Literature DB >> 8410501

Severe endocrine and nonendocrine manifestations of the McCune-Albright syndrome associated with activating mutations of stimulatory G protein GS.

A Shenker1, L S Weinstein, A Moran, O H Pescovitz, N J Charest, C M Boney, J J Van Wyk, M J Merino, P P Feuillan, A M Spiegel.   

Abstract

McCune-Albright syndrome (MCAS) is a sporadic disease classically including polyostotic fibrous dysplasia, café au lait spots, sexual precocity, and other hyperfunctional endocrinopathies. An activating missense mutation in the gene for the alpha subunit of GS, the G protein that stimulates cyclic adenosine monophosphate formation, has been reported to be present in these patients. The mutation is found in variable abundance in different affected endocrine and nonendocrine tissues, consistent with the mosaic distribution of abnormal cells generated by a somatic cell mutation early in embryogenesis. We describe three patients with MCAS who had profound endocrine and nonendocrine disease and who died in childhood. Two of the patients were severely ill neonates whose complex symptoms did not immediately suggest MCAS. A mutation of residue Arg201 of GS alpha was found in affected tissues from all three children. A review of the literature and unpublished case histories emphasizes the existence of other patients with severe and unusual clinical manifestations. We conclude that the manifestations of MCAS are more extensive than is generally appreciated, and may include hepatobiliary disease, cardiac disease, other nonendocrine abnormalities, and sudden or premature death.

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Year:  1993        PMID: 8410501     DOI: 10.1016/s0022-3476(05)80943-6

Source DB:  PubMed          Journal:  J Pediatr        ISSN: 0022-3476            Impact factor:   4.406


  47 in total

1.  Primary bimorphic adrenocortical disease: cause of hypercortisolism in McCune-Albright syndrome.

Authors:  J Aidan Carney; William F Young; Constantine A Stratakis
Journal:  Am J Surg Pathol       Date:  2011-09       Impact factor: 6.394

2.  Increased IL-6-production by cells isolated from the fibrous bone dysplasia tissues in patients with McCune-Albright syndrome.

Authors:  T Yamamoto; K Ozono; S Kasayama; K Yoh; K Hiroshima; M Takagi; S Matsumoto; T Michigami; K Yamaoka; T Kishimoto; S Okada
Journal:  J Clin Invest       Date:  1996-07-01       Impact factor: 14.808

3.  Dental perspectives in fibrous dysplasia and McCune-Albright syndrome.

Authors:  Sunday O Akintoye; Alison M Boyce; Michael T Collins
Journal:  Oral Surg Oral Med Oral Pathol Oral Radiol       Date:  2013-09

4.  Heterotrimeric G Stimulatory Protein α Subunit Is Required for Intestinal Smooth Muscle Contraction in Mice.

Authors:  Xiaoteng Qin; Shangming Liu; Qiulun Lu; Meng Zhang; Xiuxin Jiang; Sanyuan Hu; Jingxin Li; Cheng Zhang; Jiangang Gao; Min-Sheng Zhu; Robert Feil; Huashun Li; Min Chen; Lee S Weinstein; Yun Zhang; Wencheng Zhang
Journal:  Gastroenterology       Date:  2016-12-30       Impact factor: 22.682

Review 5.  Advances in endocrinology.

Authors:  P E Clayton; V Tillmann
Journal:  Arch Dis Child       Date:  1998-03       Impact factor: 3.791

Review 6.  Fibrous dysplasia of bone: the bone lesion unmasked.

Authors:  F R Singer
Journal:  Am J Pathol       Date:  1997-12       Impact factor: 4.307

7.  Mutations that rescue the paralysis of Caenorhabditis elegans ric-8 (synembryn) mutants activate the G alpha(s) pathway and define a third major branch of the synaptic signaling network.

Authors:  Michael A Schade; Nicole K Reynolds; Claudia M Dollins; Kenneth G Miller
Journal:  Genetics       Date:  2004-10-16       Impact factor: 4.562

Review 8.  Fetal neonatal hyperthyroidism: diagnostic and therapeutic approachment.

Authors:  Selim Kurtoğlu; Ahmet Özdemir
Journal:  Turk Pediatri Ars       Date:  2017-03-01

9.  Genetic diagnosis of multiple affected tissues in a patient with McCune-Albright syndrome.

Authors:  Ji Zhou; Li-hao Sun; Bin Cui; Huai-dong Song; Xiao-ying Li; Guang Ning; Jian-min Liu
Journal:  Endocrine       Date:  2007-04       Impact factor: 3.633

10.  FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1.

Authors:  Jyothsna Gattineni; Carlton Bates; Katherine Twombley; Vangipuram Dwarakanath; Michael L Robinson; Regina Goetz; Moosa Mohammadi; Michel Baum
Journal:  Am J Physiol Renal Physiol       Date:  2009-06-10
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