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Case Reports
. 2020 Aug;36(4):338-342.
doi: 10.1159/000508740. Epub 2020 Jun 5.

Mild COVID-19 Symptoms in an Infliximab-Treated Ulcerative Colitis Patient: Can Ongoing Anti-TNF Therapy Protect against the Viral Hyperinflammatory Response and Avoid Aggravated Outcomes?

Affiliations
Case Reports

Mild COVID-19 Symptoms in an Infliximab-Treated Ulcerative Colitis Patient: Can Ongoing Anti-TNF Therapy Protect against the Viral Hyperinflammatory Response and Avoid Aggravated Outcomes?

Abdullah Abdullah et al. Visc Med. 2020 Aug.

Abstract

The ongoing coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2, represents a potentially major challenge to patients with immune-mediated inflammatory diseases who are treated with immunomodulatory therapies. We report the case of an 18-year-old ulcerative colitis patient in sustained clinical remission who 4 days after application of her ongoing therapy with the anti-TNF antibody infliximab developed mild respiratory and abdominal symptoms. The patient was subsequently diagnosed with COVID-19 but did not need hospitalization. The clinical symptoms completely resolved within 1 week after onset and there was no change in ulcerative colitis activity. The recently applied anti-TNF therapy did not lead to exacerbation of the infectious symptoms. Current recommendations strongly favor continuation of effective maintenance anti-TNF therapy in inflammatory bowel disease patients, as there is no evidence for aggravated CO-VID-19 upon infection. It is unclear whether anti-TNF treatment might even have assisted in preventing worsening of COVID-19 and improving outcome. Further data in the group of immune-mediated inflammatory disease patients under anti-TNF therapy are urgently needed.

Keywords: Anti-TNF antibody; COVID-19; Cytokine storm; Infliximab; SARS-CoV-2; Ulcerative colitis.

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Conflict of interest statement

R. Atreya has served as a speaker, or consultant, or received research grants from AbbVie, Biogen, Boehringer Ingelheim GmbH & Co. KG, Dr. Falk Pharma GmbH, Ferring GmbH, Glaxo­SmithKline plc, InDex Pharmaceuticals AG, Janssen-Cilag GmbH, MSD Sharp & Dome GmbH, Pfizer Inc., Roche Pharma, Samsung Bioepis, Stelic Institute, Takeda GmbH & Co. KG, and Tillotts Pharma AG. M.F. Neurath reports research grants and/or personal fees from AbbVie, MSD, Takeda, Boehringer, Roche, Pfizer, Janssen, Pentax, and PPD.

Figures

Fig. 1
Fig. 1
Hyperinflammatory state in severe COVID-19. Binding of SARS-CoV-2 to the receptor ACE2 that is expressed on the host epithelial cell (lung/intestine) leads to the entrance of the virus upon cleavage of the viral spike protein by the host TMPRSS2. This leads to overwhelming immune cell activation and exaggerated production of cytokines and chemokines, led by IL-6 and TNF. This sort of cytokine storm perpetuates the hyperinflammatory state that leads to severe COVID-19. ACE2, angiotensin-converting enzyme 2; COVID-19, coronavirus disease 2019; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TMPRSS2, transmembrane serine protease 2.

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