Human chorionic gonadotropin (hCG) prevents luteolysis in early pregnancy. Beyond 10–12 weeks, the corpus luteum involutes despite persistently high hCG levels. What physiological event explains this 'luteo-placental shift'?
- A The placenta acquires sufficient 3β-HSD activity to synthesise progesterone independently, making corpus luteum support unnecessary ✓
- B Rising estrogen inhibits hCG receptors on the corpus luteum
- C Maternal immune tolerance fails, causing autoimmune destruction of the corpus luteum
- D Falling LH receptors on luteal cells despite normal hCG levels
Explanation
During the first 8–10 weeks of pregnancy, the corpus luteum is the sole source of progesterone required to maintain decidual support and suppress uterine contractions. As the syncytiotrophoblast matures and acquires 3β-hydroxysteroid dehydrogenase (3β-HSD) enzyme activity, the placenta becomes capable of synthesising adequate progesterone from cholesterol independently. This luteo-placental shift means the embryo is no longer dependent on the corpus luteum for progesterone, and its involution can proceed without threatening the pregnancy.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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