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We read with great interest the recent publication from Ungaro and colleagues,1 reporting the latest data from the Surveillance Epidemiology of Coronavirus Under Research Exclusion (SECURE-IBD) registry. These data, while raising concerns regarding the use of thiopurine and corticosteroid therapy in the SARS-CoV-2 pandemic, also provide valuable reassurance that monotherapy with anticytokine therapies, in particular those directed against tumour necrosis factor (TNF), are not associated with adverse outcomes in patients with IBD developing COVID-19. It has been postulated that anticytokine therapies may ameliorate or abrogate the ‘cytokine storm’ associated with severe COVID-19,2 with anti-IL6 strategies now approved for use.3
We have assessed the SARS-CoV-2 antibody seroprevalence in patients with IBD, receiving either intravenous anti-TNF therapy, or anti-integrin therapy, during the first wave of the pandemic in the UK.
Sera from 640 patients attending for maintenance infliximab or vedolizumab infusions between April and June 2020 at the John Radcliffe Hospital (Oxford, UK) and Royal London Hospital (London, UK) were tested using the Abbott SARS-CoV-2 IgG assay. Adults (180) and paediatric (56) patients were included from London. Demographic and clinical data are summarised (online supplemental tables 1, 2). Key differences between the Oxford and London adult cohorts included ethnicity, smoking, comorbidities, disease type, concomitant thiopurines and biologic; in our data set, patients attending Royal London Hospital had significantly greater evidence for deprivation than Oxford (deprivation score 4 (3–6.3) vs 8 (6–9.3), p<0.001). Seroprevalence data were compared with available data from a contemporaneous healthy healthcare worker …
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Contributors CGCM—patient recruitment, analysis, drafting of manuscript. AA—analysis, drafting of manuscript. RS—sample analysis, manuscript revision. CVA-C, RP, TA, OB, AW, SPLT, JL, NC—patient recruitment, manuscript revision. PK—manuscript revision. JS—initiation of research, recruitment, drafting and revision of manuscript
Funding This work was partly supported by the Helmsley Trust as part of the ICARUS study [Grant Number 2107–04731]. CGCM is funded by an ECCO Pioneer Award. AA, CVA-C, AW, OB, and ST are funded by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC).
Disclaimer The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.
Competing interests CVA-C has received grants from Celgene and Takeda outside the scope of the submitted work. AW reports personal fees outside the submitted work from Ferring Pharmaceuticals, Janssen, and Takeda. ST reports outside the submitted work receipt of grants/research support from AbbVie, Buhlmann, Celgene, IOIBD, Janssen, Lilly, Pfizer, Takeda, UCB, Vifor, and Norman Collisson Foundation; consulting fees from AbbVie, Allergan, Amgen, Arena, Asahi, Astellas, Biocare, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Buhlmann, Celgene, Chemocentryx, Cosmo, Enterome, Ferring, Giuliani SpA, GSK, Genentech, Immunocore, Immunometabolism, Indigo, Janssen, Lexicon, Lilly, Merck, MSD, Neovacs, Novartis, NovoNordisk, NPS Pharmaceuticals, Pfizer, Proximagen, Receptos, Roche, Sensyne, Shire, Sigmoid Pharma, SynDermix, Takeda, Theravance, Tillotts, Topivert, UCB, VHsquared, Vifor, and Zeria; speaker fees from AbbVie, Amgen, Biogen, Ferring, Janssen, Lilly, Pfizer, Shire, and Takeda; no stocks or share options. NMC reports research grants outside the submitted from Abbvie, Shire, Takeda, Pfizer, Eli Lilly, Jansenn, 4D Pharma, and lecture fees Abbvie. JS has received lecture fees from Takeda and from the Falk Foundation.
Provenance and peer review Not commissioned; externally peer reviewed.
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