key: cord-284694-bk6bnox0
authors: Wang, Changsong; Kang, Kai; Gao, Yan; Ye, Ming; Lan, Xiuwen; Li, Xueting; Zhao, Mingyan; Yu, Kaijiang
title: Cytokine Levels in the Body Fluids of a Patient With COVID-19 and Acute Respiratory Distress Syndrome: A Case Report
date: 2020-05-12
journal: Ann Intern Med
DOI: 10.7326/l20-0354
sha: 
doc_id: 284694
cord_uid: bk6bnox0

nan

during this patient's illness to see whether they could help us decide how to modify his treatment as the disease progressed. We found high and fluctuating levels of these cytokines in his peripheral blood, bronchoalveolar lavage fluid, and pleural fluid. However, these levels correlated only inconsistently with the treatments we administered, even for plasmapheresis, which was intended to dilute circulating cytokines, and for a dialysis filter that was designed to adsorb cytokines ( Figure) . In addition, these cytokine levels correlated inconsistently with his clinical course, except that the levels increased dramatically in the last days before he died.

We suspect that this patient's immune system was partially suppressed due to his advanced age and multiple chronic conditions, which might have contributed to the virus's continued replication and the disease's progress. In addition, the time from symptom onset to confirmation of COVID-19 diagnosis was relatively long, the patient's hospital course was longer, and we wonder whether this long duration of viral replication contributed to the high cytokine levels we measured.

Other studies have reported that patients with COVID-19 have evidence of local damage, which includes diffuse alveolar injury with cellular fibrous mucus-like exudates (2). We measured IL-6 levels in bronchoalveolar lavage fluid that were higher than the corresponding serum levels. On one occasion (7 March), the IL-6 level was approximately 10 times higher. This difference is even more remarkable because the process of collecting bronchoalveolar fluid dilutes the specimen. In addition, the level of IL-6 in pleural effusion was higher than the corresponding serum levels on the 2 times we measured it. If these observations indicate a cytokine storm, we propose that the local storm may be worse than the systemic storm.

Interleukin-6 blockers have been used to treat cytokine storm in patients with other causes of cytokine storm (3), and tocilizumab has been suggested for immunotherapy for severe patients with extensive lung lesions and elevated IL-6 levels (3). As a result, we wonder whether tocilizumab would have affected the IL-6 levels we observed and whether it might have improved this patient's disease course, especially because others have reported that as COVID-19 progresses to its middle and late stages, the expression of inflammatory cytokines is related to the severity of the disease (4). On the basis of our experience, we encourage additional research to determine whether inflammatory cytokines in the lungs predict the clinical course of COVID-19 and whether these cytokines should be a target for intervention and treatment.

In summary, this case suggests an increased inflammatory response in the lung tissues of critically ill patients with COVID-19, and it suggests that future research should include examinations of local inflammation in the lungs. Continued on the following page 

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