Primary hyperparathyroidism is caused by a parathyroid adenoma in 80-85% of patients and by parathyroid hyperplasia in the remaining 10-15%. Parathyroid cancer is a very uncommon cause of primary hyperparathyroidism.
The excess serum calcium found in hyperparathyroidism occurs through three mechanisms:
The serum phosphorus in patients with hyperparathyroidism is typically low because parathyroid hormone decreases phosphate absorption in the proximal renal tubule.
Consequences include increased plasma calcium, decreased plasma phosphate, polyuria and calcinuria, and decreased bone mass.
Most patients are asymptomatic.
Symptoms may include weakness and constipation (“groans”), abdominal/flank pain due to kidney stones or acute pancreatitis, depression (“psychiatric overtones”).
Radiological signs of hyperparathyroidism often include subperiosteal thinning with cystic degeneration, appearing as subperiosteal erosions in the medial sides of the second and third phalanges of the hand, and a granular "salt-and-pepper" appearance of the calvarium.
Osteitis fibrosa cystica, characterized by cystic bone spaces filled with brown fibrous tissue (“brown tumor” consisting of deposited hemosiderin from hemorrhages), causes bone pain.
Bone manifestations include osteitis fibrosa cystica, where there's an increase in osteoclasts in scalloped areas of the surface bone and replacement of marrow elements with fibrous tissue. Increased alkaline phosphatase is due to high bone turnover.
Other symptoms include increased plasma alkaline phosphatase, osteocalcin and increased excretion of cAMP (the second messenger for PTH in the kidney), and hydroxyproline.