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

doi:10.1056/NEJM198410183111607

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

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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 language	English (US)
Pages (from-to)	1032-1036
Number of pages	5
Journal	New England Journal of Medicine
Volume	311
Issue number	16
DOIs	https://doi.org/10.1056/NEJM198410183111607
State	Published - Oct 18 1984
Externally published	Yes

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General Medicine

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title = "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, caf{\'e}-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.",

author = "Florence Comite and Shawker, {Thomas H.} and Pescovitz, {Ora H.} and Loriaux, {D. Lynn} and Cutler, {Gordon B.}",

year = "1984",

month = oct,

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doi = "10.1056/NEJM198410183111607",

language = "English (US)",

volume = "311",

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AU - Comite, Florence

AU - Shawker, Thomas H.

AU - Pescovitz, Ora H.

AU - Loriaux, D. Lynn

AU - Cutler, Gordon B.

PY - 1984/10/18

Y1 - 1984/10/18

N2 - 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.

AB - 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.

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

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