title: Metabolic and inflammatory responses to pulmonary exacerbation in adults with cystic fibrosis.
abstract: BACKGROUND
  We hypothesized that increased resting energy expenditure in adults with cystic fibrosis was related to chronic inflammation secondary to pulmonary infection and could be modified by treatment of the underlying infection.
  
  
  METHODS
  To determine the relationship between resting energy expenditure and the inflammatory and metabolic responses, we studied 22 adults with cystic fibrosis and chronic Pseudomonas aeruginosa infection before and after treatment of a respiratory exacerbation. Resting energy expenditure was measured by indirect calorimetry. Spirometry and circulating concentrations of C-reactive protein, neutrophil elastase alpha1-antiproteinase complex, catecholamines, non-esterified fatty acids and glycerol were determined.
  
  
  RESULTS
  The mean (95% confidence interval)% predicted FEV1 was 28.5% (20.6, 36.4) and mean body weight 50.7 kg (47.4, 54.1). Following treatment, 1-s forced expiratory volume (FEV1) and weight increased, while C-reactive protein (P<0.0001) and neutrophil elastase alpha1-antiproteinase complex concentrations (P<0.0001) were reduced. Resting energy expenditure decreased from 6.8 (6.3, 7.2) to 6.25 (5.9, 6.6) MJ day-1 by day 15 (P<0.001). Changes in resting energy expenditure and C-reactive protein were related (r = 0.66, P< 0.0001). Weight gain was inversely related to resting energy expenditure (r = 0.43, P = 0.02) and unrelated to energy intake (r = 0.02, P = 0.47). Post-treatment reduction in norepinephrine was related to changes in heart rate (r = 0.57, P<0.01), resting energy expenditure (r = 0.51, P = 0.001) and non-esterified fatty acids (r = 0.42, P< 0.05).
  
  
  CONCLUSIONS
  A parallel reduction in the host inflammatory and catabolic responses followed treatment of a respiratory exacerbation and may have contributed to weight gain.
authors.affiliation: Llandough Hospital and Community NHS Trust, Cardiff, UK. bells@health.qld.gov.au
authors.forename: S C
authors.initials: SC
authors.lastname: Bell
authors.forename: A M
authors.initials: AM
authors.lastname: Bowerman
authors.forename: L E
authors.initials: LE
authors.lastname: Nixon
authors.forename: I A
authors.initials: IA
authors.lastname: Macdonald
authors.forename: J S
authors.initials: JS
authors.lastname: Elborn
authors.forename: D J
authors.initials: DJ
authors.lastname: Shale
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D002100:Cachexia / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D002908:Chronic Disease; D003550:Cystic Fibrosis / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D004435:Eating; D004734:Energy Metabolism; D004837:Epinephrine / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005541:Forced Expiratory Volume; D006339:Heart Rate; D006801:Humans; D008168:Lung / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology; D009638:Norepinephrine / Q000097:blood; D015596:Nutrition Assessment; D018410:Pneumonia, Bacterial / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D011552:Pseudomonas Infections / Q000276:immunology* / Q000378:metabolism*; D011550:Pseudomonas aeruginosa; D014280:Triglycerides / Q000097:blood
chemical_list: D005230:Fatty Acids, Nonesterified; D014280:Triglycerides; D002097:C-Reactive Protein; D009638:Norepinephrine; D004837:Epinephrine