This 50-year-old man with cerebellar syndrome was admitted for a pulmonary embolism, and CT scan showed osteocondensation lesions. QWBT was obtained 3 hours after 99mTc-hydroxymethylene diphosphonate (HDP) injection, as previously described (Bahloul et al, 2021), and initial QWBT images exhibited rib and sacrum fractures, as well as highly-contrasted areas typical of ECD and affecting the mandible and long bones symmetrically, whilst sparing epiphyseal regions (Mazor et al, 2013). The corresponding Maximal Intensity Projection (MIP) images are displayed in A (May 2021), as well as through rotating cine-loops in a supplemental file, with a conventional 0–13 SUV scaling (Bahloul et al, 2021) and an additional display where red lines represent the limits of hypermetabolism areas (i.e., those > 7.5 SUV (Bahloul et al, 2021)) located on limbs and skull and thus, likely due to ECD (Mazor et al, 2013).
Biopsy identified ECD with BRAF-V600 mutation and 18F-FDG PET identified a cerebellum hypometabolism (B, June 2021) in line with ECD-related atrophy at MRI (Na et al, 2008). It is of note, however, that the bone abnormalities exhibited a higher contrast on the QWBT than on PET pre-therapeutic images.
On the following QWBTs (A), the volume of ECD-related abnormalities exhibited a slight increase from 522 to 677 cm3 in December 2021, despite 5-months of α-interferon treatment, but a subsequent 50% reduction down to 329 cm3 on May 2022, after 3-months of more effectively targeted therapy by BRAF-inhibitors (Goyal et al, 2020). It is of note that the bone metabolism abnormalities still appeared much easier to delineate on the post-therapeutic QWBT images than on the PET images. This may be explained by the higher bone specificity of 99mTc-HDP than of 18F-FDG, and to the difference in physiopathological mechanisms imaged by the two radiotracers (i.e., reactive osteosynthesis for 99mTc-HDP vs. inflammatory cells infiltrate for 18F-FDG (Ohara et al, 2019)).