Our findings revealed a significantly higher incidence of early-onset thrombocytopenia in neonates born to mothers with PIH than those born to healthy mothers. Notably, neonates born to mothers with preeclampsia were at a significantly higher risk of thrombocytopenia than those born to mothers with gestational hypertension and normotensive mothers. These findings support the hypothesis that maternal gestational hypertension is associated with an increased incidence of early-onset neonatal thrombocytopenia.
The incidence of thrombocytopenia in neonates born to mothers with gestational hypertension was 13.3%, which is similar to that reported in previous studies (6.7–11.1%) [20, 21]. However, the precise mechanism by which maternal gestational hypertension increases neonatal thrombocytopenia remains unclear. However, an association between neonatal thrombocytopenia and placental lesions is linked to poor maternal perfusion or affects fetal vasculature [22, 23].
Angiogenic imbalance is the main pathological feature in mothers with hypertension. Although this condition is less severe in gestational hypertension than in preeclampsia, gestational hypertension is still associated with placental hypoperfusion [13, 24–27]. Based on the limited literature, we inferred that fetal hypoxia caused by maternal gestational hypertension affects megakaryocyte and platelet production; however, further studies are required to elucidate this mechanism.
The risk of thrombocytopenia is significantly increased in neonates with body weight < 1500 g than those with body weight > 1500 g [23, 28]. Our findings corroborate this finding. Furthermore, we observed that neonatal hypoglycemia was associated with an increased risk of early-onset neonatal thrombocytopenia. Approximately 50% of the glucose from maternal circulation is consumed in the placenta, and only 20% is transferred to the fetus. Transplacental glucose transport depends on the glucose gradient from the mother to the fetus, as well as the uteroplacental blood flow. Chronic hypoxia, ischemia, and inflammation would result in increased energy consumption in the placenta and reduced glucose transfer to the fetus, which increases the risk of hypoglycemia after birth [8, 13, 24–27, 29]. Soluble vascular endothelial growth factor receptor-1(sFlt-1) is released by the placenta when its capacity is insufficient, and sFlt-1 is released in large amounts during neonatal hypoglycemia [30]. High sFlt-1 concentration inhibits megakaryocyte maturation and increases platelet activation, leading to thrombocytopenia [30, 31]. However, the exact underlying mechanism requires further investigation.
We compared the incidence of early-onset neonatal thrombocytopenia among neonates born to mothers with gestational hypertension, preeclampsia, and normotension. We also observed that not only maternal preeclampsia, but also maternal gestational hypertension is associated with an increased incidence of early-onset neonatal thrombocytopenia. This study has several limitations. First, the incidence of neonatal thrombocytopenia in mothers with eclampsia was not included, and we could not determine whether the incidence differed among mothers with eclampsia, preeclampsia, or gestational hypertension. Second, we did not analyze whether maternal blood pressure control affected the incidence of neonatal thrombocytopenia. Third, the sample source was limited to neonates hospitalized in a single center, which may have resulted in a selection bias. Furthermore, neonatal blood samples were collected within 72 h but not simultaneously after birth. In addition, the confounding factor of perinatal infection on neonatal thrombocytopenia was not excluded.