Cyclical Ovarian Function Resistant to Treatment with an Analogue of Luteinizing Hormone Releasing Hormone in McCune–Albright Syndrome

Abstract

THE McCune–Albright syndrome was originally described in the 1930s as the triad of polyostotic fibrous dysplasia, café-au-lait pigmentation, and precocious puberty.^{1 , 2} The mechanism of the precocious puberty has been unclear, with evidence for gonadotropin-mediated central precocious puberty in some cases and for gonadotropin-independent ovarian function in others.^{3 4 5 6 7 8 9 10 11 12 13 14 15} Other endocrinopathies in patients with the McCune–Albright syndrome have included hyperthyroidism, hyperparathyroidism, acromegaly, Cushing's syndrome, and hyperprolactinemia.^{1 2 3 4 , 6 7 8 9 10 , 13 , 14 , 16 17 18 19 20} These observations have led to the hypothesis that autonomous hyperfunction of several endocrine glands might explain the different syndromes of excess hormone production.^{5 6 7 8} In addition, autopsy evidence has shown hyperplasia of endocrine glands in the McCune–Albright . . .