COVID-19-associated hyperinflammation and escalation of patient care: a retrospective longitudinal cohort study

Abstract

Background A subset of patients with severe COVID-19 develop a hyperinflammatory syndrome, which might contribute to morbidity and mortality. This study explores a specific phenotype of COVID-19-associated hyperinflammation (COV-HI), and its associations with escalation of respiratory support and survival. Methods In this retrospective cohort study, we enrolled consecutive inpatients (aged ≥18 years) admitted to University College London Hospitals and Newcastle upon Tyne Hospitals in the UK with PCR-confirmed COVID-19 during the first wave of community-acquired infection. Demographic data, laboratory tests, and clinical status were recorded from the day of admission until death or discharge, with a minimum follow-up time of 28 days. We defined COV-HI as a C-reactive protein concentration greater than 150 mg/L or doubling within 24 h from greater than 50 mg/L, or a ferritin concentration greater than 1500 μg/L. Respiratory support was categorised as oxygen only, non-invasive ventilation, and intubation. Initial and repeated measures of hyperinflammation were evaluated in relation to the next-day risk of death or need for escalation of respiratory support (as a combined endpoint), using a multi-level logistic regression model. Findings We included 269 patients admitted to one of the study hospitals between March 1 and March 31, 2020, among whom 178 (66%) were eligible for escalation of respiratory support and 91 (34%) patients were not eligible. Of the whole cohort, 90 (33%) patients met the COV-HI criteria at admission. Despite having a younger median age and lower median Charlson Comorbidity Index scores, a higher proportion of patients with COV-HI on admission died during follow-up (36 [40%] of 90 patients) compared with the patients without COV-HI on admission (46 [26%] of 179). Among the 178 patients who were eligible for full respiratory support, 65 (37%) met the definition for COV-HI at admission, and 67 (74%) of the 90 patients whose respiratory care was escalated met the criteria by the day of escalation. Meeting the COV-HI criteria was significantly associated with the risk of next-day escalation of respiratory support or death (hazard ratio 2·24 [95% CI 1·62–2·87]) after adjustment for age, sex, and comorbidity. Interpretation Associations between elevated inflammatory markers, escalation of respiratory support, and survival in people with COVID-19 indicate the existence of a high-risk inflammatory phenotype. COV-HI might be useful to stratify patient groups in trial design. Funding None.

Systemic Inflammatory Index Is a Novel Predictor of Intubation Requirement and Mortality after SARS-CoV-2 Infection

“…Our work extends the lists of inflammation-associated proposals for predictive biomarkers for the course of SARS-CoV-2 infections. As such, the respiratory inflammation index [ 16 , 17 ], cytokine signature [ 18 , 19 , 20 ], hyper inflammation signature [ 21 , 22 ], lymphocyte subsets [ 23 , 24 , 25 ], diet-instructed immune index [ 26 ], amongst others (the authors acknowledge the rapidly evolving literature on this topic, making it impossible to comprehensively cite all relevant work), have been proposed to predict severity of the disease course. As a remark, our results are in line with very recently published work identifying the value of SSI to predict the risk of in-hospital mortality of COVID-19 patients [ 27 ].…”

Polymyxin B haemoperfusion treatment for respiratory failure and hyperferritinaemia due to COVID‐19

“…Although the precise pathogenesis of severe COVID-19-induced ARDS remains unclear, hyperferritinaemia, which is categorized as hyperinflammation, is associated with severity and poor outcomes in COVID-19 [1,2]. Hyperinflammation is defined as follows: CRP concentration greater than 15 mg/dL; a doubling of CRP concentration within 24 h from a concentration of greater than 5 mg/dL; or a ferritin concentration of greater than 1500 ng/dL [1]. Ferritin levels at admission in COVID-19 non-survivors were reported to be around 1400 ng/mL [3].…”

Daylight is critical to preserve 5-methoxytryptophol levels in suspected and confirmed COVID-19 patients

“…However, this counterattack results in failure and ultimately causes a hyperinflammatory response. This situation determines the course of the disease [13] . According to published studies that SARS-COV infection played a role in the inflammation caused by tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) by affecting proteins on T cells [14] .…”