Effect of calcitonin replacement therapy in idiopathic juvenile osteoporosis
E. C. Jackson, C. F. Strife, R. C. Tsang and H. K. Marder
Department of Pediatrics, University of Kentucky Medical Center, Lexington 40536.
An 8-year-old boy with idiopathic juvenile osteoporosis and multiple
fractures had three abnormalities of bone mineral metabolism: calcitonin
deficiency, elevated serum calcitriol concentrations, and hypercalciuria.
Calcitonin deficiency was documented by two attempts to stimulate
calcitonin secretion with intravenous calcium and pentagastrin. Treatment
for 11 months with daily subcutaneous injections of human calcitonin and
oral administration of calcitriol failed to reduce the excessive bone
resorption observed on bone biopsy, and the fracture rate did not decrease.
Treatment was discontinued for two months, then resumed with calcitonin
injections and oral calcium supplementation. The fracture rate decreased
but bone biopsy continued to show excessive resorption. Therapy was
discontinued. After the onset of puberty, endogenous calcitonin was
detectable. Exogenous calcitonin therapy may have failed to control bone
resorption for several reasons: insufficient dose, reduction of bone
receptors from long-term calcitonin exposure, secondary
hyperparathyroidism, or lack of association between calcitonin deficiency
and the bone disease.
