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Condition caused by increased functioning of the parathyroid glands.



a disease caused by excessive production of the hormone of the parathyroid glands, usually occurring as the result of adenoma of those glands.

An excess of parathyroid hormone mobilizes the calcium in the bones, raises its level in the blood and lowers the level of phosphorus, and raises the quantity of calcium and phosphorus in the urine (which is then discharged). Softening and deformation of the bones is the result of this process, making possible spontaneous fracture or fracture caused by minimal injury. Visceropathic forms of hyperparathyroidism are characterized by calcium deposits in the internal organs. The most widespread is the renal form (formation of calculi in the kidneys and urinary tracts). The cause of formation of adenomas in the parathyroid glands is not known. Hyperparathyroidism is more commonly found in women. Treatment involves removal of the tumor; orthopedic treatment is necessary when the disease affects the bones, and removal of the calculi is necessary in nephrolithiasis.


References in periodicals archive ?
Caption: Figure 8: Bony resorption of greater trochanters of both femoral bones typical of untreated hyperparathyroid bone disease at the locations of the patient's pain (denoted by arrow).
26 mmol/liter), in patient with hyperparathyroid coma it raised up to 5.
The development of type II compounds proceeded with an eye on future use in hyperparathyroid states.
For all stone types, acute management involves hydration and evaluation for associated conditions such as obesity, insulin resistance, kidney structural changes, urinary tract infection, chronic kidney disease, and hyperparathyroid ism.
Last years, hyperparathyroid nature of these processes is more often mentioned, especially in combination of bones' demineralization with forming stones kidneys (Moosgaard et al.
Two hyperparathyroid glands were enlarged and hypercellular (weighing 2.
Short-term administration of the bisphosphonate ibandronate increases bone volume and prevents hyperparathyroid bone changes in mild experimental renal failure.
At one time, the only way to treat hyperparathyroid disease was to push serum calcium levels to the point of hypercalcemia, not appreciating the "calcium load" and what happened to the calcium.
Regardless of the degree of maternal hypercalcemia, it is advisable to carefully monitor the mother for hyperparathyroid crisis postpartum, and to monitor the neonate for signs of hypocalcemia or impending tetany.
Thirty-one of the drain patients had adenomas, and 6 were hyperparathyroid secondary to hyperplastic glands.
Because aminobisphosphonates block bone resorption, they can lead to hypocalcemia followed by a secondary hyperparathyroid response to restore normocalcemia.