Parathyroid hormone (PTH), an 84 amino acid polypeptide, plays a critical role in the regulation of mineral homeostasis and bone metabolism [1]. The measurement of PTH is used in conjunction with calcium determinations to assess disorders in calcium metabolism [2-4]. PTH affects mineral homeostasis by regulating the rate of kidney mediated reabsorption of calcium and phosphorus and by stimulating the synthesis of calcitriol in the kidney. The direct effect of PTH on bone is to stimulate osteoclastic bone resorption, which is coupled with an increase in bone formation. PTH is an important regulator of calcium homeostasis.
The measurement of PTH has proven to be difficult due to the heterogeneity of peptides that occur in both the gland and circulation [5]. In addition to the formation of fragments within the gland, there is further proteolytic breakdown of PTH once it is released into the circulation [6,7]. Parathyroid hormone and its fragments are cleared from the circulation by both the kidneys and liver [8]. The clearance of C-terminal fragments is slower than the clearance of the intact hormone and is more dependent upon renal mechanisms [9].
Primary and secondary hyperparathyroidism, kidney insufficiency, malabsorption-syndrome and pseudo-hypoparathyroidism result in elevated concentrations of PTH [10]. Decreased concentrations of PTH coincide with high doses of vitamin-D fortified milk, milk-alkali-syndrome, Morbus Boeck (sarcoidosis), hyperthyreosis, ingestion of thiazide and hypercalcemia of malignancy.
PTH concentration is also decreased with absorptive hypercalciuria and hypoparathyroidism.
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