为了分析社会人口统计学的潜在影响,临床和生物学因素对中度和重度COVID-19存活患者长期认知结局的影响。
我们评估了710名成年参与者(平均年龄=55±14;48.3%为女性)出院后6至11个月的完整认知电池,以及精神病患者,临床和实验室评估。使用了大量的推理统计方法来预测与任何长期认知障碍相关的潜在变量。重点研究了28种细胞因子和其他血液炎症和疾病严重程度标志物。
关于认知表现的主观评估,36.1%的人报告总体认知表现稍差,14.6%的人报告受到严重影响,与他们在COVID-19之前的状态相比。多变量分析发现性别,年龄,种族,教育,合并症,虚弱和体力活动与一般认知相关。双变量分析发现G-CSF,IFN-alfa2、IL13、IL15、IL1。RA,EL1.阿尔法,IL45,IL5,IL6,IL7,TNF-β,VEGF,后续C反应蛋白,随访D-二聚体与一般认知显著相关(p<.05)。然而,包括所有后续变量的LASSO回归,炎症标志物和细胞因子不支持这些发现.
虽然我们发现了一些社会人口统计学特征,可以预防SARS-CoV-2感染后的认知障碍,我们的数据不支持临床状态(COVID-19急性期和长期期)或炎症背景(COVID-19急性期和长期期)在解释COVID-19感染后的认知缺陷方面发挥重要作用.
To analyze the potential impact of sociodemographic, clinical and biological factors on the long-term cognitive outcome of patients who survived moderate and severe forms of COVID-19.
We assessed 710 adult participants (Mean age = 55 ± 14; 48.3% were female) 6 to 11 months after hospital discharge with a complete cognitive battery, as well as a psychiatric, clinical and laboratory evaluation. A large set of inferential statistical methods was used to predict potential variables associated with any long-term cognitive impairment, with a focus on a panel of 28 cytokines and other blood inflammatory and disease severity markers.
Concerning the subjective assessment of cognitive performance, 36.1% reported a slightly poorer overall cognitive performance, and 14.6% reported being severely impacted, compared to their pre-COVID-19 status. Multivariate analysis found sex, age, ethnicity, education, comorbidity, frailty and physical activity associated with general cognition. A bivariate analysis found that G-CSF, IFN-alfa2, IL13, IL15, IL1.RA, EL1.alfa, IL45, IL5, IL6, IL7, TNF-Beta, VEGF, Follow-up C-Reactive Protein, and Follow-up D-Dimer were significantly (p<.05) associated with general cognition. However, a LASSO regression that included all follow-up variables, inflammatory markers and cytokines did not support these findings.
Though we identified several sociodemographic characteristics that might protect against cognitive impairment following SARS-CoV-2 infection, our data do not support a prominent role for clinical status (both during acute and long-stage of COVID-19) or inflammatory background (also during acute and long-stage of COVID-19) to explain the cognitive deficits that can follow COVID-19 infection.