Abstract
Introduction: Immune checkpoint inhibitor-induced inflammatory arthritis (ICI-IA) is a relatively new disease entity caused by ICI agents during cancer therapy. Reactive arthritis (ReA) is a well-known disease entity caused by urogenital or gastrointestinal bacterial infection or pneumonia. In this sense, ICI-IA and ReA are both defined by a reaction to a well-specified causal event. As a result, comparing these diseases may help to determine therapeutic strategies. Methods: We compared ICI-IA and ReA with special focus on pharmacological management. Specifically regarding treatment, we conducted a literature search of studies published in the PubMed database. Inclusion criteria were studies on treatment with non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoids (GC), or disease modifying antirheumatic drugs (DMARDs) in ICI-IA or ReA. During systematic selection, 21 studies evaluating ICI-IA and 14 studies evaluating ReA were included. Results: In ICI-IA, prospective and retrospective studies have shown effects of non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoid (GC), sulfasalazine (SSZ), methotrexate (MTX), hydroxychloroquine (HCQ) and TNFi. In ReA, retrospective studies evaluated NSAIDs and GC. A randomized controlled trial reported the effect of SSZ, and a retrospective study reported the effect of MTX and SSZ in combination with tumor necrosis factor alpha inhibition (TNFi). For both entities, small case reports show treatment effects of interleukin 6 receptor inhibition (IL-6Ri). Discussion: This literature review identified both similarities and differences regarding the pathogenesis and clinical features of ReA and ICI-IA. Studies on treatment reported effectiveness of NSAIDs, GC, MTX, SSZ and TNFi in both diseases. Further, small case reports showed effects of IL-6Ri.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 112687 |
| Tidsskrift | Biomedicine & Pharmacotherapy |
| Vol/bind | 148 |
| Antal sider | 9 |
| ISSN | 0753-3322 |
| DOI | |
| Status | Udgivet - apr. 2022 |
Bibliografisk note
Funding Information:TWK was supported by a grant from Independent Research Fund Denmark ( 9039–00015B ).
Funding Information:
T. Kragstrup has received the Gilead Nordic Fellowship grant, has engaged in educational activities receiving speaking fees from Pfizer, Bristol-Myers Squibb, Eli Lilly, Novartis, UCB, and Abbvie, has received consultancy fees from Bristol-Myers Squibb, Gilead, Galapagos, and UCB, and is co-founder and clinical developer in iBiotech ApS developing diagnostic and therapeutic solutions for people with autoimmune diseases and cancer. J. Leipe received grant/research support from: Novartis, Pfizer; Abbvie, BMS, Gilead, Janssen, Sanofi; honoraria for consulting or speaking: Abbvie, BMS, Galapagos, Janssen-Cilag, Gilead, Lilly, Medac, MSD, Novartis, Pfizer, Roche/Chugai, Sanofi, UCB. V.Schäfer received grant/research support from: Novartis, Hexal, Lilly, Roche, Celgene, University of Bonn, honoraria for consulting or speaking: Chugai, AbbVie, Celgene, Sanofi, Lilly, Pfizer, Amgen, BMS, Roche, Gilead, Novartis, BMS, Medac, Sanofi, Lilly, Pfizer, Janssen, Roche, Schire, Onkowissen.