Literature DB >> 19250271

Skeletal consequences of familial hypocalciuric hypercalcaemia vs. primary hyperparathyroidism.

Signe Engkjaer Christensen1, Peter H Nissen, Peter Vestergaard, Lene Heickendorff, Lars Rejnmark, Kim Brixen, Leif Mosekilde.   

Abstract

OBJECTIVES: Bone metabolism is only superficially described in familiar hypocalciuric hypercalcaemia (FHH). We describe and compare biochemical and osteodensitometric variables in FHH and primary hyperparathyroidism (PHPT) and assess whether they can improve the diagnostic discrimination between the groups.
DESIGN: Cross-sectional. PATIENTS: Sixty-six FHH patients with known calcium-sensing receptor (CASR) gene mutations and 147 PHPT patients. MEASUREMENTS: We determined calcium, creatinine, phosphate, magnesium, parathyroid hormone (PTH), 25OHD, 1,25(OH)(2) D and alkaline phosphatase (AP) in plasma, NTx/creatinine ratio in urine and calculated the calcium/creatinine clearance ratio (CCCR). We performed dual energy X-ray absorptiometry at the lumbar spine, hip, forearm and whole body.
RESULTS: When compared with normal controls, the FHH patients had increased levels of PTH and AP with normal U-NTx and regional Z-scores. Increased phenotypic expression of CASR mutations in terms of hypercalcaemia was associated with higher lumbar spine bone mineral density, but not with bone markers. FHH were younger and leaner than the PHPT patients. They had comparable plasma Ca(2+) and 25OHD, but lower levels of PTH, 1,25(OH)(2) D, AP and U-NTx. They had higher Z-scores in the hip and in the forearm. We achieved the best discrimination between groups by multiplying CCCR with AP, 1,25(OH)(2) D and PTH, but the difference between the area under the curves by receiver operating characteristic analysis remained insignificant.
CONCLUSION: Familiar hypocalciuric hypercalcaemia is associated with increased PTH and AP compared to normal controls, but not with bone loss irrespective of the severity of the CASR mutations. A multiplicative model including CCCR, AP, 1,25(OH)(2) D and PTH insignificantly improved the power of the CCCR to differentiate between FHH and PHPT. However, we still recommend CASR gene analysis in patients with a CCCR <0.020.
© 2009 Blackwell Publishing Ltd.

Entities:  

Mesh:

Substances:

Year:  2009        PMID: 19250271     DOI: 10.1111/j.1365-2265.2009.03557.x

Source DB:  PubMed          Journal:  Clin Endocrinol (Oxf)        ISSN: 0300-0664            Impact factor:   3.478


  14 in total

1.  The calcium-sensing receptor complements parathyroid hormone-induced bone turnover in discrete skeletal compartments in mice.

Authors:  Yingben Xue; Yongjun Xiao; Jingning Liu; Andrew C Karaplis; Martin R Pollak; Edward M Brown; Dengshun Miao; David Goltzman
Journal:  Am J Physiol Endocrinol Metab       Date:  2012-01-24       Impact factor: 4.310

Review 2.  The calcium-sensing receptor in bone--mechanistic and therapeutic insights.

Authors:  David Goltzman; Geoffrey N Hendy
Journal:  Nat Rev Endocrinol       Date:  2015-03-10       Impact factor: 43.330

Review 3.  Familial hypocalciuric hypercalcemia and related disorders.

Authors:  Janet Y Lee; Dolores M Shoback
Journal:  Best Pract Res Clin Endocrinol Metab       Date:  2018-05-26       Impact factor: 4.690

Review 4.  The calcium-sensing receptor in bone metabolism: from bench to bedside and back.

Authors:  L Cianferotti; A R Gomes; S Fabbri; A Tanini; M L Brandi
Journal:  Osteoporos Int       Date:  2015-06-23       Impact factor: 4.507

5.  Deficiency of the calcium-sensing receptor in the kidney causes parathyroid hormone-independent hypocalciuria.

Authors:  Hakan R Toka; Khaldoun Al-Romaih; Jacob M Koshy; Salvatore DiBartolo; Claudine H Kos; Stephen J Quinn; Gary C Curhan; David B Mount; Edward M Brown; Martin R Pollak
Journal:  J Am Soc Nephrol       Date:  2012-09-20       Impact factor: 10.121

6.  A phase 2, randomized, placebo-controlled, dose-ranging study of the calcium-sensing receptor antagonist MK-5442 in the treatment of postmenopausal women with osteoporosis.

Authors:  Johan Halse; Susan Greenspan; Felicia Cosman; Graham Ellis; Arthur Santora; Albert Leung; Norman Heyden; Suvajit Samanta; Steven Doleckyj; Elizabeth Rosenberg; Andrew E Denker
Journal:  J Clin Endocrinol Metab       Date:  2014-08-28       Impact factor: 5.958

7.  Atypical skeletal manifestations of rickets in a familial hypocalciuric hypercalcemia patient.

Authors:  Bo Wu; Ou Wang; Yan Jiang; Mei Li; Xiaoping Xing; Weibo Xia
Journal:  Bone Res       Date:  2017-06-27       Impact factor: 13.567

8.  Adaptor protein-2 sigma subunit mutations causing familial hypocalciuric hypercalcaemia type 3 (FHH3) demonstrate genotype-phenotype correlations, codon bias and dominant-negative effects.

Authors:  Fadil M Hannan; Sarah A Howles; Angela Rogers; Treena Cranston; Caroline M Gorvin; Valerie N Babinsky; Anita A Reed; Clare E Thakker; Detlef Bockenhauer; Rosalind S Brown; John M Connell; Jacqueline Cook; Ken Darzy; Sarah Ehtisham; Una Graham; Tony Hulse; Steven J Hunter; Louise Izatt; Dhavendra Kumar; Malachi J McKenna; John A McKnight; Patrick J Morrison; M Zulf Mughal; Domhnall O'Halloran; Simon H Pearce; Mary E Porteous; Mushtaqur Rahman; Tristan Richardson; Robert Robinson; Isabelle Scheers; Haroon Siddique; William G Van't Hoff; Timothy Wang; Michael P Whyte; M Andrew Nesbit; Rajesh V Thakker
Journal:  Hum Mol Genet       Date:  2015-06-16       Impact factor: 6.150

9.  Existing data sources for clinical epidemiology: Danish registries for studies of medical genetic diseases.

Authors:  Mary Nguyen-Nielsen; Elisabeth Svensson; Ida Vogel; Vera Ehrenstein; Lone Sunde
Journal:  Clin Epidemiol       Date:  2013-08-08       Impact factor: 4.790

10.  Familial Hypocalciuric Hypercalcemia in Pregnancy: Diagnostic Pitfalls.

Authors:  Alicia R Jones; Matthew Jl Hare; Justin Brown; Jun Yang; Caroline Meyer; Frances Milat; Carolyn A Allan
Journal:  JBMR Plus       Date:  2020-04-27
View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.