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TOPLINE
Anti-TNF therapy when used as a second-line therapy after biologics with different mechanisms of action was associated with a higher risk for treatment discontinuation in patients with ulcerative colitis (UC), but not in those with Crohn's disease (CD).
METHODOLOGY
- Researchers conducted a multicentre observational study using data from the ENEIDA registry to assess the durability and efficacy of second-line anti-TNF therapy following treatment with a biologic with a different mechanism of action in adult patients with inflammatory bowel disease (IBD).
- They included 66 patients with CD and 117 patients with UC who first received a non-anti-TNF biologic followed by an anti-TNF therapy as a second-line treatment between 2018 and 2025.
- Using propensity score matching, each case receiving anti-TNF therapy after a biologic with a different mechanism of action was matched with three of those receiving first-line anti-TNF and three of those receiving anti-TNF after another anti-TNF, resulting in 198 matched patients with CD and 351 matched patients with UC.
- Among patients previously treated with non-anti-TNF biologics, 62% of those with CD received ustekinumab and 38% received vedolizumab, whereas 90% of those with UC received vedolizumab and 10% received ustekinumab.
- The primary outcome was treatment durability, defined as treatment persistence without treatment failure or discontinuation; secondary outcomes were short-term (16-week) and long-term (52-week) clinical remission and response rates, as well as safety.
TAKEAWAY
- In patients with UC, the use of anti-TNF therapy after biologics with different mechanisms of action was independently associated with a higher risk for treatment discontinuation than the use of anti-TNF therapy following another anti-TNF therapy (adjusted hazard ratio, 1.89; P < .001).
- In patients with CD, anti-TNF therapy after exposure to biologics with different mechanisms of action was not associated with treatment persistence.
- Clinical remission rates were significantly lower among patients with UC who received anti-TNF after biologics with different mechanisms of action vs those in the two control groups at both short-term (20% vs 34% vs 39%; P < .001) and long-term (18% vs 34% vs 42%; P < .001) follow-ups. No significant difference in remission rates was observed among patients with CD in the three groups.
- Rates of treatment discontinuation due to adverse events did not differ among the three cohorts in either patients with CD or those with UC.
IN PRACTICE
"[The] study provides the first real-world evidence on the use of anti-TNF therapy after failure of a biologic agent with a different MOA [mechanism of action] in IBD," the authors wrote.
"[The] results suggest that not only the number of previous therapies, but also the specific mechanisms of action previously employed, may critically influence subsequent treatment response," they added.
SOURCE
This study was led by Carmen Yagüe Caballero, Servicio de Aparato Digestivo, Hospital Universitario Miguel Servet, Zaragoza, Spain. It was published online on August 12, 2026, in Alimentary Pharmacology & Therapeutics.
LIMITATIONS
Residual confounding cannot be ruled out due to the lack of data on baseline disease activity. Clinical response and remission were obtained on the basis of investigator judgement rather than activity indices, thereby introducing potential assessment variability and subjectivity in effectiveness outcomes. The study lacked data on patient frailty and comorbidity burden.
DISCLOSURES
One author reported receiving funding through a Juan Rodés Grant from Instituto de Salud Carlos III, and another author reported receiving support from Gobierno Vasco-Eusko Jaurlaritza. Several authors declared serving as speakers, consultants, or advisory board members; receiving research or education funding, advisory fees, and consulting fees; or having other ties with various pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
