Background: The so-called "intact parathyroid hormone (iPTH)" assay detects large C-terminal PTH fragments that are lacking several N-terminal amino acid residues in addition to 1-84 PTH molecules.
Methods: Blood samples were obtained from 65 predialysis patients (male, 35; female, 30) and 109 dialysis patients (male, 73; female, 36). The plasma 1-84 PTH levels were determined by a specific immunoradiometric assay (IRMA).
Results: The ratio of 1-84 PTH/iPTH did not show a significant correlation with glomerular filtration rate (GFR) among patients with a GFR of more than 80 ml/min, while it showed a positive correlation with GFR among patients with a GFR of less than 80 ml/min. The ratio of 1-84 PTH/iPTH demonstrated a significant tendency to decrease in the order of patients with normal renal function (0.928 +/- 0.182), those with renal dysfunction (0.836 +/- 0.186; P < 0.05 vs patients with GFR > 80 ml/min [i.e., normal renal function]), and those with maintenance hemodialysis (0.618 +/- 0.123; P < 0.01 vs patients with GFR > 80 ml/min). The plasma levels of 1-84 PTH and conventional iPTH showed a close correlation in dialysis patients. Neither 1-84 PTH levels nor secondary parameters calculated from them showed a better correlation with bone metabolic markers than iPTH levels.
Conclusions: Circulating large C-terminal PTH fragment levels are increased in uremic patients. However, this noninvasive study failed to demonstrate the superiority of the specific 1-84 assay compared with the conventional iPTH assay to evaluate bone metabolism.
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http://dx.doi.org/10.1007/s10157-003-0226-2 | DOI Listing |
Br J Clin Pharmacol
December 2024
Department of Clinical Pharmacy and Pharmacology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
Medicina (Kaunas)
November 2024
Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdańsk, 80-210 Gdańsk, Poland.
Arch Endocrinol Metab
November 2024
Universidade Federal de São Paulo Escola Paulista de Medicina Departamento de Endocrinologia e Metabolismo São PauloSP Brasil Departamento de Endocrinologia e Metabolismo, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
The main diagnostic dilemma in normocalcemic hyperparathyroidism is differentiating this condition from secondary hyperparathyroidism and other causes of elevated parathyroid hormone (PTH) levels in eucalcemic patients, including potential assay interferences. Despite the analytical sensitivity of immunoassays, they may lack adequate accuracy due to several analytical interferences, such as the presence of heterophilic antibodies. Immunoassays for PTH measurement use the immunometric "sandwich" technique, and only a few cases of interference with this assay have been reported to date.
View Article and Find Full Text PDFEndocrine
October 2024
Department of Pediatrics, IRCCS Ospedale San Raffaele, Milano, Italy.
Background: Hypoparathyroidism is a rare endocrine disease characterized by insufficient parathyroid hormone (PTH) secretion by the parathyroid glands, leading to hypocalcemia. In contrast to most hormone deficiencies for which hormone replacement is currently the mainstay of therapy, hypoparathyroidism has conventionally been treated with calcium supplements and active analogs of vitamin D. Although the advent of a replacement therapy with 1-34 and 1-84 PTH represented a major step in the therapeutic history of hypoparathyroidism, several new molecules and different management strategies have recently been developed.
View Article and Find Full Text PDFFront Pharmacol
September 2024
Division of Clinical Medicine, University of Sheffield, Sheffield, United Kingdom.
Introduction: Receptor activity-modifying proteins (RAMPs) are known to modulate the pharmacology and function of several G-protein-coupled receptors (GPCRs), including the parathyroid hormone 1 receptor (PTH1R). However, the precise effects of different RAMPs on PTH1R signalling and trafficking remain poorly understood. This study investigated the impact of RAMP2 and RAMP3 on PTH1R function using a range of PTH and PTH-related protein (PTHrP)-derived ligands.
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