ABSTRACT
PURPOSE: To evaluate the accuracy and cost benefit of a rapid molecular point-of-care testing (POCT) device detecting COVID-19 within a traumatological emergency department. BACKGROUND: Despite continuous withdrawal of COVID-19 restrictions, hospitals will remain particularly vulnerable to local outbreaks which is reflected by a higher institution-specific basic reproduction rate. Patients admitted to the emergency department with unknown COVID-19 infection status due to a- or oligosymptomatic COVID-19 infection put other patients and health care workers at risk, while fast diagnosis and treatment is necessary. Delayed testing results in additional costs to the health care system. METHODS: From the 8th of April 2021 until 31st of December 2021, all patients admitted to the emergency department were tested with routine RT-PCR and rapid molecular POCT device (Abbott ID NOW™ COVID-19). COVID-19-related additional costs for patients admitted via shock room or emergency department were calculated based on internal cost allocations. RESULTS: 1133 rapid molecular tests resulted in a sensitivity of 83.3% (95% CI 35.9-99.6%), specificity of 99.8% (95% CI 99.4-100%), a positive predictive value of 71.4% (95% CI 29-96.3%) and a negative predictive value of 99.9% (95% CI 99.5-100%) as compared to RT-PCR. Without rapid COVID-19 testing, each emergency department and shock room admission with subsequent surgery showed additional direct costs of 2631.25, without surgery of 729.01. CONCLUSION: Although rapid molecular COVID-19 testing can initially be more expensive than RT-PCR, subsequent cost savings, improved workflows and workforce protection outweigh this effect by far. The data of this study support the use of a rapid molecular POCT device in a traumatological emergency department.
ABSTRACT
SARS-CoV-2 is the causative agent of the immune response-driven disease COVID-19 for which new antiviral and anti-inflammatory treatments are urgently needed to reduce recovery time, risk of death and long COVID development. Here, we demonstrate that the immunoregulatory kinase p38 MAPK is activated during viral entry, mediated by the viral spike protein, and drives the harmful virus-induced inflammatory responses. Using primary human lung explants and lung epithelial organoids, we demonstrate that targeting p38 signal transduction with the selective and clinically pre-evaluated inhibitors PH-797804 and VX-702 markedly reduced the expression of the pro-inflammatory cytokines IL6, CXCL8, CXCL10 and TNF-α during infection, while viral replication and the interferon-mediated antiviral response of the lung epithelial barrier were largely maintained. Furthermore, our results reveal a high level of drug synergism of both p38 inhibitors in co-treatments with the nucleoside analogs Remdesivir and Molnupiravir to suppress viral replication of the SARS-CoV-2 variants of concern, revealing an exciting and novel mode of synergistic action of p38 inhibition. These results open new avenues for the improvement of the current treatment strategies for COVID-19.