title: Systemic inflammatory mediators and bone homeostasis in intestinal failure.
abstract: BACKGROUND
  A proinflammatory state has been described in patients with intestinal failure. The prevalence of metabolic bone disease in this group is considerable. It is not known whether this proinflammatory state is related to bone parameters, though bone disease is recognized as a proinflammatory process in postmenopausal women. The purpose of this study was to examine whether inflammation was related to bone disease.
  
  
  METHODS
  Eight patients with parenteral nutrition (PN)-dependent intestinal failure but no recent infections or immunosuppressive medications had serum assayed for interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, and its receptors (TNFR-I and TNFR-II), C-reactive protein, and whole blood for lymphocyte proliferation. Routine clinical laboratory measures of vitamin D, parathyroid hormone, serum calcium, and phosphorus within 3 months of the inflammatory measures were compared by Pearson's correlation to the inflammatory measures.
  
  
  RESULTS
  Mean values for calcium, phosphorus, and albumin were normal, but 25-hydroxy vitamin D was reduced and parathyroid hormone and alkaline phosphatase elevated. Serum total calcium was negatively related to TNFR-II, TNF-alpha and positively to T-helper cells. Longer PN dependence was associated with inflammation and negatively with T-helper cells.
  
  
  CONCLUSIONS
  These preliminary findings are hypothesis generating only but support an association of low calcium and longer duration of PN with inflammation in patients with intestinal failure. Whether the inflammation results from vitamin D deficiency or the vitamin D deficiency develops secondary to excessive use of activated vitamin D to modulate inflammation from some other cause, such as a component of PN or repeated infectious challenge, requires further study.
authors.affiliation: University of Pennsylvania School of Nursing, Philadelphia, Pennsylvania 19104-6096, USA. compherc@nursing.upenn.edu
authors.forename: Charlene
authors.initials: C
authors.lastname: Compher
authors.forename: Michael
authors.initials: M
authors.lastname: Pazianas
authors.forename: Stephen
authors.initials: S
authors.lastname: Benedict
authors.forename: John C
authors.initials: JC
authors.lastname: Brown
authors.forename: Bruce P
authors.initials: BP
authors.lastname: Kinosian
authors.forename: Mary
authors.initials: M
authors.lastname: Hise
mesh_terms: D000328:Adult; D000368:Aged; D001851:Bone Diseases, Metabolic / Q000097:blood / Q000453:epidemiology / Q000209:etiology* / Q000276:immunology; D001842:Bone and Bones / Q000378:metabolism*; D002118:Calcium / Q000097:blood; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism; D007410:Intestinal Diseases / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D016331:Parenteral Nutrition, Home / Q000009:adverse effects*; D013601:T-Lymphocytes; D014807:Vitamin D / Q000031:analogs & derivatives / Q000097:blood*; D014808:Vitamin D Deficiency / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology
chemical_list: D018836:Inflammation Mediators; D010281:Parathyroid Hormone; D014807:Vitamin D; C104450:25-hydroxyvitamin D; D002118:Calcium