Novel Positron Emission Tomography/Computed Tomography of Diffuse Parenchymal Lung Disease Combining a Labeled Somatostatin Receptor Analogue and 2-Deoxy-2 [F] Fluoro-D-Glucose

Abstract

We prospectively investigated the potential of positron emission tomography (PET) using the somatostatin receptor (SSTR) analogue 68 Ga-DOTATATE and 2-deoxy-2[ 18 F]fluoro-D-glucose ( 18 F-FDG) in diffuse parenchymal lung disease (DPLD). Twenty-six patients (mean age 68.9 ± 11.0 years) with DPLD were recruited for 68 Ga-DOTATATE and 18 F-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 68 Ga-DOTATATE and 18 F-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 68 Ga-DOTATATE and 2.8 ± 1.0 ( t -test, p = .018) for 18 F-FDG. The mean 68 Ga-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 68 Ga-DOTATATE SUV max and gas transfer (transfer factor of the lung for carbon monoxide [TL CO ]) was r = .34 ( p = .127) and r = .49 ( p = .028) between 18 F-FDG SUV max and TL CO . 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 18 F-FDG on PET.