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Correspondence on ‘Anti-inflammatory therapy for COVID-19 infection: the case for colchicine’
  1. Carlo Perricone1,
  2. Elena Bartoloni1,
  3. Giacomo Cafaro1,
  4. Roberto Caporali2,
  5. Roberto Gerli1
  1. 1 Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Perugia, Italy
  2. 2 Department of Clinical Sciences and Community Health, ASS G Pini, University of Milan, Milano, Italy
  1. Correspondence to Professor Roberto Gerli, Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Perugia, Italy; roberto.gerli{at}

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It is well recognised that hyperinflammation induced by SARS-CoV-2 is a major cause of disease severity and mortality in infected patients and many of the proposed treatments include agents currently used in rheumatologic clinical practice.1 One critical question, however, is which anti-inflammatory drugs are most appropriate. Among the most traditional non-biological anti-inflammatory therapies, corticosteroids appear to provide some benefit in advanced stages of the disease,2 but concerns may arise from immunosuppression induced during viral replicative phase. On the contrary, no data are available on possible effects of non-steroidal anti-inflammatory drugs (NSAIDs).

In their interesting paper,3 Reyes et al highlighted the potential anti-inflammatory role of colchicine in COVID-19. The primary mechanism of action of colchicine is tubulin disruption leading to down-regulation of multiple inflammatory pathways.4 Among these, colchicine is able to impair platelet aggregation and leucocyte migration through an action on adhesion molecules,5 effect shared with NSAIDs, including salicylates.6 7 However, another important anti-inflammatory effect of colchicine, not described for NSAIDs, derives from its ability to inhibit the NLR family pyrin domain containing 3

(NLRP3) inflammasome with consequent reduction of proinflammatory cytokines.4 It is for this reason that colchicine …

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  • Contributors CP conceived the idea, drafted the manuscript and revised the final version of the manuscript. EB, GC and RC revised the manuscript and approved the final version of the manuscript. RG conceived the idea and wrote the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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