title: Acute effect of pamidronate on PTH secretion in postmenopausal hemodialysis patients with secondary hyperparathyroidism.
abstract: BACKGROUND
  The purpose of this study is to evaluate the acute effect of pamidronate on plasma ionized calcium (iCa) level reduction and dynamic parathyroid hormone (PTH) secretion in postmenopausal hemodialysis-dependent women with secondary hyperparathyroidism.
  
  
  METHODS
  Twelve postmenopausal women undergoing regular hemodialysis with serum intact PTH levels greater than 200 pg/mL (200 ng/L) were included in this study. Pamidronate was administered intravenously as a single dose of 15 mg in the last hour of hemodialysis. PTH responses to hypocalcemia and hypercalcemia induced with 1 mEq/L (0.5 mmol/L) and 4 mEq/L (2 mmol/L) of dialysate calcium, respectively, were evaluated before and 1 week after pamidronate therapy.
  
  
  RESULTS
  Pamidronate therapy resulted in a decrease in predialysis basal plasma iCa (iCa(base); P < 0.05) levels and an increase in maximal serum PTH (PTHmax; P < 0.001), basal PTH (PTHbase; P < 0.001), and minimal PTH levels (P < 0.001). The set point of serum calcium and the slope of the PTH-calcium curve were not altered by pamidronate therapy. An inverse correlation was present between iCa(base) and the PTHbase-PTHmax ratio before (r = -0.66; P < 0.05) and after (r = -0.84; P < 0.001) pamidronate therapy.
  
  
  CONCLUSIONS
  Our study shows that pamidronate therapy is associated with reduced plasma iCa levels and increased PTH secretion, resulting in aggravated secondary hyperparathyroidism. These findings suggest that secondary hyperparathyroidism may worsen after the administration of pamidronate, at least in the short term, in postmenopausal hemodialysis patients.
authors.affiliation: Department of Medicine, Division of Nephrology, Tri-Service General Hospital, National Defense Medical Center, Neihu, Taipei, Taiwan.
authors.forename: Kuo-Cheng
authors.initials: KC
authors.lastname: Lu
authors.forename: Lai-King
authors.initials: LK
authors.lastname: Yeung
authors.forename: Shih-Hua
authors.initials: SH
authors.lastname: Lin
authors.forename: Yuh-Feng
authors.initials: YF
authors.lastname: Lin
authors.forename: Pauling
authors.initials: P
authors.lastname: Chu
mesh_terms: D000368:Aged; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D004164:Diphosphonates / Q000009:adverse effects* / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology*; D006996:Hypocalcemia / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications* / Q000628:therapy; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D000077268:Pamidronate; D010281:Parathyroid Hormone / Q000378:metabolism*; D017698:Postmenopause / Q000502:physiology*; D006435:Renal Dialysis
chemical_list: D004164:Diphosphonates; D010281:Parathyroid Hormone; D000077268:Pamidronate