ABSTRACT
Tissue injury in nonmalignant human disease can develop from either disproportionate inflammation or exaggerated fibrotic responses. The molecular and cellular fundamental of these 2 processes, their impact on disease prognosis and the treatment concept deviates fundamentally. Consequently, the synchronous assessment and quantification of these 2 processes in vivo is extremely desirable. Although noninvasive molecular techniques such as 18F-fluorodeoxyglucose PET offer insights into the degree of inflammatory activity, the assessment of the molecular dynamics of fibrosis remains challenging. The 68Ga-fibroblast activation protein inhibitor-46 may improve noninvasive clinical diagnostic performance in patients with both fibroinflammatory pathology and long-term CT-abnormalities after severe COVID-19.
Subject(s)
COVID-19 , Humans , COVID-19/diagnostic imaging , Positron-Emission Tomography , Inflammation , Positron Emission Tomography Computed Tomography , Gallium Radioisotopes , Fluorodeoxyglucose F18ABSTRACT
PATIENTS AND METHODS: Six post COVID-19 patients suspected for pulmonary fibrosis were scheduled for dual-tracer PET/CT with 18 F-FDG and 68 Ga-fibroblast activation protein inhibitor (FAPI)-46. The uptake of 68 Ga-FAPI-46 in the involved lung was compared with a control group of 9 non-COVID-19 patients. Clinical data and PET/CT imaging were collected and analyzed. RESULTS: PET/CT revealed in all 6 pulmonary impaired patients the reduced glucose avidity on 18 F-FDG and clear positivity on 68 Ga-FAPI-46 PET/CT in comparison to the control group. CONCLUSIONS: Enhancing fibrotic repair mechanisms, 68 Ga-FAPI PET/CT may improve noninvasive clinical diagnostic performance in patients with long-term CT abnormalities after severe COVID-19. Although this study shows promising results, additional studies in larger populations are required to establish a general diagnostic guideline.