Hyper-parathyroidism
Characterized by overactivity of one or more of the four parathyroid glands, hyperparathyroidism results from excessive secretion of parathyroid hormone (PTH). Such hypersecretion of PTH promotes bone resorption and leads to hypercalcemia and hypophosphatemia. (See Bone resorption in primary hyperparathyroidism.)
Increased renal and GI absorption of calcium occurs.
Primary hyperparathyroidism is commonly diagnosed by elevated calcium levels found on laboratory profiles in asymptomatic patients. It affects women two to three times more commonly than men.
Causes
Hyperparathyroidism may be primary or secondary:
In primary hyperparathyroidism, one or more of the parathyroid glands enlarges, increasing PTH secretion and elevating serum calcium levels. The most common cause is a single adenoma. Primary hyperparathyroidism is also a component of multiple endocrine neoplasia, in which all four glands are usually involved.
In secondary hyperparathyroidism, excessive compensatory production of PTH stems from a hypocalcemia-producing abnormality outside the parathyroid gland, such as rickets, vitamin D deficiency, chronic renal failure, and osteomalacia due to phenytoin.
Signs and symptoms
The clinical effects of primary hyperparathyroidism result from hypercalcemia and are typically present in several body systems.
Renal: nephrocalcinosis due to elevated levels of calcium and, possibly, recurring nephrolithiasis, which may lead to renal insufficiency; renal manifestations, including polyuria, are the most common effects of hyperparathyroidism
Skeletal and articular: chronic lower back pain and easy fracturing due to bone degeneration; bone tenderness; chondrocalcinosis; osteopenia and osteoporosis, especially on the vertebrae; erosions of the juxta-articular surface; subchondral fractures; traumatic synovitis; and pseudogout
GI: pancreatitis, causing constant, severe epigastric pain that radiates to the back; peptic ulcers, causing abdominal pain, anorexia, nausea, and vomiting
Neuromuscular: muscle weakness and atrophy, particularly in the legs
Central nervous system: psychomotor and personality disturbances, depression, overt psychosis, stupor and, possibly, coma
Other: skin necrosis, cataracts, calcium microthrombi to lungs and pancreas, polyuria, anemia, and subcutaneous calcification.
Similarly, in secondary hyperparathyroidism, decreased serum calcium levels may produce the same features of calcium imbalance with skeletal deformities of the long bones (rickets, for example) as well as symptoms of the underlying disease.
Diagnosis
Findings differ in primary and secondary disease.
