Assessing the levels of a protein involved in bone formation and its specific antibodies in patients with inflammatory bowel disease (IBD) may help identify those at risk of having axial joint involvement, Italian researchers found.
IBD patients commonly experience extra-intestinal symptoms, including spondyloarthritis (SpA) — inflammation of the joints and of the bone’s ligaments and tendons.
Early detection and management of IBD-associated SpA remains a challenge in clinical practice, mainly due to lack of accurate measures of disease activity and inflammation. This may be particularly difficult in cases of SpA with hidden active IBD.
The study, “Sclerostin and Antisclerostin Antibody Serum Levels Predict the Presence of Axial Spondyloarthritis in Patients with Inflammatory Bowel Disease,” was published in The Journal of Rheumatology.
Researchers evaluated the diagnostic potential of the protein sclerostin and anti-sclerostin antibodies as blood biomarkers in IBD patients.
Previous studies suggested that sclerostin is decreased in the blood of patients with ankylosing spondylitis (AS) compared to healthy people, or controls, and that its total amount correlates with radiographic progression of the disease.
Antibodies that block sclerostin activity have also been suggested as important contributors in the development of ankylosing spondylitis.
The research team evaluated the levels of sclerostin and anti-sclerostin antibodies in 85 patients with axial or peripheral SpA/IBD, 40 IBD patients without joint symptoms, 20 patients with AS, 20 with rheumatoid arthritis, and 20 healthy volunteers.
Sclerostin blood levels were significantly lower in SpA/IBD patients compared to IBD, rheumatoid arthritis, and healthy controls. As in previous reports, patients with AS had the lowest levels of serum sclerostin.
Interestingly, when SpA/IBD patients were separated according to joint involvement of the disease — either axial or peripheral SpA, depending on whether the axial joints of the spine or the peripheral joints of the arms and legs are affected — they had significantly different sclerostin levels.
Sclerostin levels in axial SpA/IBD patients were similar to those seen in AS patients, whereas peripheral SpA/IBD levels were similar to those in IBD, rheumatoid arthritis, and healthy controls.
Although all groups of patients showed increased levels of anti-sclerostin antibodies circulating in their blood compared to healthy controls, these were significantly higher in axial SpA/IBD and ankylosing spondylitis patients.
Also, peripheral SpA/IBD patients had much lower levels of these antibodies compared to AS, axial SpA/IBD, and IBD patients.
Levels of sclerostin and anti-sclerostin antibodies were not associated with IBD or articular disease activity. Still, these two blood biomarkers effectively predicted the presence of axial SpA in about 85% of IBD patients. IBD patients with sclerostin serum levels lower than 169.3 pg/ml had a 5.92 times greater risk of developing axial SpA, and those with anti-sclerostin antibodies levels higher than 32.25 IU/ml were 3.9 times more like to develop the disease.
“Our study may have great relevance for both clinical practice and translational research,” the researchers wrote. “We have demonstrated that sclerostin and anti-sclerostin antibody serum levels could represent novel biomarkers to assess the presence of axial SpA in patients with IBD.”
The researchers believe that assessing sclerostin serum levels could help clinicians identify patients who may benefit the most from additional imaging tests to establish an early diagnosis of SpA/IBD and improve management of the disease.
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