Uninterrupted oral bisphosphonate (pamidronate) therapy of patients with osteoporosis is not associated with chronic stimulation of parathyroid hormone secretion.

Abstract

We have previously reported that long-term uninterrupted treatment of patients with osteoporosis with oral pamidronate is associated with increases in bone mineral content (BMC) of the lumbar spine which could not be explained by the antiresorptive action of the drug alone, raising the possibility of an additional effect of the treatment on skeletal tissue. Administration of suppressive doses of the bisphosphonate to patients with excessive osteoclastic resorption is followed by transient decreases in serum calcium and increases in parathyroid hormone (PTH) concentrations. It is possible, therefore, that chronic pamidronate therapy may stimulate PTH secretion, which in turn has been previously shown to have anabolic effects on the skeleton. To test this hypothesis we examined the changes in serum calcium. PTH and phosphate concentrations every 6 months in 33 patients with vertebral osteoporosis and no biochemical evidence of increased bone turnover, treated with oral pamidronate 150 mg daily. Serum alkaline phosphatase and urinary hydroxyproline excretion decreased significantly by 20% and 28%, respectively, after 6 months of treatment and remained at this level for the following 18 months. These changes were associated with significant increases in spinal BMC, as expected. Serum calcium, PTH and phosphate did not change from baseline values either in the whole group or when the patients were divided according to the use or not of calcium supplements. Our results exclude chronic stimulation of PTH secretion as a factor contributing to long-term increases in bone mass in patients with osteoporosis and adequate calcium intake during continuous oral pamidronate therapy.