title: Oral vitamin D supplementation reduces the incidence of eucalcemic PTH elevation after surgery for primary hyperparathyroidism.
abstract: BACKGROUND
  As many as 43% of patients will have normocalcemic intact parathyroid hormone (PTH) elevation after undergoing curative parathyroidectomy for primary hyperparathyroidism. This phenomenon may be due in part to an absolute or relative deficiency of vitamin D, which is under-recognized in patients with primary hyperparathyroidism.
  
  
  METHODS
  From September 1, 2004, to September 30, 2005, 86 consecutive patients underwent parathyroidectomy for primary sporadic hyperparathyroidism (psHPT). The patients were segregated into 2 groups based on postoperative management. Group 1 was composed of 26 patients who received routine oral calcitriol and calcium carbonate postoperatively. The 60 patients in the second group (group 2) received calcium carbonate postoperatively at the discretion of the primary surgeon.
  
  
  RESULTS
  A total of 85 patients (99%) achieved postoperative cure with sustained reduction in serum calcium. Within 30 days postoperatively, mean serum PTH levels normalized in both groups (41 +/- 31 vs 39 +/- 31 pg/ml; P = .91). However, at 1 to 3 months postoperatively, mean serum calcium levels remained similar (9.5 +/- 0.7 vs 9.3 +/- 0.5 mg/dl; P = .39) whereas mean serum PTH levels in groups 1 and 2 were 43 +/- 25 pg/ml and 67 +/- 45 pg/ml (P = .02), respectively. At 4 to 6 months postoperatively, mean PTH was again higher in group 2 (36 +/- 22 vs 67 +/- 35; P = .03), whereas mean serum calcium levels were normal (9.2 +/- 0.8 vs 9.6 +/- 0.4 mg/dl; P = .18). The incidence of postoperative normocalcemic PTH elevation was significantly higher in group 2 at 1 to 3 months (14% vs 39%; P = .04) and at 7 to 12 months (22% vs 83%; P = .04).
  
  
  CONCLUSIONS
  Vitamin D supplementation following parathyroidectomy for primary hyperparathyroidism reduces the incidence of postoperative eucalcemic PTH elevation.
authors.affiliation: Department of Surgery, Rush University Medical Center, Chicago, Ill. 60612, USA.
authors.forename: Todd D
authors.initials: TD
authors.lastname: Beyer
authors.forename: Carmen C
authors.initials: CC
authors.lastname: Solorzano
authors.forename: Richard A
authors.initials: RA
authors.lastname: Prinz
authors.forename: Ambika
authors.initials: A
authors.lastname: Babu
authors.forename: Naris
authors.initials: N
authors.lastname: Nilubol
authors.forename: Subhash
authors.initials: S
authors.lastname: Patel
mesh_terms: D000284:Administration, Oral; D000368:Aged; D002117:Calcitriol / Q000627:therapeutic use; D002118:Calcium / Q000097:blood*; D002119:Calcium Carbonate / Q000627:therapeutic use; D002120:Calcium Channel Agonists / Q000627:therapeutic use; D005260:Female; D006801:Humans; D049950:Hyperparathyroidism, Primary / Q000097:blood* / Q000601:surgery*; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000037:antagonists & inhibitors / Q000097:blood*; D016105:Parathyroidectomy; D011182:Postoperative Care; D011184:Postoperative Period; D013997:Time Factors; D014807:Vitamin D / Q000008:administration & dosage* / Q000627:therapeutic use
chemical_list: D002120:Calcium Channel Agonists; C470125:PTH protein, human; D010281:Parathyroid Hormone; D014807:Vitamin D; D002117:Calcitriol; D002119:Calcium Carbonate; D002118:Calcium