Effect of long-term calcitonin therapy on the clinical course of osteogenesis imperfecta.

10 children with osteogenesis imperfecta, 4 with "tarda" and 6 with "congenita" varieties of the disease, were treated with salmon calcitonin (SCT) for intervals ranging from 14 to 35 months. Responses to SCT therapy in patients with osteogenesis imperfecta tarda were characterized by an apparent decreased fracture incidence in three, a fall in either alkaline or acid phosphatase, and a rate of increase in forearm bone mass which was greater than that observed in an untreated "tarda" population. The chemical response SCT therapy varied in children with osteogenesis imperfecta congenita, only one demonstrating a decrease in both acid phosphatase and urinary hydroxyproline. Three others responded with a rise in acid phosphatase, two of whom also demonstrated a fall in urinary hydroxyproline; in two other "congenita" patients urinary hydroxyproline was actually higher after SCT treatment and acid phosphatase relatively unchanged. Alkaline phosphatase was normal in all "congenita" patients before and following the SCT treatment interval. These varied biochemical responses were associated with temporary increments in bone mass early in the treatment course, although in bone mass early in the treatment course, although one "congenita" patient with the largest calciuric response to SCT and an increase in hydroxyproline excretion demonstrated progressive increments in skeletal mineral content during a 14-month treatment interval. In both "tarda" and "congenita" subjects, parathyroid hormone was unchanged by chronic SCT treatment; SCT-antibodies were detectable although biological responsivity to SCT persisted.