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Background <p>Children are at increased risk for neuropsychiatric disorders following COVID-19. However, information regarding the clinical, metabolic, and cerebrospinal fluid (CSF) characteristics in patients with neuropsychiatric disorders associated with COVID-19 is limited. In this study, we described the clinical features and retrospectively assessed the metabolic and inflammatory profiles of 13 pediatric patients who exhibited subacute neuropsychiatric symptoms within one month of SARS-CoV-2 infection (NP-COVID-19).</p> Methods <p>We retrospectively reviewed and analyzed the clinical and paraclinical data of 13 children with NP-COVID-19 admitted to Qilu hospital from December 15, 2022, to January 31, 2023. Healthy children (HC, <i>n</i> = 21) and pre-pandemic migraine patients (<i>n</i> = 12) were included as controls. Systemic metabolic and inflammatory parameters in NP-COVID-19 patients including thyroid hormone levels and neutrophil-to-lymphocyte ratio were compared with HC. Blood-brain barrier (BBB) integrity and CSF biomarkers of intrathecal inflammation including cytokines and immunoglobulin G index were compared with migraine patients.</p> Results <p>CSF SARS-CoV-2 RNA was negative in all patients with NP-COVID-19. No differences in systemic inflammatory parameters were found between NP-COVID-19 patients and HC. However, NP-COVID-19 patients with intact BBB integrity exhibited significantly higher CSF interleukin (IL)-8 levels than migraine controls. In addition, serum free triiodothyronine (FT3) levels were lower in NP-COVID-19 patients than HC and low-T3 syndrome occurred in 61.5% of NP-COVID-19 children.</p> Conclusions <p>Systemic inflammation rarely occurred in children with NP-COVID-19. Low-T3 syndrome is prevalent in NP-COVID-19 pediatric patients and the neuroinflammatory activation is mainly characterized by elevated CSF IL-8. Further study is required to investigate the pathophysiologic mechanisms in NP-COVID-19.</p>

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Clinical, thyroid metabolic, and inflammatory features in pediatric patients with post-acute COVID-19 neuropsychiatric symptoms

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月30日

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  • Ping Yin,
  • Dongqing Zhang,
  • Baomin Li,
  • Gefei Lei,
  • Xiafei Fu

摘要

Background

Children are at increased risk for neuropsychiatric disorders following COVID-19. However, information regarding the clinical, metabolic, and cerebrospinal fluid (CSF) characteristics in patients with neuropsychiatric disorders associated with COVID-19 is limited. In this study, we described the clinical features and retrospectively assessed the metabolic and inflammatory profiles of 13 pediatric patients who exhibited subacute neuropsychiatric symptoms within one month of SARS-CoV-2 infection (NP-COVID-19).

Methods

We retrospectively reviewed and analyzed the clinical and paraclinical data of 13 children with NP-COVID-19 admitted to Qilu hospital from December 15, 2022, to January 31, 2023. Healthy children (HC, n = 21) and pre-pandemic migraine patients (n = 12) were included as controls. Systemic metabolic and inflammatory parameters in NP-COVID-19 patients including thyroid hormone levels and neutrophil-to-lymphocyte ratio were compared with HC. Blood-brain barrier (BBB) integrity and CSF biomarkers of intrathecal inflammation including cytokines and immunoglobulin G index were compared with migraine patients.

Results

CSF SARS-CoV-2 RNA was negative in all patients with NP-COVID-19. No differences in systemic inflammatory parameters were found between NP-COVID-19 patients and HC. However, NP-COVID-19 patients with intact BBB integrity exhibited significantly higher CSF interleukin (IL)-8 levels than migraine controls. In addition, serum free triiodothyronine (FT3) levels were lower in NP-COVID-19 patients than HC and low-T3 syndrome occurred in 61.5% of NP-COVID-19 children.

Conclusions

Systemic inflammation rarely occurred in children with NP-COVID-19. Low-T3 syndrome is prevalent in NP-COVID-19 pediatric patients and the neuroinflammatory activation is mainly characterized by elevated CSF IL-8. Further study is required to investigate the pathophysiologic mechanisms in NP-COVID-19.