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Familial Vitamin D Resistant Rickets in Untreated AdultBony Proliferation of Neural Arches With Cord Compression
C. CONRAD JOHNSTON, JR., MD;
GERALD J. KURLANDER, MD;
DAVID M. SMITH, MD;
JULIUS M. GOODMAN, MD;
ROBERT L CAMPBELL, MD
Arch Intern Med. 1966;117(1):141-147.
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RICKETS ICKETS in the growing child and osteomalacia in the adult are now rarely due to simple vitamin-D deficiency. Renal tubular defects and intestinal malabsorption are frequently associated with the clinical picture of rickets, and large doses of vitamin D are usually required for healing. One syndrome, familial vitamin D resistant rickets, is well characterized genetically and clinically.1,2 This disease is inherited as a sex-linked dominant. The children present a picture of rickets, which is usually more marked in the lower extremities. Large doses of vitamin D are necessary for treatment, but the results have not been especially satisfactory.3,4,5 Although active rickets cease at the time of closure of the epiphyses, these patients remain dwarfed with deformities of the lower extremities, and have been confused with achondroplastic dwarfs. The clinical picture of osteomalacia, with roentgenographic evidence of decreased bone density and pseudofractures, is unusual in adults with familial
. . . [Full Text PDF of this Article]
Author Affiliations
INDIANAPOLIS
From the departments of medicine and radiology and division of neurological surgery, Indiana University School of Medicine.
Footnotes
Submitted for publication May 21, 1965; accepted July 28.
Reprint requests to 1100 W Michigan St, Indianapolis, Ind 46207 (Dr. Johnston).
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