Adding a DMARD or Switching Away From Anti-TNF Drugs Helps Patients With IBD and Paradoxical Arthritis

The authors of a recent study report that the addition of a disease-modifying anti-rheumatic drug (DMARD) or a switch to ustekinumab showed greater efficacy than changing anti–tumor necrosis factor (anti-TNF) treatments in patients with inflammatory bowel disease (IBD) who develop paradoxical arthritis. 
The Center for Biosimilars Staff
May 28, 2018
Patients who receive treatment with anti–tumor necrosis factor (anti-TNF) drugs for inflammatory bowel disease (IBD) may develop arthritis, despite the fact that anti-TNFs can be used successfully to treat conditions such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Currently, there are no predictors of paradoxical arthritis, and optimal clinical management is debated.

A recent study sought to evaluate the histological features of paired synovial tissue and colonic mucosa tissue in patients who have IBD and develop paradoxical arthritis while undergoing treatment.

Patients with Crohn disease (CD) or ulcerative colitis (UC) who were in stable clinical or endoscopic remission, and who had no history of joint involvement but developed paradoxical arthritis during maintenance therapy with anti-TNFs, were enrolled in a prospective study from January 2015 to April 2017. In total, 10 patients with IBD (6 with CD and 4 with UC) were enrolled.

The patients underwent rheumatological evaluation and immunological parameters were recorded, and they also underwent ultrasound assessment. A multidisciplinary team recommended 1 of 3 treatment modifications for these patients: the addition of a disease-modifying anti-rheumatic drug (DMARD), either methotrexate or sulphasalazine; a switch to a different anti-TNF agent; or a switch to ustekinumab. Patients were followed every 2 months for at least 6 months.

Ultrasound assessment showed that there were no significant differences between patients with IBD who developed arthritis while taking anti-TNFs than in patients with PsA or RA, but the patients showed greater similarity, in terms of tender joint count and swollen joint count, to PsA than to RA. They also showed similar histological findings in terms of synovial-resident CD68+, CD21+, CD20+, CD3+, and CD117+ cells versus comparator patients who had PsA or RA.

Additionally, the colonic mucosa (CM) of patients with IBD showed signs of histologically proven subclinical inflammation, even in the case of clinical and endoscopic remission or mild disease activity. All of the patients with IBD had CD68+ cells present in their CM samples, and 70%, 60% and 50%, respectively, had CD3+, CD117+ and CD20+ cells present.

Among the 10 patients, 6 added a DMARD to their treatment, 2 switched to another anti-TNF drug, and 2 switched to ustekinumab. All of the patients who added a DMARD showed a reduced disease activity score (DAS) at 6 months of follow-up, and among those who changed treatments, only patients who switched to ustekinumab had a reduced DAS at followup.

Despite the small study size, the authors say that the addition of a DMARD or a switch to ustekinumab showed greater efficacy than changing anti-TNF treatments in patients with IBD and paradoxical arthritis under anti-TNF treatment.

Reference
Alivernini A, Pugliese D, Tolusso B, et al. Paradoxical arthritis occurring during anti-TNF in patients with inflammatory bowel disease: histological and immunological features of a complex synovitis. RMD Open. 2018;4(1):e000667. doi: 10.1136/rmdopen-2018-000667.

 

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