(18)F-FDG brain PET hypometabolism in patients with long COVID.

(18)F-FDG brain PET hypometabolism in patients with long COVID.
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DOI:
10.1007/s00259-021-05215-4
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发表时间:
2021-08
影响因子:
9.1
通讯作者:
Eldin C
Eldin C
中科院分区:
医学1区
文献类型:
--
作者:
Guedj E;Campion JY;Dudouet P;Kaphan E;Bregeon F;Tissot-Dupont H;Guis S;Barthelemy F;Habert P;Ceccaldi M;Million M;Raoult D;Cammilleri S;Eldin C

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在全球爆发严重急性呼吸综合征冠状病毒2(SARS-CoV-2)的背景下,一些患者在从COVID-19中明显康复后报告功能性投诉。这种临床表现被称为“长期COVID”。我们在此对来自同一中心的长期COVID患者进行了18F-FDG脑PET的回顾性分析,这些患者在生物学上被确诊为SARS-CoV-2感染,并且在初次感染后至少3周持续存在功能性主诉。使用基于全脑体素的分析将35名长期COVID患者的PET扫描与44名健康受试者的本地数据库进行了比较,以描述大脑代谢低下的特征。评价该代谢特征的个体相关性,以将患者和健康受试者分类。最后,将PET异常与患者的特征和功能主诉进行探索性比较。与健康受试者相比,长期COVID患者在双侧直肠/眶回(包括嗅回)、右侧颞叶(包括杏仁核和海马,延伸至右侧丘脑)、双侧脑桥/延髓脑干、双侧小脑(未校正的p体素< 0.001,校正的p簇< 0.05 FWE)中表现出双侧代谢减退。这些代谢聚类具有高度判别性,可区分患者和健康受试者(100%正确分类)。这些低代谢簇与更多的功能性主诉(脑干和小脑簇)显著相关,并且都与某些症状(嗅觉减退/嗅觉缺失、记忆/认知障碍、疼痛和失眠)的发生相关(p < 0.05)。在更初步的分析中,包括嗅回在内的额簇的代谢在7名接受ACE药物治疗高血压的患者中更差(p = 0.032),而在感染期使用鼻减充血剂喷雾剂的3名患者中更好(p < 0.001)。这项研究证明了长期COVID患者的脑PET代谢低下的概况,这些患者具有生物学证实的SARS-CoV-2,并且在初始感染症状后超过3周存在持续的功能性主诉,涉及嗅回和连接的边缘/边缘区,延伸到脑干和小脑。这些低代谢与患者的症状相关,具有生物标志物价值以识别和潜在地跟踪这些患者。包括嗅回在内的额叶簇的代谢减退似乎与高血压患者的ACE药物有关,在使用鼻减充血剂喷雾的患者中,该嗅觉区域的代谢也更好,这表明ACE受体可能作为这种神经向性的嗅觉通道。
In the context of the worldwide outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), some patients report functional complaints after apparent recovery from COVID-19. This clinical presentation has been referred as “long COVID.” We here present a retrospective analysis of 18F-FDG brain PET of long COVID patients from the same center with a biologically confirmed diagnosis of SARS-CoV-2 infection and persistent functional complaints at least 3 weeks after the initial infection. PET scans of 35 patients with long COVID were compared using whole-brain voxel-based analysis to a local database of 44 healthy subjects controlled for age and sex to characterize cerebral hypometabolism. The individual relevance of this metabolic profile was evaluated to classify patients and healthy subjects. Finally, the PET abnormalities were exploratory compared with the patients’ characteristics and functional complaints. In comparison to healthy subjects, patients with long COVID exhibited bilateral hypometabolism in the bilateral rectal/orbital gyrus, including the olfactory gyrus; the right temporal lobe, including the amygdala and the hippocampus, extending to the right thalamus; the bilateral pons/medulla brainstem; the bilateral cerebellum (p-voxel < 0.001 uncorrected, p-cluster < 0.05 FWE-corrected). These metabolic clusters were highly discriminant to distinguish patients and healthy subjects (100% correct classification). These clusters of hypometabolism were significantly associated with more numerous functional complaints (brainstem and cerebellar clusters), and all associated with the occurrence of certain symptoms (hyposmia/anosmia, memory/cognitive impairment, pain and insomnia) (p < 0.05). In a more preliminary analysis, the metabolism of the frontal cluster which included the olfactory gyrus was worse in the 7 patients treated by ACE drugs for high blood pressure (p = 0.032), and better in the 3 patients that had used nasal decongestant spray at the infectious stage (p < 0.001). This study demonstrates a profile of brain PET hypometabolism in long COVID patients with biologically confirmed SARS-CoV-2 and persistent functional complaints more than 3 weeks after the initial infection symptoms, involving the olfactory gyrus and connected limbic/paralimbic regions, extended to the brainstem and the cerebellum. These hypometabolisms are associated with patients’ symptoms, with a biomarker value to identify and potentially follow these patients. The hypometabolism of the frontal cluster, which included the olfactory gyrus, seems to be linked to ACE drugs in patients with high blood pressure, with also a better metabolism of this olfactory region in patients using nasal decongestant spray, suggesting a possible role of ACE receptors as an olfactory gateway for this neurotropism.
DOI: 10.1186/1471-2377-11-37
发表时间: 2011-03-24
期刊: BMC neurology
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