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

Florence Comite, Thomas H. Shawker, Ora H. Pescovitz, D. Lynn Loriaux, Gordon B. Cutler

Research output: Contribution to journalArticle

35 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1032-1036
Number of pages5
JournalNew England Journal of Medicine
Volume311
Issue number16
DOIs
StatePublished - Oct 18 1984

ASJC Scopus subject areas

  • Medicine(all)

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