title: Altered diurnal regulation of blood ionized calcium and serum parathyroid hormone concentrations during parenteral nutrition.
abstract: BACKGROUND
  Little is known about parathyroid gland function in patients receiving total parenteral nutrition (TPN).
  
  
  OBJECTIVE
  Our objective was to determine whether parathyroid gland function is abnormal in TPN recipients.
  
  
  METHODS
  Six patients with a mean (+/-1 SD) age of 45.5 +/- 8.0 y who had been receiving TPN for 18.7 +/- 2. 8 y underwent bone biopsy, bone mass measurements with dual-energy X-ray absorptiometry, and dynamic tests of parathyroid gland function. Diurnal variations in blood ionized calcium (iCa(2+)) and serum parathyroid hormone (PTH) concentrations were also assessed. Results were compared with those of healthy volunteers.
  
  
  RESULTS
  Bone mass and bone formation were subnormal in all patients. Basal serum PTH concentrations were moderately higher in the TPN recipients than in healthy volunteers, and values obtained every 30 min over 24 h were significantly higher (P < 0.001) in TPN recipients (5.0 +/- 0.9 pmol/L) than in healthy volunteers (2.6 +/- 0.6 pmol/L). The percentage increase in serum PTH during citrate-induced hypocalcemia was lower in the TPN recipients, consistent with secondary hyperparathyroidism. Evening infusions of calcium-containing TPN eliminated the nocturnal rise in serum PTH, increased the amplitude of change for iCa(2+) and PTH over 24 h, increased the orderliness of change for iCa(2+) and PTH as measured by approximate entropy (ApEn), and enhanced the synchrony of change between iCa(2+) and PTH. Treatment for 10 d with calcium-free TPN restored the nocturnal rise in serum PTH and increased ApEn for PTH. ApEn for iCa(2+) remained low, suggesting that a component of nutrient solutions, but not calcium per se, enhances the regularity of PTH release in TPN recipients.
  
  
  CONCLUSIONS
  Parathyroid gland function is abnormal in long-term TPN recipients, which may contribute to disturbances in bone metabolism.
authors.affiliation: Departments of Medicine and Pediatrics, University of California Los Angeles School of Medicine, CA 90095, USA. wgoodman@ucla.edu
authors.forename: W G
authors.initials: WG
authors.lastname: Goodman
authors.forename: S
authors.initials: S
authors.lastname: Misra
authors.forename: J D
authors.initials: JD
authors.lastname: Veldhuis
authors.forename: A A
authors.initials: AA
authors.lastname: Portale
authors.forename: H J
authors.initials: HJ
authors.lastname: Wang
authors.forename: M E
authors.initials: ME
authors.lastname: Ament
authors.forename: I B
authors.initials: IB
authors.lastname: Salusky
mesh_terms: D000328:Adult; D015519:Bone Density; D016723:Bone Remodeling; D002118:Calcium / Q000097:blood* / Q000652:urine; D002940:Circadian Rhythm; D002951:Citrates; D005260:Female; D005272:Femur Neck; D006801:Humans; D008159:Lumbar Vertebrae; D008297:Male; D008875:Middle Aged; D010280:Parathyroid Glands / Q000378:metabolism / Q000503:physiopathology*; D010281:Parathyroid Hormone / Q000097:blood*; D010289:Parenteral Nutrition, Total / Q000009:adverse effects; D010343:Patient Admission; D000077559:Sodium Citrate; D013997:Time Factors; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D002951:Citrates; D010281:Parathyroid Hormone; D014807:Vitamin D; D000077559:Sodium Citrate; C097949:1,25-dihydroxyvitamin D; C104450:25-hydroxyvitamin D; D002118:Calcium