key: cord-256143-9u5a0jqz
authors: Grassia, Roberto; Soro, Sara; Conti, Clara Benedetta
title: Inflammatory Bowel Diseases and Biological Treatment in SARS-CoV-2 Era. Why Not?
date: 2020-05-09
journal: Inflamm Bowel Dis
DOI: 10.1093/ibd/izaa110
sha: 
doc_id: 256143
cord_uid: 9u5a0jqz

nan

In December 2019, a new β-coronavirus (SARS-CoV-2) and its related disease, COVID-19, spread first in China and then worldwide, becoming a pandemic. The patients affected by chronic diseases seem to be at a higher risk to develop severe pneumonia. 1 In this setting, the initial indication from the inflammatory bowel disease (IBD) center in Wuhan was to discontinue all biological and immunosuppressive treatments. There, among 318 IBD patients, none developed COVID-19. 2 Subsequent guidelines suggested for patients with IBD to continue all treatments to avoid relapse. 3 In an Italian observational study, among 522 IBD patients (89% adults), 16% under biological therapy, none was hospitalized for COVID-19. 4 We confirm this observation.

On April 19, 2020, Italy officially registered 178.972 SARS-Cov-2 infected people. Particularly, our province of Cremona reports the highest rate of infected people in the world: 1 of 73 inhabitants. However, the prevalence could be even higher, as these data are based on hospitalized and symptomatic patients only. Our IBD cohort includes 251 patients, 41 (16.3%) under biological treatment (median time of treatment, 23 months), 20 males (48.8%), 30 with Crohn's disease (CD), and 11 ulcerative colitis (RCU) (mean age 48.6; SD±15.2). Thirty patients are treated with antitumor necrosis factor alpha (anti-TNFα), 10 with vedolizumab, and 1 with ustekinumab. None of the patients under biological treatment reported COVID-19 symptoms.

Some IBD constitutional and therapeutic aspects could support these data. First, SARS-CoV-2 binds to the cells through angiotensin-converting enzyme 2 (ACE2). Two distinct formsfull-length and soluble ACE2-exist. The soluble form circulates in the blood, acting as a competitive interceptor of SARS-CoV-2. Interestingly, soluble ACE2 is upregulated in the blood of IBD patients. Again, the severity of COVID-19 seems to be linked to the "cytokines storm" syndrome, with massive production of interleukin (IL)-2, IL-6, TNF, and interferon-γ. In this direction, tocilizumab, a IL-6 receptor antagonist, has been included in the COVID-19 therapy trials. The suppression of the inflammatory response in IBD by biological drugs could help against both the mucosal inflammation and the COVID-19 pneumonia, sustained by the abnormal "cytokine storm." 5 On the other hand, we anecdotally report only 1 case of COVID-19 in our IBD cohort in a patient under azathioprine therapy.

Further studies are needed to investigate if IBD patients under biological treatment could be protected against the COVID-19 pneumonia, whereas those under immunosuppressive therapy (ie, thiopurines) could remain at higher risk of developing the disease due to the different mechanism of action.

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

Protection of 318 Inflammatory Bowel Disease Patients from the Outbreak and Rapid Spread of COVID-19 Infection in Wuhan

AGA clinical practice update on management of inflammatory bowel disease during the COVID-19 pandemic: expert commentary

Uneventful course in IBD patients during SARS-CoV-2 outbreak in northern Italy

Are patients with inflammatory bowel disease at increased risk for Covid-19 infection?