Interpretations

Intact PTH (1-84) is a biologically active hormone produced by parathyroid hormones and secreted into systemic circulation. It exerts its effects through the interaction of its first 34 amino acids with the type 1 PTH/PTHrP receptor (PTHR1). PTH fragments, containing carboxyl-(C) or amino-terminal (N-terminal) portions of the molecule arise from either intra-glandular or peripheral degradation of the hormone, are also present in the circulation. As a result, circulating immune-reactive PTH in normocalcemic subjects comprises: PTH 1-84, C-terminal fragments and N-terminal fragments. An increasing body of evidence suggests that some of these fragments, particularly the N-terminally truncated fragment PTH 7-84 (also referred to as non-PTH 1-84), interact with distinct receptors (C-PTH receptor, C-PTHR) and thereby may have important roles in the regulation of bone resorption and serum calcium concentration.
 

The intact (1-84) PTH has a short half-life of about 5 minutes, whereas the carboxy and midmolecule fragments, which are biologically inactive, have half-lives 10- to 20-fold higher make up >90% of the total circulating PTH and are primarily cleared by the kidneys. In patients with renal failure, PTH-C fragments can accumulate to high levels. PTH 1-84 is also elevated in these patients.
 

Intact PTH assays measures not only PTH (1-84) but other fragments including PTH (7-84) which may accumulate in patients with renal insufficiency.
 

The serum calcium level regulates PTH secretion via negative feedback through the parathyroid calcium sensing receptor (CASR). Decreased calcium levels stimulate PTH release. Secreted PTH causes rapid increase in renal tubular reabsorption of calcium and decrease in phosphorus reabsorption. PTH also functions by enhancing mobilization of calcium from bone and increasing renal synthesis of 1,25-dihydroxy vitamin D, which, in turn, increases intestinal calcium absorption. In rare inherited syndromes of parathyroid hormone resistance or unresponsiveness and in renal failure, PTH release may not increase serum calcium levels.
 

Parathyroid hormone (PTH) values should be interpreted in conjunction with serum calcium and phosphorus levels, and the overall clinical presentation and history of the patient.
 

An elevated PTH value with normal serum calcium are not always necessarily indicative of primary hyperparathyroidism. It is possible that the elevation in PTH is due to secondary causes, the most likely cause is due vitamin D deficiency.