Areas of normal pulmonary parenchyma on HRCT exhibit increased FDG PET signal in IPF patientsReport as inadecuate




Areas of normal pulmonary parenchyma on HRCT exhibit increased FDG PET signal in IPF patients - Download this document for free, or read online. Document in PDF available to download.

European Journal of Nuclear Medicine and Molecular Imaging

, Volume 41, Issue 2, pp 337–342

First Online: 14 August 2013Received: 29 January 2013Accepted: 07 July 2013DOI: 10.1007-s00259-013-2514-8

Cite this article as: Win, T., Thomas, B.A., Lambrou, T. et al. Eur J Nucl Med Mol Imaging 2014 41: 337. doi:10.1007-s00259-013-2514-8

Abstract

PurposePatients with idiopathic pulmonary fibrosis IPF show increased PET signal at sites of morphological abnormality on high-resolution computed tomography HRCT. The purpose of this investigation was to investigate the PET signal at sites of normal-appearing lung on HRCT in IPF.

MethodsConsecutive IPF patients 22 men, 3 women were prospectively recruited. The patients underwent F-FDG PET-HRCT. The pulmonary imaging findings in the IPF patients were compared to the findings in a control population. Pulmonary uptake of F-FDG mean SUV was quantified at sites of morphologically normal parenchyma on HRCT. SUVs were also corrected for tissue fraction TF. The mean SUV in IPF patients was compared with that in 25 controls patients with lymphoma in remission or suspected paraneoplastic syndrome with normal PET-CT appearances.

ResultsThe pulmonary SUV mean ± SD uncorrected for TF in the controls was 0.48 ± 0.14 and 0.78 ± 0.24 taken from normal lung regions in IPF patients p < 0.001. The TF-corrected mean SUV in the controls was 2.24 ± 0.29 and 3.24 ± 0.84 in IPF patients p < 0.001.

ConclusionIPF patients have increased pulmonary uptake of F-FDG on PET in areas of lung with a normal morphological appearance on HRCT. This may have implications for determining disease mechanisms and treatment monitoring.

KeywordsIdiopathic pulmonary fibrosis PET-CT  Download fulltext PDF



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Source: https://link.springer.com/







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