title: Methylglyoxal concentrations differ in standard and washed neonatal packed red blood cells.
abstract: BACKGROUND
  Preterm infants have a greater risk of necrotizing enterocolitis following transfusion. It is hypothesized that high glucose concentrations in red blood cell (RBC) preservatives lead to increased methylglyoxal (MG) metabolism, causing glycation-driven damage to transfused RBCs. Such changes to the RBCs could promote a proinflammatory state in transfusion recipients.
  
  
  METHODS
  Standard and washed RBCs in Adsol-3, two common neonatal preparations, were studied. Consecutive measurements were performed of glucose, MG, reduced glutathione, glyoxalase I activity (GLO-I), and D-lactate, the stable end product of MG detoxification by glyoxalase enzymes over the 42-d storage period.
  
  
  RESULTS
  RBC units consume glucose and produceD-lactate and MG during storage. In 28/30 units, the MG concentrations showed only small variations during storage. Two units had elevated MG levels (>10 pmol/mg Hb) during the first half of storage. Washing of the RBCs significantly reduced both MG and D-lactate.
  
  
  CONCLUSIONS
  This study shows two patterns of MG metabolism in packed RBCs for neonatal transfusion and raises the possibility that RBC units with higher MG levels may have increased glycation-driven damage in the transfused RBCs. Whether transfused MG could trigger an inflammatory response such as necrotizing enterocolitis in preterm neonates and whether washing could prevent this require further study.
authors.affiliation: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: Autumn S
authors.initials: AS
authors.lastname: Kiefer
authors.affiliation: Department of Internal Medicine and Clinical Chemistry, University of Heidelberg, Heidelberg, Germany.
authors.forename: Thomas
authors.initials: T
authors.lastname: Fleming
authors.affiliation: Department of Biostatistics, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: George J
authors.initials: GJ
authors.lastname: Eckert
authors.affiliation: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: Brenda B
authors.initials: BB
authors.lastname: Poindexter
authors.affiliation: Department of Internal Medicine and Clinical Chemistry, University of Heidelberg, Heidelberg, Germany.
authors.forename: Peter P
authors.initials: PP
authors.lastname: Nawroth
authors.affiliation: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: Mervin C
authors.initials: MC
authors.lastname: Yoder
mesh_terms: D000225:Adenine; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001793:Blood Preservation / Q000009:adverse effects*; D020345:Enterocolitis, Necrotizing / Q000139:chemically induced*; D004912:Erythrocytes / Q000737:chemistry*; D005947:Glucose; D005978:Glutathione / Q000097:blood; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D019344:Lactic Acid / Q000097:blood; D007791:Lactoylglutathione Lyase / Q000097:blood; D008353:Mannitol; D011310:Preservatives, Pharmaceutical; D011765:Pyruvaldehyde / Q000009:adverse effects / Q000378:metabolism*; D012965:Sodium Chloride; D065227:Transfusion Reaction
chemical_list: C037839:ADSOL; D001786:Blood Glucose; D011310:Preservatives, Pharmaceutical; D019344:Lactic Acid; D008353:Mannitol; D012965:Sodium Chloride; D011765:Pyruvaldehyde; D007791:Lactoylglutathione Lyase; D005978:Glutathione; D005947:Glucose; D000225:Adenine