Oral pulse therapy with vitamin D3 for control of secondary hyperparathyroidism
Hebrew University-Hadassah Medical School Pediatric Nephrology
(Impact Factor: 2.86).
11/1994; 8(6):724-726. DOI: 10.1007/BF00869102
Twelve dialysis patients received oral pulse therapy with 1--hydroxyvitamin D3 in a dose of 0.1 g/kg body weight twice weekly and daily calcium carbonate (1.5–3.5 g) for a period of 8–12 months. This treatment was very effective in suppressing secondary hyperparathyroidism without causing hypercalcaemia and/or hyperphosphataemia.
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ABSTRACT: To review the medical literature on management of end-stage renal disease (ESRD) and its complications in the pediatric patient.
MEDLINE searches (1970-1997) of the English-language literature. Clinical trials and reviews of drug therapy management were included, and bibliographies were reviewed for relevant articles.
Principles of renal replacement therapy in children have been expanded to include maintenance of fluid and electrolyte balance and to manage the complications of ESRD in children. Types of renal replacement and their complications are reviewed. Complications of ESRD are reviewed with emphasis on drug therapy management of anemia of chronic renal failure, growth retardation, and hypertension. A discussion of the use of vitamins and supplements to maintain bone and mineral homeostasis is provided, and specific recommendations for vaccination of children with ESRD are given.
Children with end-stage renal failure present a unique challenge to the pharmacist. Renal replacement therapy for children with ESRD involves some form of dialysis and an intensive medication regimen. Complications must be treated with appropriate drug therapy. Drug therapy must be monitored closely for dosage adjustment, clinical response, drug interactions, and toxicity. Patients and families must receive continuous education and follow-up to encourage compliance. The pharmacist must work closely with the healthcare team to optimize drug therapy and improve patient education and compliance.
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ABSTRACT: Vitamin D toxicity can be life-threatening and associated with substantial morbidity, if not identified quickly. Hypervitaminosis D with hypercalcemia may be secondary to excessive intake of parent vitamin D, its metabolites 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), or vitamin D analogs; to increased production of 25(OH)D or 1,25(OH)2D from exogenous substrate; and even to topical applications of potent vitamin D analogs. Vitamin D toxicity is not a common cause of hypercalcemia, but it can be life threatening if not identified promptly. The major causes of hypercalcemia are primary hyperparathyroidism and malignancy. If these two etiologies are excluded, vitamin D toxicity becomes an important diagnostic consideration. Many different mechanisms have been proposed to account for vitamin D toxicity, including the vitamin D metabolite itself, vitamin D receptor (VDR) number, activity of 1α-hydroxylase, inhibition of vitamin D metabolism, and the capacity of vitamin-D-binding protein (DBP). Mounting evidence that higher levels of vitamin D may have beneficial effects on bone and cellular health may predispose to enhanced administration of vitamin D in the future and thereby increased frequency of vitamin D toxicity.
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