– Hyperactivity of one or more of the parathyroid glands, which is manifested as hypercalcemia.
Causes and Incidence
Primary hyperparathyroidism is caused by a parathyroid adenoma, multiple endocrine neoplasia, or a genetic defect. Secondary hyperparathyroidism is caused by underlying disease such as rickets, renal failure, or osteomalacia; pregnancy; vitamin D or calcium deficiency; or an excessive intake of laxatives. The disease most often occurs in adults 30 to 70 years of age. Women are more likely than men to be diagnosed (3:2 ratio).
In primary hyperparathyroidism, one or more of the parathyroid glands hypertrophies, increasing secretion of parathyroid hormone (PTH) and elevating serum calcium levels. Increased PTH causes an increase in osteoblast formation, which increases bone turnover rate. Cysts and fibrous tissue invade the bone. Increased calcium causes renal calculi, a decrease in neuromuscular excitability, a delay in gastrointestinal motility, defects in cardiac conduction, and decreased neuronal permeability. In secondary disease the elevated PTH stems from a hypocalcemia-producing abnormality outside the gland that stimulates the gland to produce more calcium.
Manifestations include bone pain, backache, pain on weight bearing, pathologic fractures, dilute urine and hematuria, fatigue, clumsiness, constipation, acute abdominal pain, mood swings, and paranoia.
Renal failure, cardiac arrhythmias, cardiac failure, central nervous system coma, and death are complications associated with untreated hyperparathyroidism.
Increases in total serum calcium, ionized calcium, PTH, uric acid, and chloride are the usual diagnostic findings. A thyroid scan, ultrasound, computed tomography, or magnetic resonance imaging may be used to locate parathyroid lesions. X-ray studies reveal bone demineralization. Intact PTH is used to distinguish primary from secondary and malignant disease.
Parathyroidectomy to remove adenoma or other abnormal parathyroid tissue.
Diuretics (no thiazides, since they can lead to hypercalcemia) to increase urinary secretion of calcium; phosphate as an antihypercalcemic.
Treatment of the underlying disease in secondary hyperparathyroidism; increased fluid intake; restriction of dietary intake of calcium; monitoring of daily serum calcium, blood urea nitrogen, and potassium and magnesium levels.