Laboratory of Pulmonary Engineering, Biomedical Engineering Program, Alberto Luiz Coimbra Institute of Post-Graduation and Research in Engineering, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Department of Radiology, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Clin Nucl Med. 2022 Dec 1;47(12):1019-1025. doi: 10.1097/RLU.0000000000004376. Epub 2022 Aug 26.
We quantified lung glycolytic metabolic activity, clinical symptoms and inflammation, coagulation, and endothelial activation biomarkers in 2019 coronavirus disease (COVID-19) pneumonia survivors.
Adults previously hospitalized with moderate to severe COVID-19 pneumonia were prospectively included. Subjects filled out a questionnaire on clinical consequences, underwent chest CT and 18 F-FDG PET/CT, and provided blood samples on the same day. Forty-five volunteers served as control subjects. Analysis of CT images and quantitative voxel-based analysis of PET/CT images were performed for both groups. 18 F-FDG uptake in the whole-lung volume and in high- and low-attenuation areas was calculated and normalized to liver values. Quantification of plasma markers of inflammation (interleukin 6), d -dimer, and endothelial cell activation (angiopoietins 1 and 2, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1) was also performed.
We enrolled 53 COVID-19 survivors (62.3% were male; median age, 50 years). All survivors reported at least 1 persistent symptom, and 41.5% reported more than 6 symptoms. The mean lung density was greater in survivors than in control subjects, and more metabolic activity was observed in normal and dense lung areas, even months after symptom onset. Plasma proinflammatory, coagulation, and endothelial activation biomarker concentrations were also significantly higher in survivors.
We observed more metabolic activity in areas of high and normal lung attenuation several months after moderate to severe COVID-19 pneumonia. In addition, plasma markers of thromboinflammation and endothelial activation persisted. These findings may have implications for our understanding of the in vivo pathogenesis and long-lasting effects of COVID-19 pneumonia.
我们量化了 2019 年冠状病毒病（COVID-19）肺炎幸存者的肺糖酵解代谢活性、临床症状和炎症、凝血和内皮激活生物标志物。
前瞻性纳入先前因中度至重度 COVID-19 肺炎住院的成年人。受试者填写临床后果问卷，进行胸部 CT 和 18 F-FDG PET/CT 检查，并在同一天提供血液样本。45 名志愿者作为对照组。对两组 CT 图像进行分析，并对 PET/CT 图像进行定量体素分析。计算并归一化整个肺体积和高、低衰减区域的 18 F-FDG 摄取值到肝值。还定量测定了血浆炎症标志物（白细胞介素 6）、D-二聚体和内皮细胞激活标志物（血管生成素 1 和 2、血管细胞黏附分子 1 和细胞间黏附分子 1）。
我们纳入了 53 名 COVID-19 幸存者（62.3%为男性；中位年龄 50 岁）。所有幸存者均报告至少 1 种持续症状，41.5%报告超过 6 种症状。与对照组相比，幸存者的肺部密度更高，在正常和致密肺区观察到更多的代谢活性，甚至在症状出现后数月。幸存者的血浆促炎、凝血和内皮激活生物标志物浓度也明显更高。
我们观察到，在中度至重度 COVID-19 肺炎数月后，高衰减和正常肺区的代谢活性更高。此外，血栓炎症和内皮激活的血浆标志物持续存在。这些发现可能对我们理解 COVID-19 肺炎的体内发病机制和长期影响具有重要意义。
