Literature DB >> 28323910

Progressive Development of PTH Resistance in Patients With Inactivating Mutations on the Maternal Allele of GNAS.

Alessia Usardi1, Asmaa Mamoune1, Elodie Nattes2, Jean-Claude Carel3, Anya Rothenbuhler1,2, Agnès Linglart1,2,4.   

Abstract

Context: Parathormone (PTH) resistance is characterized by hypocalcaemia, hyperphosphatemia, and elevated PTH in the absence of vitamin D deficiency. Pseudohypoparathyroidism type 1A [PHP1A, or inactivating parathormone (PTH)/PTHrp signaling disorder 2, according to the new classification (iPPSD2)], is caused by mutations in the maternal GNAS allele. Objective: To assess PTH resistance over time in 20 patients affected by iPPSD2 (PHP1A), diagnosed because of family history, ectopic ossification, or short stature, and carrying a GNAS mutation.
Methods: We gathered retrospective data for calcium, phosphate, thyrotropin (TSH), and PTH levels at regular intervals. PTH infusion testing (teriparatide) was performed in 1 patient.
Results: Patients were diagnosed at a mean age of 3.9 years and had a mean follow-up of 2 years. TSH resistance was already present at diagnosis in all patients (TSH, 13.3 ± 9.0 mIU/L). Over time, PTH levels increased (179 to 306 pg/mL; P < 0.05), and calcium levels decreased (2.31 to 2.21 mmol/L; P < 0.05), but phosphate levels did not decrease with age as expected for healthy individuals. One patient born with ectopic ossifications showed an increase in cyclic adenosine monophosphate upon PTH infusion, similar to that of controls, at 7 months of age, but an impaired response at 4 years of age. Conclusions: In patients with iPPSD2 (PHP1A), PTH resistance and hypocalcemia develop over time. These findings highlight the importance of screening for maternal GNAS mutations in the presence of ectopic ossifications or family history, even in the absence of PTH resistance and hypocalcemia. The follow-up of these patients should include regular assessments of calcium, phosphate, and PTH levels.
Copyright © 2017 Endocrine Society

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Year:  2017        PMID: 28323910     DOI: 10.1210/jc.2016-3544

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  11 in total

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Authors:  Monica Reyes; Bert Bravenboer; Harald Jüppner
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Review 2.  Molecular Definition of Pseudohypoparathyroidism Variants.

Authors:  Harald Jüppner
Journal:  J Clin Endocrinol Metab       Date:  2021-05-13       Impact factor: 5.958

3.  Progression of PTH Resistance in Autosomal Dominant Pseudohypoparathyroidism Type Ib Due to Maternal STX16 Deletions.

Authors:  Zentaro Kiuchi; Monica Reyes; Patrick Hanna; Anu Sharma; Terry DeClue; Robert C Olney; Peter Tebben; Harald Jüppner
Journal:  J Clin Endocrinol Metab       Date:  2022-01-18       Impact factor: 6.134

Review 4.  Management of pseudohypoparathyroidism.

Authors:  Emily L Germain-Lee
Journal:  Curr Opin Pediatr       Date:  2019-08       Impact factor: 2.856

5.  Pseudohypoparathyroidism: application of the Italian common healthcare-pathway for a homogeneous clinical approach and a shared follow up.

Authors:  Daniele Tessaris; Elisa Bonino; Giovanna Weber; Malgorzata Wasniewska; Domenico Corica; Marco Pitea; Giuseppe Scirè; Manuela Caruso-Nicoletti; Danilo Fintini; Luisa de Sanctis
Journal:  Ital J Pediatr       Date:  2021-03-04       Impact factor: 2.638

6.  Calcitriol and Levothyroxine Dosing for Patients With Pseudohypoparathyroidism.

Authors:  Jacqueline Antoun; Dylan Williamson; Merla Hubler; Ashley H Shoemaker
Journal:  J Endocr Soc       Date:  2021-10-27

7.  A novel variant in the GNAS complex locus causes Albright hereditary osteodystrophy with pseudopseudohypoparathyroidism.

Authors:  Jeffrey S Smith; Abdulrahman A Aldeeri; Scott A Elman; Joel B Krier; Joseph F Merola
Journal:  JAAD Case Rep       Date:  2022-01-19

8.  GNAS mutation is an unusual cause of primary adrenal insufficiency: a case report.

Authors:  Yajie Tong; Dongmei Yue; Ying Xin; Dan Zhang
Journal:  BMC Pediatr       Date:  2022-08-04       Impact factor: 2.567

9.  Case report: An infantile lethal form of Albright hereditary osteodystrophy due to a GNAS mutation.

Authors:  Valérie Leclercq; Valérie Benoit; Damien Lederer; Melanie Delaunoy; Marcela Ruiz; Claire de Halleux; Olivier Robaux; Catherine Wanty; Isabelle Maystadt
Journal:  Clin Case Rep       Date:  2018-08-16

10.  Dental anomalies and orthodontic characteristics in patients with pseudohypoparathyroidism.

Authors:  Jane Hejlesen; Line Underbjerg; Hans Gjørup; Tanja Sikjaer; Lars Rejnmark; Dorte Haubek
Journal:  BMC Oral Health       Date:  2019-12-31       Impact factor: 2.757

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