HELLP syndrome and fetal growth restriction (FGR) are usually treated as distinct maternal and fetal disorders, yet both may arise from a shared disturbance within the coupled maternal–placental–fetal circulation.This paper models the maternal and fetal circulatory systems as two mechanically coupled circuits linked by the placenta and uses pressure difference, blood flow, and vascular resistance as the principal variables. Within this framework, the placenta is defined not only as an exchange organ but also as a resistive interface that governs perfusion balance between the two circulations. In this model, increased placental resistance appears on the maternal side as compensatory hypertension, endothelial injury, and susceptibility to HELLP syndrome, while on the fetal side it appears as reduced perfusion and impaired growth. Placenta-derived factors such as sFlt-1 are positioned as amplifying mechanisms that intensify maternal vascular dysfunction once placental stress is established. The proposed framework reframes HELLP syndrome and FGR as divergent maternal and fetal responses to a common placental circulatory abnormality, offering a unified explanation for why these conditions may coexist, partially overlap, or occur independently.
Takako Okubo (Fri,) studied this question.