Spondyloarthritis patients with microscopic gut inflammation had to start anti–tumor necrosis factor treatment sooner in the course of their disease than patients without gut inflammation in a prospective, observational study of 63 Belgian patients with the axial form of spondyloarthritis, the peripheral form, or both.
The finding "is in line with the hypothesis that in SpA [spondyloarthritis] gut inflammation may drive disease," Dr. Heleen Cypers said at the annual European Congress of Rheumatology.
Dr. Heleen Cypers
SpA patients with microscopic gut inflammation initiated anti–tumor necrosis factor (TNF) therapy roughly twice as quickly as those without gut inflammation at each time period examined – at 6, 12, and 18 months after their initial diagnosis. After 18 months, 56% of patients with inflammation were on treatment with an anti-TNF agent, compared with almost 29% of the followed patients without microscopic gut inflammation, said Dr. Cypers, a rheumatologist at Ghent (Belgium) University.
The link between microscopic gut inflammation and a faster need to start on biologic treatment occurred at nearly identical rates in both the subset of 11 patients with acute gut inflammation and the subset of 21 patients with chronic inflammation.
Previous research by Dr. Cypers’ group had shown that chronic inflammation in the gut was associated with more extensive bone marrow edema of the sacroiliac joints, a higher risk of progression to ankylosing spondylitis, and a higher risk of developing Crohn’s disease. No information existed on the impact of gut inflammation on therapeutic decision-making in SpA, however.
The current study followed the Ghent Inflammatory Arthritis and Spondylitis Cohort (GIANT) of 63 newly diagnosed patients who underwent an ileocolonoscopy at baseline. Patients were not taking anti-TNF agents and were followed for 18 months. The decision to start anti-TNF treatment was made by a rheumatologist who was unaware of the patient’s gut history.
SpA patients who had microscopic gut inflammation at baseline were more likely to start anti-TNF treatment sooner than were patients without gut inflammation. During follow-up, just under a third of patients (9 of 31) with normal gut histology started anti-TNFs, compared with over half (18 of 32) of the patients with gut inflammation at baseline.
In most cases, anti-TNF drugs were started because first-line therapy had failed, Dr. Cypers reported. Her analysis also showed that initiation of an anti-TNF drug during follow-up was significantly linked with a higher level of C-reactive protein at baseline.
According to Dr. Cypers, the findings support the hypothesis that bowel inflammation in SpA induces a more chronic, persevering disease.
"The findings identify gut inflammation as a marker of a poor prognosis and have relevance for therapeutic decision-making in daily clinical practice. It is conceivable that assessment of gut inflammation will be included in future models for risk stratification of SpA," she said in an interview.
The underlying mechanisms explaining the link are still under investigation, but several studies have suggested that inflammation in the gut may be a triggering factor for SpA development. Interactions in the intestinal immune system also may play an important role, she said.
Future research by the group will focus on ruling out the interdependency of all of these factors, predicting response to biologic therapy based on gut histology, and determining whether therapies aiming at treating microscopic gut inflammation can affect the evolution of the disease.
Dr. Cypers said that she and her associates had no disclosures.