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REGULATION OF CALCIUM‐PARATHYROID HORMONE FEEDBACK IN PRIMARY HYPERPARATHYROIDISM: EFFECTS OF BISPHOSPHONATE TREATMENT
Author(s) -
ADAMI S.,
MIAN M.,
BERTOLDO F.,
ROSSINI M.,
JAYAWERRA P.,
O'RIORDAN J. L. H.,
CASCIO V.
Publication year - 1990
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1990.tb00504.x
Subject(s) - endocrinology , medicine , bone resorption , primary hyperparathyroidism , parathyroid hormone , hypercalcaemia , bisphosphonate , hyperparathyroidism , calcium metabolism , bone disease , calcium , osteoporosis
SUMMARY Dichloromethylene bisphosphonate (C12MBP), a powerful inhibitor of bone resorption, was administered to 27 patients with primary hyperparathyroidism. It was given by either intravenous infusion (six patients, 500‐1000 mg day), or by intramuscular injection (six patients, 100‐200 mg/day) or by mouth (15 patients, 1600‐2400 mg/day) for 20–180 days. Sustained suppression of bone resorption was observed in all patients, as judged by a fall in the urinary hydroxyproline excretion. In contrast, the hypocalcaemic effect was inconsistent and short‐lived, particularly in the patients without overt bone disease. The fall in serum calcium seemed largely to be due to a transient dissociation between bone resorption and bone formation and was associated with increases in circulating parathyroid hormone (PTH). In ten patients given the bisphosphonate orally for 6 months, serum calcium was unchanged but serum PTH was significantly raised. These results suggest that Cl2MBP may be of use for short‐term correction of severe hypercalcaemia due to hyperparathyroidism, particularly in the patients with overt bone disease. However, its long‐term use should not be recommended because of increased PTH secretion.