title: Airway glucose concentrations and effect on growth of respiratory pathogens in cystic fibrosis.
abstract: BACKGROUND
  Pulmonary decline accelerates in cystic fibrosis-related diabetes (CFRD) proportional to severity of glucose intolerance, but mechanisms are unclear. In people without CF, airway glucose (AG) concentrations are elevated when blood glucose (BG)> or =8 mmol L(-1) (airway threshold), and are associated with acquisition of respiratory infection.
  
  
  METHODS
  To determine the relationship between BG and AG, 40 CF patients underwent paired BG and AG (nasal) measurements. Daily time with BG>airway threshold was compared in 10 CFRD, 10 CF patients with normal glucose tolerance (CF-NGT) and 10 healthy volunteers by continuous BG monitoring. The effect of glucose at airway concentrations on bacterial growth was determined in vitro by optical densitometry.
  
  
  RESULTS
  AG was present more frequently (85%-vs.-19%, p<0.0001) and at higher concentrations (0.5-3 mmol L(-1)-vs.-0.5-1 mmol L(-1), p<0.0001) when BG was > or =8 mmol L(-1)-vs.-<8 mmol L(-1). Daily time with BG> or =8 mmol L(-1) was CFRD (49+/-25%), CF-NGT (6+/-5%), healthy volunteers (1+/-3%), p<0.0001. Staphylococcus aureus growth increased at > or =0.5 mmol L(-1) (p=0.006) and Pseudomonas aeruginosa growth above 1-4 mmol L(-1) glucose (p=0.039).
  
  
  CONCLUSIONS
  BG> or =8 mmol L(-1) predicted elevated AG concentrations in CF, at least in nasal secretions. CFRD patients spent approximately 50% day with BG>airway threshold, implying persistently elevated AG concentrations. Further studies are required to determine whether elevated airway glucose concentrations contribute to accelerated pulmonary decline in CFRD.
authors.affiliation: Glucose and Pulmonary Infection Group, St George's, University of London, Room 66, Ground Floor Jenner Wing, Cardiac and Vascular Sciences (Respiratory), Cranmer Terrace, SW17 0RE, London, United Kingdom.
authors.forename: Amanda L
authors.initials: AL
authors.lastname: Brennan
authors.forename: Khin M
authors.initials: KM
authors.lastname: Gyi
authors.forename: David M
authors.initials: DM
authors.lastname: Wood
authors.forename: Julie
authors.initials: J
authors.lastname: Johnson
authors.forename: Rick
authors.initials: R
authors.lastname: Holliman
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Baines
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Philips
authors.forename: Duncan M
authors.initials: DM
authors.lastname: Geddes
authors.forename: Margaret E
authors.initials: ME
authors.lastname: Hodson
authors.forename: Emma H
authors.initials: EH
authors.lastname: Baker
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D003550:Cystic Fibrosis / Q000378:metabolism* / Q000382:microbiology; D005260:Female; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D018149:Glucose Intolerance / Q000150:complications / Q000235:genetics / Q000378:metabolism; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D008297:Male; D011550:Pseudomonas aeruginosa / Q000187:drug effects* / Q000254:growth & development; D012137:Respiratory System / Q000378:metabolism / Q000382:microbiology; D013211:Staphylococcus aureus / Q000187:drug effects* / Q000254:growth & development
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005947:Glucose