Bone Status Among Patients With Nonsurgical Hypoparathyroidism, Autosomal Dominant Hypocalcaemia, an

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Share Nonsurgical hypoparathyroidism (Ns-HypoPT) and pseudohypoparathyroidism (PHP) are both rare diseases, characterized by hypocalcemia. In Ns-HypoPT, PTH levels are low, whereas patients with PHP often have very high levels due to receptor-insensitivity to PTH (PTH-resistance). Accordingly, we hypothesized that indices of bone turnover and bone mineralization/architecture are similar in Ns-HypoPT and PHP despite marked differences in PTH levels. We studied 62 patients with Ns-HypoPT and 31 with PHP as well as a group of age- and sex-matched healthy controls. We found a significantly higher areal BMD (aBMD) by DXA among patients with Ns-HypoPT, both compared with PHP and the background population. Compared with Ns-HypoPT, PHP patients had significantly lower total and trabecular volumetric BMD (vBMD) assessed by quantitative computed tomography (QCT) scans at the spine and hip. High-resolution peripheral quantitative computed tomography (HRpQCT) scans showed a lower trabecular area and vBMD as well as a lower trabecular number at the tibia in PHP compared to Ns-HypoPT and matched controls. In PHP, PTH levels correlated with levels of markers of bone formation (osteocalcin, bone-specific alkaline phosphatase, P1NP), and bone resorption (CTx). In adult males, levels of bone markers were significantly higher in PHP compared with Ns-HypoPT. Levels of procalcitonin and calcitonin were significantly higher in PHP compared with Ns-HypoPT. In conclusion, indices of bone turnover, density, and microarchitecture differ between patients with Ns-HypoPT and PHP. Our data suggest that patients with PHP do not have a complete skeletal resistance to PTH and that the effects of chronically high PTH levels in PHP are mostly confined to the trabecular tissue. © 2017 American Society for Bone and Mineral Research. Underbjerg L, et al. Clin Endocrinol (Oxf). 2018 Jun;88(6):838-847. doi: 10.1111/cen.13593. Epub 2018 Apr 3. Clin Endocrinol (Oxf). 2018. PMID: 29520810 Underbjerg L, et al. Clin Endocrinol (Oxf). 2019 Apr;90(4):592-600. doi: 10.1111/cen.13927. Epub 2019 Jan 27. Clin Endocrinol (Oxf). 2019. PMID: 30589959 Silva BC, et al. Osteoporos Int. 2017 Feb;28(2):463-471. doi: 10.1007/s00198-016-3750-0. Epub 2016 Aug 30. Osteoporos Int. 2017. PMID: 27577725 Review. Santa Rosa RG, et al. Endocrine. 2023 Dec;82(3):673-680. doi: 10.1007/s12020-023-03495-4. Epub 2023 Aug 25. Endocrine. 2023. PMID: 37624475 Silva BC, et al. Rev Endocr Metab Disord. 2021 Dec;22(4):789-802. doi: 10.1007/s11154-020-09614-0. Epub 2020 Nov 16. Rev Endocr Metab Disord. 2021. PMID: 33200346 Review. Ferrari D, et al. J Clin Med. 2023 Dec 6;12(24):7525. doi: 10.3390/jcm12247525. J Clin Med. 2023. PMID: 38137593 Free PMC article. Review. Wang Y, et al. Curr Osteoporos Rep. 2023 Jun;21(3):311-321. doi: 10.1007/s11914-023-00787-6. Epub 2023 Apr 4. Curr Osteoporos Rep. 2023. PMID: 37014531 Review. Nielsen CV, et al. Calcif Tissue Int. 2021 Jun;108(6):775-784. doi: 10.1007/s00223-021-00814-7. Epub 2021 Feb 12. Calcif Tissue Int. 2021. PMID: 33576839 Zanchetta MB, et al. J Endocr Soc. 2020 Nov 28;5(2):bvaa181. doi: 10.1210/jendso/bvaa181. eCollection 2021 Feb 1. J Endocr Soc. 2020. PMID: 33409439 Free PMC article. Mantovani G, Bastepe M, Monk D, de Sanctis L, Thiele S, Ahmed SF, Bufo R, Choplin T, De Filippo G, Devernois G, Eggermann T, Elli FM, Garcia Ramirez A, Germain-Lee EL, Groussin L, Hamdy NAT, Hanna P, Hiort O, Jüppner H, Kamenický P, Knight N, Le Norcy E, Lecumberri B, Levine MA, Mäkitie O, Martin R, Martos-Moreno GÁ, Minagawa M, Murray P, Pereda A, Pignolo R, Rejnmark L, Rodado R, Rothenbuhler A, Saraff V, Shoemaker AH, Shore EM, Silve C, Turan S, Woods P, Zillikens MC, Perez de Nanclares G, Linglart A. Mantovani G, et al. Horm Res Paediatr. 2020;93(3):182-196. doi: 10.1159/000508985. Epub 2020 Aug 5. Horm Res Paediatr. 2020. PMID: 32756064 Free PMC article. Review.