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.1,2This 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.3,4,5Although 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