title: In vivo and in vitro hepatic phosphorus-31 magnetic resonance spectroscopy and electron microscopy in chronic ductopenic rejection of human liver allografts.
abstract: BACKGROUND
  In vivo hepatic phosphorus-31 magnetic resonance spectroscopy (MRS) provides non-invasive information about phospholipid metabolism.
  
  
  OBJECTIVE
  To delineate MRS abnormalities in patients with chronic ductopenic rejection (CDR) and to characterise spectral changes by in vitro MRS and electron microscopy.
  
  
  METHODS
  Sixteen liver transplant recipients (four with CDR; 12 with good graft function) and 29 controls (23 healthy volunteers; six patients with biliary duct strictures) were studied with in vivo 31P MRS. Peak area ratios of phosphomonoesters (PME) and phosphodiesters (PDE), relative to nucleotide triphosphates (NTP) were measured. In vitro MRS and electron microscopy were performed on biopsy specimens from five patients with CDR, freeze clamped at retransplantation. Phosphoethanolamine (PE), phosphocholine (PC), glycerophosphorylethanolamine (GPE), and glycerophosphorylcholine (GPC) concentrations were measured.
  
  
  RESULTS
  The 12 patients with good graft function displayed no spectral abnormalities in vivo; the four patients with CDR showed significantly elevated PME:NTP (p < 0.01) and PDE:NTP ratios (p < 0.005). Patients with biliary strictures had significant differences in PME:NTP (p < 0.01) from patients with CDR, but not in mean PDE:NTP. In vitro spectra from CDR patients showed elevated PE and PC, mirroring the in vivo changes in PME, but reduced GPE and GPC concentrations were observed, at variance with the in vivo PDE findings. On electron microscopy, there was no proliferation in hepatocyte endoplasmic reticulum.
  
  
  CONCLUSIONS
  The increase in PME:NTP reflects altered phospholipid metabolism in patients with CDR, while the increase in PDE:NTP may represent a significant contribution from bile phospholipid.
authors.affiliation: Robert Steiner MR Unit, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
authors.forename: S D
authors.initials: SD
authors.lastname: Taylor-Robinson
authors.forename: J
authors.initials: J
authors.lastname: Sargentoni
authors.forename: J D
authors.initials: JD
authors.lastname: Bell
authors.forename: E L
authors.initials: EL
authors.lastname: Thomas
authors.forename: C D
authors.initials: CD
authors.lastname: Marcus
authors.forename: K K
authors.initials: KK
authors.lastname: Changani
authors.forename: N
authors.initials: N
authors.lastname: Saeed
authors.forename: H J
authors.initials: HJ
authors.lastname: Hodgson
authors.forename: B R
authors.initials: BR
authors.lastname: Davidson
authors.forename: A K
authors.initials: AK
authors.lastname: Burroughs
authors.forename: K
authors.initials: K
authors.lastname: Rolles
authors.forename: C S
authors.initials: CS
authors.lastname: Foster
authors.forename: I J
authors.initials: IJ
authors.lastname: Cox
mesh_terms: D000328:Adult; D000368:Aged; D001653:Bile Ducts, Intrahepatic / Q000473:pathology; D004983:Ethanolamines / Q000378:metabolism; D005260:Female; D006084:Graft Rejection / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D016031:Liver Transplantation / Q000473:pathology*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009711:Nucleotides / Q000378:metabolism; D010714:Phosphatidylethanolamines / Q000378:metabolism; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D010759:Phosphorus Isotopes; D012086:Reoperation
chemical_list: D004983:Ethanolamines; D009711:Nucleotides; D010714:Phosphatidylethanolamines; D010759:Phosphorus Isotopes; C002449:glycerophosphoethanolamine; C005448:phosphorylethanolamine; D010744:Phosphoric Monoester Hydrolases; D010727:Phosphoric Diester Hydrolases; C020677:glycerophosphocholine phosphodiesterase