Pediatric Hyperparathyroidism Medication
- Author: Gordon L Klein, MD, MPH; Chief Editor: Stephen Kemp, MD, PhD more...
At present, satisfactory medical therapy for primary hyperparathyroidism is being developed and early studies are promising. Pharmacologic treatment for secondary hyperparathyroidism is currently oral or parenteral calcitriol (1,25-dihydroxyvitamin D) in patients with renal failure. However, increasing use of paricalcitol or cinacalcet may reduce the need for surgical resection.
Vitamin D analogs
These agents regulate serum calcium levels via actions on calcium and phosphorus metabolism at intestinal, renal, and skeletal sites. The kidney appears to play a central role in this system. It produces calcitriol (ie, 1,25-dihydroxyvitamin D, the primary active metabolite of vitamin D3), which acts on distal organs, and at the same time is the target organ for parathyroid hormone (PTH), calcitonin, and possibly calcitriol. Calcitriol is administered to help suppress excessive PTH release and blunt the hyperparathyroid response to chronic renal failure.
Unlike calcitriol, a new vitamin D analog, paricalcitol, can treat secondary hyperparathyroidism without raising serum calcium and phosphorus levels. Paricalcitol is not yet extensively used in pediatric patients, but articles by Sanchez and Seeherunvong et al have described initial data suggesting safety and effectiveness in children.[16, 17]
Used in attempted suppression of PTH secretion stimulated by inability of the kidneys to excrete phosphate, with its consequent accumulation in blood. Increases calcium levels by promoting absorption of calcium in the intestines and retention in the kidneys. Has not been tried in patients with other causes of secondary hyperparathyroidism.
For treatment of secondary hyperparathyroidism in ESRD. Reduces PTH levels, stimulates calcium and phosphorous absorption, and stimulates bone mineralization.
Sodium chloride 0.9% fluid is used to supply intravenous hydration to replace fluids lost by emesis for patients with acute hypercalcemia of any etiology.
Commonly used solution that is designed to replace circulating crystalloid lost by emesis.
Once hydration has been established, use of a diuretic (eg, furosemide) can help increase calciuresis without adding to the dehydration caused by hypercalcemia.
Increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.
The published doses of 80-100 mg for adults and 25-50 mg for children IV q4h should be reserved for the most severe cases.
Bisphosphonates are antiresorptive agents that are used to help preserve bone mass. They are available in oral and parenteral forms. The inhibition of bone resorption produces a hypocalcemic effect. These agents are used in the management of conditions associated with increased bone resorption (eg, osteoporosis, Paget disease, management of hypercalcemia [especially that associated with malignancy]).
In case of acute hypercalcemia with vomiting, parenteral therapy is recommended. By reducing bone resorption, a calcium-lowering effect in the blood may occur.
IV bisphosphonate that acts as an antiresorptive agent. Inhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization. Currently accepted uses include the treatment of hypercalcemia associated with neoplasms and metastases as well as for treatment of Paget disease. This category of drugs is not approved for the treatment of hypercalcemia secondary to hyperparathyroidism; however, in practice, can be used for this as well as in the management of postmenopausal osteoporosis. Now being used in pediatrics to treat osteogenesis imperfecta and idiopathic juvenile osteoporosis. Preliminary study results on its use to prevent bone loss following severe burns appear promising.
These agents reduce PTH levels. A small clinical trial by Muscheites et al in children showed an 80% decrease in serum PTH levels.
Directly lowers intact parathyroid hormone (iPTH) levels by increasing sensitivity of calcium sensing receptor on chief cell of parathyroid gland to extracellular calcium. Also results in concomitant serum calcium decrease. Indicated for secondary hyperparathyroidism in patients with chronic kidney disease on dialysis.
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