PTH

PTH, or parathyroid hormone, is a peptide hormone produced by the chief cells of the parathyroid glands. In humans, the hormone is synthesized as a larger precursor and processed to an 84‑amino acid peptide; the active portion is the N‑terminal 34 amino acids. PTH regulates calcium and phosphate homeostasis and acts through the PTH1R receptor on bone and kidney.

PTH raises serum calcium and lowers serum phosphate. In bone, it stimulates osteoblasts to express RANKL, promoting osteoclast formation and bone resorption, which releases calcium and phosphate. In the kidney, PTH increases calcium reabsorption in the distal tubule and reduces phosphate reabsorption in the proximal tubule. It also stimulates 1α‑hydroxylase (CYP27B1), increasing production of 1,25‑dihydroxyvitamin D3, which enhances intestinal absorption of calcium and phosphate.

Secretion is primarily driven by low serum calcium, with the calcium‑sensing receptor on parathyroid cells mediating feedback. Calcitriol and high calcium exert negative feedback on PTH release. Magnesium status and phosphate levels can also influence secretion.

Clinically, PTH is central to disorders of calcium balance. Primary hyperparathyroidism (often due to a parathyroid adenoma) causes hypercalcemia and low phosphate. Secondary hyperparathyroidism, common in chronic kidney disease, presents with hypocalcemia and hyperphosphatemia; tertiary hyperparathyroidism can follow prolonged secondary disease. Hypoparathyroidism causes hypocalcemia. Therapeutic considerations include PTH analogs such as teriparatide for osteoporosis, and calcimimetics like cinacalcet to suppress PTH in CKD.