English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The severe acute respiratory coronavirus 2 (SARS-CoV2) pandemic has prompted search for therapeutics tackling both the pathogen and the overwhelming host response, on an unprecedented scale. In a minority of patients, the disease may cause frequently lethal complications from acute respiratory distress syndrome to multisystem organ failure presumably driven by a cytokine storm [1]. Therefore, anti-cytokine therapies may be helpful to prevent tissue injury. However, these antiinflammatory drugs constitute double-edged swords; while they can prevent organ damage, they increase the risk of concomitant (super)infection. Recently, Neurath argued for a protective effect of tumor necrosis factor (TNF) inhibitors in severe COVID-19 [2]. Specifically, TNF may aggravate lymphopenia through direct killing via TNF/TNFR1 signaling in T cells [3], and T cell dysfunction reflects an important yet underestimated target for immunomodulatory interventions [4]. Thus, anti-TNF strategies may be an interesting option in severe COVID-19. This is supported by data from patients with inflammatory bowel disease (IBD) already on anti-TNF treatment. As of June 16, 2020, outcome data from 1511 IBD patients with COVID-19, among them, 433 patients on anti-TNF, are available from the SECURE-IBD registry [5]. Of these, 16% were hospitalized but only three patients (0.7%) died. Compared to other anti-inflammatory drugs such as steroids, thiopurines, or JAK inhibitors from SECURE-IBD, the safety signal of anti-TNF therapy seems simply the best. These positive clinical data in the absence of a causative therapy encouraged us to use infliximab (IFX), a chimeric monoclonal anti-TNF antibody, as an experimental therapy in patients with severe COVID-19 in the absence of IBD. In this case series, we retrospectively explore the possible impact of IFX in critically ill patients with confirmed COVID-19 in comparison with a contemporaneous group of COVID-19 receiving supportive therapy only. Seven patients (47–70 years; one woman) were treated with a single infusion of IFX (5 mg/kg body weight) between 0 and 3 days after admission. One of the six had no known preexisting medical conditions apart from obesity, which was present in all cases (Table 1). In all IFX-treated patients, a rapid and at least temporary decrease of proinflammatory cytokines such as IL-6 (see Fig. 1) and other inflammatory markers (CRP, LDH) was observed along with clinical improvement in six of seven patients. Lymphocyte count (available in six of seven patients) before IFX infusion was initially below 1 Gpt/l and increased in five patients after IFX (Fig. 1b). The 17 patients of the control group showed 35% overall mortality at a similar stage of hospitalization along with prolonged systemic inflammation.

Infliximab against severe COVID-19-induced cytokine storm syndrome with organ failure—a cautionary case series