PARATHORMONE DOSAGE AND SERUM CALCIUM AND PHOSPHORUS IN EXPERIMENTAL CHRONIC HYPERPARATHYROIDISM LEADING TO OSTITIS FIBROSA

1. On a low calcium intake hypercalcemia tended to disappear in chronic hyperparathyroidism on a given dose of parathormone (as large as 6 units per kg.), apparently due to the reduction of a readily available calcium reserve. An increase of either the calcium intake or of the daily dose of parathormone caused a rise of serum calcium and symptoms of overdosage. 2. Hypocalcemia developed in chronic hyperparathyroidism in young puppies on a low calcium diet. Tetany occurred at a calcium level which was higher and a phosphorus level which was lower than in tetania parathyreopriva of young puppies. About 0.1 gm. of calcium daily was apparently sufficient to maintain the serum calcium at a normal level. 3. The serum phosphorus in chronic hyperparathyroidism in young puppies continued at or rose above the high level normal for young animals. Toward the end of long periods of treatment on large parathormone doses (about 5 units per kg.) serum phosphorus approached normal levels, pronounced hypercalcemia was absent but hypotonia and other symptoms of hyperparathyroidism were present. 4. A single dose of parathormone caused early in the treatment and on liberal calcium intakes a more marked relative rise of serum calcium than in normal adult dogs, confirming previous observations (5, 8). Later in the treatment and on low calcium intakes this effect was greatly reduced. Serum phosphorus rose after a single injection of parathormone, even when the effect on the serum calcium was slight or absent. 5. The continued effect of parathormone on serum calcium after prolonged periods of treatment, and the modified response of the serum phosphorus indicate tolerance due to some compensation, rather than immunity. 6. The bone lesions, presenting the essential features of ostitis fibrosa cystica (von Recklinghausen's disease) in varying degrees of severity, depending on the relation of the parathormone dose to the calcium intake and to the duration of the treatment, were most prominent on low calcium intakes, which permitted the use of large doses of parathormone without fatal hypercalcemia and without symptoms of overdosage. 7. Clinical and experimental hyperparathyroidism are compared and discussed.