title: Acute changes in calcium homeostasis during treatment of primary hyperparathyroidism with risedronate.
abstract: We administered risedronate, a potent oral bisphosphonate, to patients with mild primary hyperparathyroidism in order to 1) determine if we could normalize the serum calcium concentration in the short term, and 2) analyze changes in the homeostatic mechanisms responsible for maintaining hypercalcemia in this patient population. When administered for 7 days, risedronate reduced fasting serum calcium concentrations without significant toxicity in patients with primary hyperparathyroidism. The decrease in serum calcium was accompanied by evidence of inhibition of bone resorption, as assessed by measurement of urinary hydroxyproline, increased serum immunoreactive PTH concentrations, enhanced renal tubular reabsorption of calcium, and a progressive decrease in serum alkaline phosphatase. Serum PTH was partially suppressed by an oral calcium load in untreated patients as well as in patients treated with risedronate. Although patients treated with risedronate had normal fasting serum calcium levels, serum calcium values in these normocalcemic patients were labile after oral ingestion of calcium. After daily calcium intake of 2 g, serum calcium levels in risedronate-treated patients were similar to those in untreated patients with primary hyperparathyroidism, suggesting that there are likely to be fluctuations in serum calcium in risedronate-treated patients with normal fasting serum calcium during postprandial periods. These studies show that risedronate lowers fasting serum calcium during short term treatment. However, further studies are required to determine whether the lability in serum calcium in these patients after an oral calcium load has clinical significance, and whether longer term treatment would maintain serum calcium in the normal range.
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio 78284-7877.
authors.forename: C A
authors.initials: CA
authors.lastname: Reasner
authors.forename: M D
authors.initials: MD
authors.lastname: Stone
authors.forename: D J
authors.initials: DJ
authors.lastname: Hosking
authors.forename: A
authors.initials: A
authors.lastname: Ballah
authors.forename: G R
authors.initials: GR
authors.lastname: Mundy
mesh_terms: D000284:Administration, Oral; D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood; D000704:Analysis of Variance; D001862:Bone Resorption; D002118:Calcium / Q000008:administration & dosage / Q000378:metabolism*; D012968:Etidronic Acid / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D006909:Hydroxyproline / Q000652:urine; D006961:Hyperparathyroidism / Q000188:drug therapy* / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000187:drug effects / Q000378:metabolism; D010281:Parathyroid Hormone / Q000097:blood; D017698:Postmenopause; D000068296:Risedronic Acid
chemical_list: D010281:Parathyroid Hormone; D000469:Alkaline Phosphatase; D000068296:Risedronic Acid; D012968:Etidronic Acid; D006909:Hydroxyproline; D002118:Calcium