title: Metabolic origin of hypovitaminosis C in acutely hospitalized patients.
abstract: OBJECTIVE
  Recent studies have indicated a high prevalence of hypovitaminosis C in acutely hospitalized patients. It is unclear whether hypovitaminosis C in this setting represents deficiency or tissue redistribution of the vitamin as part of the acute-phase response.
  
  
  METHODS
  We administered vitamin C for 1 wk to acutely hospitalized, but not critically ill patients with hypovitaminosis C, on the assumption that a large increase in plasma and mononuclear leukocyte vitamin C concentrations, a decrease in metabolic markers of oxidative stress, or an improvement in psychologic mood state would implicate the initial condition as nutritional deficiency rather than tissue redistribution.
  
  
  RESULTS
  Vitamin C administration increased plasma and mononuclear leukocyte vitamin C concentrations from subnormal (16.3 ± 12.4 μmol/L and 6.5 ± 5.5 mmol/L, respectively) to normal (71.0 ± 30.9 μmol/L, P < 0.0001, and 8.2 ± 6.8 mmol/L, P < 0.015); the mood disturbance score improved by 33% (P < 0.008). There was no increase in plasma glutathione concentrations or a reduction in plasma or mononuclear leukocyte malondialdehyde concentrations. An inverse relation was observed between plasma C-reactive protein and plasma vitamin C concentrations (P = 0.006).
  
  
  CONCLUSIONS
  Although associated with systemic inflammation, the metabolic features of hypovitaminosis C in acutely hospitalized, non-critically ill patients are more consistent with deficiency than with tissue redistribution.
authors.affiliation: Lady Davis Institute for Medical Research, McGill University and Jewish General Hospital, Montreal, Quebec, Canada.
authors.forename: Rebecca
authors.initials: R
authors.lastname: Evans-Olders
authors.forename: Shaun
authors.initials: S
authors.lastname: Eintracht
authors.forename: L John
authors.initials: LJ
authors.lastname: Hoffer
mesh_terms: D000208:Acute Disease / Q000523:psychology; D000210:Acute-Phase Reaction / Q000097:blood*; D000339:Affect / Q000187:drug effects; D000368:Aged; D000369:Aged, 80 and over; D001205:Ascorbic Acid / Q000097:blood / Q000627:therapeutic use*; D001206:Ascorbic Acid Deficiency / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology / Q000209:etiology*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002170:Canada / Q000453:epidemiology; D005260:Female; D005978:Glutathione / Q000097:blood; D006760:Hospitalization; D006785:Hospitals, University; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects; D015995:Prevalence
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D005978:Glutathione; D001205:Ascorbic Acid