Abstract
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Objectives Alterations in tissue permeability due to inflammation results in non-specific increases in accumulation of tracers at these sites. L-Glucose is not a substrate for either glucose carrier proteins or hexokinase and therefore cellular penetration is minimal. Thus, an F-18 labeled L-glucose analog may be useful for delineation of sites of inflammation using PET. In this report we prepared 2-[18F]fluoro-2-deoxy-L-glucose and studied its localization in inflammatory foci.
Methods 2-[18F]fluoro-2-deoxy-L-glucose was prepared from the L-mannose triflate in a manner similar to that for 2-FDG production. Focal sites of inflammation were produced in mice by bacterial infection, turpentine injection and thermal injury. Animals with each type of inflammation were injected with ~ 0.7 mCi tracer and imaged dynamically for 30 min with a Siemens P4 microPET camera. After rebinning in 2 min frames the images were reconstructed and regions of interest were placed over the inflammatory sites and the contralateral uninvolved area.
Results This sugar analog rapidly entered infammatory sites. In infected tissues and turpentine induced inflammation, peak uptake occurred at ~ 20 min after injection (peak lesion/muscle: infection ~ 3.0, turpentine ~ 1.5) and decrease slightly thereafter. In burned tissue, peak uptake occurred at ~ 10 min after injection (peak lesion/muscle ~ 2.0) and decrease slightly thereafter. In contrast, the tracer washed-out rapidly in normal tissue beginning at ~3-4 min after injection.
Conclusions The rapid uptake of 2-[18F]fluoro-2-deoxy-L-glucose is due to increased tissue permeability and demonstrates the feasibility of using 2-[18F]fluoro-2-deoxy-L-glucose for imaging of infection and inflammation