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Am J Respir Crit Care Med. 2006 Jun 15;173(12):1363-9. Epub 2006 Mar 16.

Quantifying pulmonary inflammation in cystic fibrosis with positron emission tomography.

Author information

1
Department of Radiology, Washington University School of Medicine, Campus Box 8223, 660 S. Euclid Ave., St. Louis, MO 63110, USA. chend@mir.wustl.edu

Abstract

RATIONALE:

Although infection contributes to morbidity in patients with cystic fibrosis (CF), the host inflammatory response is also an important cause of progressive pulmonary function deterioration. Quantifying the inflammatory burden in these patients is challenging and often requires invasive procedures. Positron emission tomographic imaging with [18F]fluorodeoxyglucose ([18FDG]) could be used as a noninvasive alternative to quantify lung inflammation.

OBJECTIVE:

To determine the relationships among lung [18F]FDG uptake, bronchoalveolar lavage (BAL) neutrophil concentrations, and pulmonary function in patients with CF.

METHODS:

Twenty patients and seven healthy volunteers were studied. A subset of seven patients also consented to undergo BAL. The uptake of [18F]FDG by the lungs was measured as the net influx rate constant Ki. Patients were stratified by rate of decline in pulmonary function into stable, intermediate, and rapidly declining groups. Ki was compared among groups and was correlated against neutrophil concentrations in BAL fluid.

RESULTS:

Ki was significantly elevated (p<0.05) among patients with CF as a whole compared with healthy control subjects (0.0015+/-0.0009 versus 0.0007+/-0.0002 ml blood/ml lung/min) but especially in patients with rapidly declining pulmonary function (0.0022+/-0.0011 ml blood/ml lung/min). Ki correlated positively with the number of neutrophils present in BAL fluid.

CONCLUSION:

Imaging with [18F]fluorodeoxyglucose and positron emission tomography can be used to assess inflammatory burden in patients with CF. Elevations in Ki may be able to identify patients with more aggressive disease and may be useful in monitoring changes in inflammatory burden in response to novel treatments.

PMID:
16543553
PMCID:
PMC2662975
DOI:
10.1164/rccm.200506-934OC
[Indexed for MEDLINE]
Free PMC Article

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