Acute myelitis after SARS-CoV-2 infection: a case report.

Kang Zhao; Jucun Huang; Dan Dai; Yuwei Feng; Liming Liu; Shuke Nie

Based on our study, acute paralysis was the novel neurological symptom of COVID-19. Analysis of the clinical characteristics of 1099 patients with COVID-19 showed that the common symptoms at the onset of disease were fever (43.8% of the patients appeared on admission, while 88.7% of the patients occurred after admission), cough (67.8%), and neurological symptoms were rare 2 . However, severe patients with COVID-19 were likely to have neurological symptoms (such as headache, dizziness, hypogeusia, and neuralgia) and complications including acute cerebrovascular diseases, impaired consciousness and skeletal muscular injury 15 . According to the laboratory testing, we found that lymphopenia and eosinopenia happened in the early stage of COVID-19. The decrease of red blood cell and hemoglobin showed that bone marrow hematopoietic system was affected by SARS-CoV-2, which was expected to be further confirmed by large-scale retrospective analysis. It had been reported that ACE2 was expressed in hepatic bile duct cells and proximal renal tubules 7, 8 , hepatic and renal dysfunctions were also detected in the patients with COVID-19 16 . Liver function of this patient in this study was obviously damaged with normal renal function, the elevated levels of alanine aminotransferase and aspartate aminotransferas reached the peak on the 15th day after the onset of disease, and then recovered gradually. At the same time, the level of total protein, albumin and HDL-C significantly decreased with the process of the disease, suggesting that metabolic abnormalities contributed to the pathogenesis of COVID-19. However, the renal function was normal in this study, which was inconsistent with previous study. It had been reported that the decreased level of serum iron in patients with pneumonia was an independent risk factor for hospital death 17 .The mechanism may be related to the influence of pathogenic microorganism infection on iron uptake. In this patient, on the 7th day of the onset of the disease, the level of serum iron was only 1.8 umol/L, and gradually increased with the treatment. The level of serum iron returned to normal when the nucleic acid test of 2019-nCov turned into negative. The possible role of serum iron in the 2019-nCov infection deserved further research in the future. We believed that overactive inflammation response and immune damage occurred in COVID-19 for the high level of C-reactive protein, SAA, IL-6 and ferritin in the patient. Immune damage and cytokines released by inflammatory storms at the early stage of COVID might interpret and explain why spinal cord was implicated in the disease.