Not long ago, in these pages,1 we mourned the descent of the pituitary gland as king of the endocrine realm. Mechanisms such as the releasing factors of the hypothalamus, the feedback safety valve, and the inhibitor somatostatin had preempted the signals that loosed its fruits or contained them.
Now, it has been discovered that the pituitary has lost not its ability to govern the functions of the thyroid but its monopoly with respect to hyperthyroidism. The usurper is the hydatidiform mole, a benign neoplasm of the placenta that secretes human chorionic gonadotropin and has been found to be another thyroid-stimulating hormone (TSH).
The first observation of this unlikely maker of thyrotropin was published by Tisné et al2 in 1955, but it received little attention. In the 1960s, several investigators picked up the clue and redemonstrated the connection between the placental mole and hyperthyroidism. In 1969, Hershman and Starnes
Ricketts HT. Long Distance Hyperthyroidism. JAMA. 1976;235(3):287. doi:10.1001/jama.1976.03260290045030