGROUND: Preeclampsia (PE) is a major cause of poor maternal and perinatal outcomes. While a number of biophysical and biochemical markers have been explored for early prediction, there is a need for low-cost accessible markers. The platelet-to-high-density lipoprotein cholesterol ratio (PHR) might reflect the combined effects of impaired platelet function, inflammatory thrombosis and reduced protection against vascular injury.
METHODS: This retrospective cohort included 11,618 pregnancies assessed in early pregnancy. PHR, calculated from platelet count and high-density lipoprotein cholesterol, was analyzed per 10-unit increment. Logistic regression assessed associations with PE, subgroup analyses examined major phenotypes, and receiver operating characteristic analyses compared individual discrimination with mean arterial pressure multiples of the median (MAP MoM) and placental growth factor multiples of the median (PlGF MoM) values.
RESULTS: Among 11,618 pregnancies, 468 women (4.03%) developed PE. Median PHR per 10 was lower among women who developed PE than among those who did not (15.07 [IQR, 11.93-18.24] vs. 19.05 [IQR, 16.82-21.75]; P<0.001). In multivariable analyses controlling for maternal age, body mass index before pregnancy, parity, type of gestation, and conception by in vitro fertilization, every 10-point rise in PHR was linked to a reduced likelihood of PE (adjusted odds ratio, 0.69; 95% CI, 0.67-0.72; P<0.001). PHR values were significantly decreased in early-onset, preterm, and late-onset PE compared with pregnancies without PE (all P<0.01), but did not differ significantly across these three subtypes. Among participants with available Fetal Medicine Foundation (FMF) screening data, the AUCs were 0.732 (95% CI, 0.693-0.771) for PHR, 0.702 (95% CI, 0.669-0.738) for MAP MoM, and 0.606 (95% CI, 0.570-0.638) for PlGF MoM.
CONCLUSION: Lower early-pregnancy PHR was independently associated with subsequent PE. PHR had the highest AUC point estimate among the three individual biomarkers evaluated.
METHODS: This retrospective cohort included 11,618 pregnancies assessed in early pregnancy. PHR, calculated from platelet count and high-density lipoprotein cholesterol, was analyzed per 10-unit increment. Logistic regression assessed associations with PE, subgroup analyses examined major phenotypes, and receiver operating characteristic analyses compared individual discrimination with mean arterial pressure multiples of the median (MAP MoM) and placental growth factor multiples of the median (PlGF MoM) values.
RESULTS: Among 11,618 pregnancies, 468 women (4.03%) developed PE. Median PHR per 10 was lower among women who developed PE than among those who did not (15.07 [IQR, 11.93-18.24] vs. 19.05 [IQR, 16.82-21.75]; P<0.001). In multivariable analyses controlling for maternal age, body mass index before pregnancy, parity, type of gestation, and conception by in vitro fertilization, every 10-point rise in PHR was linked to a reduced likelihood of PE (adjusted odds ratio, 0.69; 95% CI, 0.67-0.72; P<0.001). PHR values were significantly decreased in early-onset, preterm, and late-onset PE compared with pregnancies without PE (all P<0.01), but did not differ significantly across these three subtypes. Among participants with available Fetal Medicine Foundation (FMF) screening data, the AUCs were 0.732 (95% CI, 0.693-0.771) for PHR, 0.702 (95% CI, 0.669-0.738) for MAP MoM, and 0.606 (95% CI, 0.570-0.638) for PlGF MoM.
CONCLUSION: Lower early-pregnancy PHR was independently associated with subsequent PE. PHR had the highest AUC point estimate among the three individual biomarkers evaluated.