Laboratory screening for hyperparathyroidism

Younes, Nidal A.; Shafagoj, Yanal; Khatib, Faisal; Ababneh, Mahmoud

doi:10.1016/j.cccn.2004.10.003

Cited by 43 publications

(29 citation statements)

References 83 publications

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“…At the time of presentation, the patient's plasma PTH, measured by use of the Nichols Advantage Intact PTH assay, was 6.40 pmol/L, a value inappropriately high for the patient's age [Յ5.51 pmol/L in patients Ͻ17 years (13 )] and his increased calcium concentration. The findings of hypercalcemia in combination with hypophosphatemia and nonsuppressed PTH led to a diagnosis of primary hyperparathyroidism (14 ).…”

Section: Case Historymentioning

confidence: 99%

“…The patient's fractional excretion of calcium was 0.02, providing evidence that familial hypocalciuric hypercalcemia (FHH) was unlikely to be the cause of the hypercalcemia (14,15 ). To further explore if the hypercalcemia was due to familial hyperparathyroidism, calcium and phosphorus measurements were obtained from the patient's parents and were within the appropriate reference intervals.…”

Section: Case Historymentioning

confidence: 99%

“…However, hypercalcemic patients with asymptomatic primary hyperparathyroidism can exhibit PTH values in the high-normal range. In the absence of hyperparathyroidism, PTH is normally low or undetectable in the presence of increased calcium and thus a PTH value within the reference interval is inappropriate in the context of hypercalcemia (14,19,25 ). The identification of primary hyperparathyroidism is particularly important in children because it is associated with a higher incidence of end-organ damage than in adults (1 ).…”

Section: Differential Diagnosis Of Hypercalcemia In An Adolescentmentioning

confidence: 99%

“…Patients rarely exhibit symptoms of hypercalcemia, and typically have normal or slightly increased PTH in the presence of mild hypercalcemia. A fractional excretion of calcium (Ca urine ‫ء‬ Cr serum /Ca serum ‫ء‬ Cr urine ) of Ͻ0.01 is diagnostic (14 ). The condition is generally without long-term sequelae and parathyroidectomy is not recommended.…”

Section: Differential Diagnosis Of Hypercalcemia In An Adolescentmentioning

confidence: 99%

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Persistent Hypercalcemia After Parathyroidectomy in an Adolescent and Effect of Treatment With Cinacalcet HCl

Henrich¹,

Rogol

D'Amour

et al. 2006

Clinical Chemistry

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Background: Hyperparathyroidism is uncommon in adolescence and is more likely to persist after parathyroidectomy than in adults. Cinacalcet HCl is a new calcimimetic that has been used successfully for the treatment of primary and secondary hyperparathyroidism in adults, but its use in adolescents has not been reported. Case: A 16 year-old male presented with hypercalcemia that had persisted for 1.5 years after parathyroidectomy for primary hyperparathyroidism. Parathyroid hormone (PTH) concentrations were nonsupressed despite a mean (SD) serum calcium concentration of 2.82 (0.06) mmol/L. Treatment with cinacalcet HCl was initiated and a pharmacodynamic profile was obtained for serum calcium, phosphorus, and PTH. Cinacalcet HCl normalized serum calcium. The changes in PTH were assay dependent. Issues: We use this case conference to review the evaluation of hypercalcemia in adolescents, examine the changes in relevant laboratory results during treatment with cinacalcet HCl, and discuss differences among assays for PTH. Conclusions: Interpretation of PTH results in patients treated with cinacalcet HCl requires consideration of the pharmacodynamic effects of the drug and the nature of the PTH assay.

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Section: Case Historymentioning

confidence: 99%

Section: Case Historymentioning

confidence: 99%

Section: Differential Diagnosis Of Hypercalcemia In An Adolescentmentioning

confidence: 99%

Section: Differential Diagnosis Of Hypercalcemia In An Adolescentmentioning

confidence: 99%

See 2 more Smart Citations

Persistent Hypercalcemia After Parathyroidectomy in an Adolescent and Effect of Treatment With Cinacalcet HCl

Henrich¹,

Rogol

D'Amour

et al. 2006

Clinical Chemistry

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“…Some authors suggest that the long-term stimulation of parathyroids in S-HPTH results in their hyperplasia. Presumably, it could also induce benign transformation and overt autonomy of glands in T-HPTH as proposed by some investigators (9). A similar condition predominantly characterizes primary HPTH (P-HPTH) with the adenoma morphology of parathyroids and high levels of serum PTH.…”

Section: Introductionmentioning

confidence: 98%

The calcium-sensing receptor and vitamin D receptor expression in tertiary hyperparathyroidism

Grzela

Chudziński²,

Lasiecka³

et al. 2006

Int J Mol Med

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Abstract. The parathormone (PTH) production is controlled by calcium and vitamin D, which interact with the calciumsensing receptor (CaSR) and vitamin D receptor (VDR), respectively. All of these elements control calcium homeostasis, which is crucial for many physiological processes. Thus, impairment of the upstream component of this system, e.g. a decrease of CaSR and/or VDR, could result in hyperparathyroidism (HPTH). Therefore, the aim of this study was to assess the expression of CaSR and VDR in a tertiary form of HPTH (T-HPTH). The study involved 19 T-HPTH patients qualified for parathyroidectomy and 21 control parathyroids harvested from multi-organ cadaver donors. The small fragments of harvested glands were homogenized and used for Western blot analysis, whereas the remaining tissues underwent routine hematoxylin-eosin staining or immunostaining for CaSR and VDR. Among 64 T-HPTH parathyroids, 58 revealed the morphology of benign hyperplasia, 2 were identified as adenoma and 4 were classified as normal; some glands displayed a mixed histological phenotype. Western blot analysis revealed a decrease of CaSR and VDR in hyperplasia and adenomaderived samples. However, no correlation between the types of hyperplasia and receptor expression was observed. On the other hand, microscopic analysis of CaSR-and VDRimmunostained sections revealed a highly differentiated and significantly decreased mean expression of both receptors, which correlated with parathyroid histology. The reason behind the impaired expression of CaSR and VDR in T-HPTH is unclear. It presumably results from constant parathyroid stimulation at the stage of S-HPTH, followed by further development of polyclonal autonomy. However, the verification of this thesis requires further study. IntroductionThe production and secretion of parathormone (PTH), a main hormone produced by chief cells of parathyroid glands, remains under the control of calcium ions and vitamin D metabolites. The target molecules for these two key regulatory factors are calcium-sensing receptor (CaSR) and vitamin D receptor (VDR), respectively (1).Calcium-sensing receptor, which belongs to the class III of G-protein coupled receptors, could be activated by various di-and tri-valent cations, especially Ca 2+ and Mg 2+ , but also L-amino acids and other positively charged molecules (2). The triggering of CaSR by these agonists has been shown to post-transcriptionally down-regulate PTH expression, primarily by influencing the PTH-mRNA stability (1). The activation of CaSR also appears to inhibit parathyroid cell proliferation, however, the detailed molecular mechanism of this action remains unclear (3). Presumably, a useful model for the more precise determination of CaSR biological significance could be patients with loss-of-function receptor mutations, resulting in familial benign (hypocalciuric) hypercalcaemia (FBHH) or neonatal severe primary hyperparathyroidism (NSP-HPTH) (4).The receptor for vitamin D is the intracellular phosphoprotein belonging to the nuclear receptor superfa...

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Endokrinologische Labordiagnostik

Obermayer-Pietsch¹

Labormedizin

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Laboratory screening for hyperparathyroidism

Cited by 43 publications

References 83 publications

Persistent Hypercalcemia After Parathyroidectomy in an Adolescent and Effect of Treatment With Cinacalcet HCl

Persistent Hypercalcemia After Parathyroidectomy in an Adolescent and Effect of Treatment With Cinacalcet HCl

The calcium-sensing receptor and vitamin D receptor expression in tertiary hyperparathyroidism

Endokrinologische Labordiagnostik

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