Novel Positron Emission Tomography/Computed Tomography of Diffuse Parenchymal Lung Disease Combining a Labeled Somatostatin Receptor Analogue and 2-Deoxy-2[F-18]Fluoro-D-Glucose
Department of Respiratory Medicine, Lister Hospital, Stevenage, UK. Molecular Imaging
(Impact Factor: 1.96).
04/2012; 11(2):91-8. DOI: 10.2310/7290.2011.00030
We prospectively investigated the potential of positron emission tomography (PET) using the somatostatin receptor (SSTR) analogue ⁶⁸Ga-DOTATATE and 2-deoxy-2[¹⁸F]fluoro-D-glucose (¹⁸F-FDG) in diffuse parenchymal lung disease (DPLD). Twenty-six patients (mean age 68.9 ± 11.0 years) with DPLD were recruited for ⁶⁸Ga-DOTATATE and ¹⁸F-FDG combined PET/high-resolution computed tomography (HRCT) studies. Ten patients had idiopathic pulmonary fibrosis (IPF), 12 patients had nonspecific interstitial pneumonia (NSIP), and 4 patients had other forms of DPLD. Using PET, the pulmonary tracer uptake (maximum standardized uptake value [SUV(max)]) was calculated. The distribution of PET tracer was compared to the distribution of lung parenchymal changes on HRCT. All patients demonstrated increased pulmonary PET signal with ⁶⁸Ga-DOTATATE and ¹⁸F-FDG. The distribution of parenchymal uptake was similar, with both tracers corresponding to the distribution of HRCT changes. The mean SUV(max) was 2.2 ± 0.7 for ⁶⁸Ga-DOTATATE and 2.8 ± 1.0 (t-test, p = .018) for ¹⁸F-FDG. The mean ⁶⁸Ga-DOTATATE SUV(max) in IPF patients was 2.5 ± 0.9, whereas it was 2.0 ± 0.7 (p = .235) in NSIP patients. The correlation between ⁶⁸Ga-DOTATATE SUV(max) and gas transfer (transfer factor of the lung for carbon monoxide [TLCO]) was r = -.34 (p = .127) and r = -.49 (p = .028) between ¹⁸F-FDG SUV(max) and TLCO. We provide noninvasive in vivo evidence in humans showing that SSTRs may be detected in the lungs of patients with DPLD in a similar distribution to sites of increased uptake of ¹⁸F-FDG on PET.
Available from: Robin J Green
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ABSTRACT: There is a lack of objective tools to reliably diagnose exacerbations in bronchiectasis. The primary aim of this study was to assess the ability of fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) to detect sites of active inflammation in children with human immunodeficiency virus (HIV)-related bronchiectasis with or without exacerbations. The secondary aim was to assess whether ¹⁸F-FDG-PET/CT results are in agreement with local and systemic inflammatory markers and markers of HIV disease activity. Forty-one children with HIV-related bronchiectasis underwent ¹⁸F-FDG PET/CT. Data on the presence of a clinical exacerbation were recorded. Serum was collected for CD4 count, HIV viral load, C-reactive protein (CRP) and cytokines IL-8, INF-γ and TNF-α. Induced sputum samples were processed for microbiological culture and for IL-8, INF-γ and TNF-α.Mean age of all children was 8.2 ± 2.2 years. Twelve subjects showed F-FDG lung uptake while six of them had an exacerbation. There was no difference in the ¹⁸F-FDG uptake in participants with or without an exacerbation (P=0.613). Fluorine- 18-FDG-PET had a good correlation with the presence of consolidation (P=0.01, OR=6.67). The mean CRP was higher in the subjects with (18)F-FDG uptake when compared to those without uptake (51.96 ± 95.12 vs. 13.26 ± 19.87), although this difference was not significant (P=0.09). In conclusion, the ¹⁸F-FDG-PET lung uptake technique could not reliably predict the presence of an exacerbation in children with HIV and bronchiectasis, and its diagnostic value was limited to identifying disease activity on the scan in acute pneumonia cases. Fluorine-18-FDG-PET had no significant correlation with CRP or with other inflammatory biomarkers and markers of HIV disease activity.
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ABSTRACT: Noninvasive markers of disease activity in patients with idiopathic pulmonary fibrosis (IPF) are lacking. We performed this study to investigate the reproducibility of pulmonary (18)F-FDG PET/CT in patients with IPF.
The study group comprised 13 patients (11 men, 2 women; mean age 71.1 ± 9.9 years) with IPF recruited for two thoracic (18)F-FDG PET/CT studies performed within 2 weeks of each other. All patients were diagnosed with IPF in consensus at multidisciplinary meetings as a result of typical clinical, high-resolution CT and pulmonary function test features. Three methods for evaluating pulmonary (18)F-FDG uptake were used. The maximal (18)F-FDG pulmonary uptake (SUVmax) in the lungs was determined using manual region-of-interest placement. An (18)F-FDG uptake intensity histogram was automatically constructed from segmented lungs to evaluate the distribution of SUVs. Finally, mean SUV was determined for volumes-of-interest in pulmonary regions with interstitial lung changes identified on CT scans. Processing included correction for tissue fraction effects. Bland-Altman analysis was performed and interclass correlation coefficients (ICC) were determined to assess the reproducibility between the first and second PET scans, as well as the level of intraobserver and interobserver agreement.
The mean time between the two scans was 6.3 ± 4.3 days. The interscan ICCs for pulmonary SUVmax analysis and mean SUV corrected for tissue fraction effects were 0.90 and 0.91, respectively. Intensity histograms were different in only 1 of the 13 paired studies. Intraobserver agreement was also excellent (0.80 and 0.85, respectively). Some bias was observed between observers, suggesting that serial studies would benefit from analysis by the same observer.
This study demonstrated that there is excellent short-term reproducibility in pulmonary (18)F-FDG uptake in patients with IPF.
Available from: Toby M Maher
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ABSTRACT: Patients 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.
Consecutive IPF patients (22 men, 3 women) were prospectively recruited. The patients underwent (18)F-FDG PET/HRCT. The pulmonary imaging findings in the IPF patients were compared to the findings in a control population. Pulmonary uptake of (18)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).
The 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).
IPF patients have increased pulmonary uptake of (18)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.
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