A 28-year-old primigravida at 34 weeks gestation has BP 158/104 mmHg, proteinuria 2+ on dipstick, and new-onset headache. sFlt-1/PlGF ratio is measured at 85. Which of the following statements best characterises the pathophysiology of her condition?
- A Excessive placental secretion of PlGF causes endothelial activation via the VEGFR-1 receptor
- B Deficiency of soluble endoglin reduces TGF-β signalling and promotes vasoconstriction
- C Elevated sFlt-1 sequesters free VEGF and PlGF, leading to systemic endothelial dysfunction ✓
- D Increased placental nitric oxide production causes paradoxical vasoconstriction in the uteroplacental bed
Correct answer: C. Elevated sFlt-1 sequesters free VEGF and PlGF, leading to systemic endothelial dysfunction
Explanation
In pre-eclampsia, the placenta releases excess soluble Flt-1 (sFlt-1), a decoy receptor that binds and neutralises circulating VEGF and PlGF, depriving endothelium of essential survival factors and causing widespread endothelial dysfunction, hypertension, and proteinuria. PlGF is not elevated but rather consumed/sequestered. Soluble endoglin is also elevated and compounds TGF-β inhibition, but the primary anti-angiogenic culprit is sFlt-1. Nitric oxide is reduced, not increased, in pre-eclampsia.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.