LETTER
Bone Density and Vitamin D Intoxication
Barbara B. Sterkel, MD
15 March 1998 | Volume 128 Issue 6 | Page 507
TO THE EDITOR:
The diagnosis "hypervitaminosis D" is more appropriate than "vitamin D intoxication" for the four patients that Adams and Lee [1] observed to have 25-hydroxyvitamin D [25(OH)D] levels twice the upper limit of normal and elevated ratios of fasting urinary calcium to creatinine. These patients do not meet the "vitamin D poisoning" criteria of hypercalcemia, hyperphosphatemia, nephrolithiasis, nephrocalcinosis, or ectopic calcifications described by Albright and Reifenstein in their book Parathyroid Glands and Metabolic Bone Disease.
In the presence of elevated 25(OH)D levels and adequate calcium intake, intestinal hyperabsorption is more likely to be the cause of hypercalciuria [2] than is a presumed increase from mobilization of skeletal calcium. No biochemical measurement of bone turnover was obtained, and bone loss was not documented by measurement of bone density before the elevated 25(OH)D levels were detected. Furthermore, the measured gain in bone density cannot be entirely attributed to normalized 25(OH)D levels alone because all four patients were given calcium and vitamin D supplementation, and two received estrogen; these therapies are expected to increase mineralization [3]. Radiography and lateral morphometry were not performed to exclude vertebral compression or degenerative arthritis. These conditions may account for increased mineralization as measured by anteroposterior dual-energy x-ray absorptiometry of the spine.
Vitamin D deficiency is common in elderly populations [4], and supplementation has been shown to reduce fracture rates in nursing home residents [5], prevent demineralization in patients receiving glucocorticoids, and prevent postmenopausal bone loss. The need to obtain a full history of dietary and supplemental vitamin intake is an important message. However, for fear of an unquantitated toxicity, Adams and Lee may inappropriately discourage physicians from incorporating this important substance into the therapeutic regimen for elderly, relatively immobilized patients, who are prone to occult forms of vitamin D deficiency.
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Author and Article Information
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Washington University School of Medicine; St. Louis, MO 63110
1. Adams JS, Lee G. Gains in bone mineral density with resolution of vitamin D intoxication. Ann Intern Med. 1997; 127:203-6.
2. Pak CY, Oata M, Lawrence EC, Snyder W. The hypercalciurias: causes, parathyroid functions, and diagnositic criteria. J Clin Invest. 1974; 54:387-400.
3. Lindsay R, Tohme JF. Estrogen treatment of patients with established postmenopausal osteoporosis. Obstet Gynecol. 1990; 76:290-5.
4. Villareal DT, Civitelli R, Chines A, Avioli LV. Subclinical vitamin D deficiency in postmenopausal women with low vertebral bone mass. J Clin Endocrinol Metab. 1991; 72:628-34.
5. Chapuy MC, Arlot M, Duboeuf F, Brun J, Crouzet B, Arnaud S, et al. Vitamin D3 and calcium to prevent hip fracture in elderly women. N Engl J Med. 1992; 327:1637-42.
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