|PTH measured by chemiluminescent immunoassay uring the ADVIA Centaur.
Parathyroid hormone (PTH) is secreted by the parathyroid glands and plays an important role in calcium homeostasis by maintaining the concentration of ionised calcium within the precise limits necessary to achieve metabolic and neuroregulatory function of this essential mineral. The parathyroid glands comprise four small glands, located in pairs against each of the two lobes of the thyroid gland. The target tissues for PTH are the bone and kidneys. In bone, PTH promotes the dissolution of bone material, increasing the flow of calcium and phosphate from the bone to the plasma. In the kidneys, PTH reduces the renal clearance of calcium and decreases phosphate reabsorption from the renal tubular fluid, causing phosphaturia. This action tends to decrease the plasma phosphate concentration. PTH also stimulates the kidneys to secrete Vitamin D, the latter increases the efficiency of calcium absorption by the intestinal tract. Measurement of PTH and calcium provide important information for the evaluation of calcium metabolism disorders, such as primary and secondary hyperparathyroidism, hypoparathyroidism and tumour related hypercalcaemia. Primary hyperparathyroidism is usually due to a parathyroid adenoma, less often to diffuse hyperplasia of the glands and only rarely to a parathyroid carcinoma, and is an elevation of PTH which causes an excessive retention of calcium that can precipitate in the kidneys, resulting in stone formation. Secondary hyperparathyroidism is an appropriate increase in the PTH concentration caused by a decrease in the calcium concentration, frequently due to renal disease and Vitamin D deficiency. Both these conditions are associated with decreased synthesis of calcitriol, which causes hypocalcaemia, and the increase in PTH secretion is an appropriate physiological response. The increase in PTH may not, however, normalise the serum calcium; in the absence of adequate calcitriol, there is resistance to the calcium-mobilising effect of PTH on the bone. Occasionally patients with end-stage renal failure become hypercalcaemic, due to the development of autonomous PTH secretion, presumably as a result of the prolonged hypocalcaemic stimulus. It may be seen for the first time in a patient given a renal transplant, who can then metabolise Vitamin D normally. This is termed tertiary hyperparathyroidism. Hypoparathyroidism is a low concentration of PTH that causes a decrease in the plasma calcium concentration that can lead to tetany. Tumour related hypercalcaemia is characterised by a decreased PTH concentration with an elevated concentration of calcium due to bone resorption or the production of compounds by the tumour.