The treatment of hypervitaminosis D with hypercalcemia consists of immediate withdrawal of the vitamin, a low calcium diet, generous intake of fluids, along with symptomatic and supportive treatment. Decline in the average rate of linear growth and increased mineralization of bones in infants and children (dwarfism).
Bone demineralization (osteoporosis) in adults occurs concomitantly. Widespread calcification of the soft tissues, including the heart, blood vessels, renal tubules, and lungs. Impairment of renal function with polyuria, nocturia, polydipsia, hypercalciuria, reversible azotemia, hypertension, nephrocalcinosis, generalized vascular calcification, or irreversible renal insufficiency which may result in death. Hypercalcemia with anorexia, nausea, weakness, weight loss, vague aches and stiffness, constipation, mental retardation, anemia, and mild acidosis. Hypervitaminosis D is characterized by: 1. The effects of administered vitamin D can persist for two or more months after cessation of treatment.
Maintenance of a normal serum phosphorous level by dietary phosphate restriction and/or administration of aluminum gels as intestinal phosphate binders in those patients with hyperphosphatemia as frequently seen in renal osteodystrophy is essential to prevent metastatic calcification.Īdequate dietary calcium is necessary for clinical response to vitamin D therapy. In the treatment of hypoparathyroidism, intravenous calcium, parathyroid hormone, and/or dihydrotachysterol may be required. When high therapeutic doses are used progress should be followed with frequent blood calcium determinations. IN VITAMIN D RESISTANT RICKETS THE RANGE BETWEEN THERAPEUTIC AND TOXIC DOSES IS NARROW. Dosage levels must be individualized and great care exercised to prevent serious toxic effects. Therapeutic dosage should be readjusted as soon as there is clinical improvement. Vitamin D administration from fortified foods, dietary supplements, self-administered and prescription drug sources should be evaluated.
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