In-Ho Song1, Kay-Geert Hermann2, Hildrun Haibel3, Christian E Althoff2, Denis Poddubnyy3, Joachim Listing4, Anja Weiß4, Bruce Freundlich5, Ekkehard Lange6, Martin Rudwaleit7, Joachim Sieper3. 1. Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Rheumatology, Med. Clinic I, Rheumatology, Hindenburgdamm 30, 12203 Berlin, Germany. Electronic address: in-ho@gmx.de. 2. Charité Universitätsmedizin Berlin, Campus Mitte, Radiology, Berlin, Germany. 3. Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Rheumatology, Med. Clinic I, Rheumatology, Hindenburgdamm 30, 12203 Berlin, Germany. 4. German Rheumatism Research Center, Berlin, Germany. 5. Division of Rheumatology, University of Pennsylvania, Philadelphia, PA. 6. Pfizer, Germany, Berlin, Germany. 7. Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Rheumatology, Med. Clinic I, Rheumatology, Hindenburgdamm 30, 12203 Berlin, Germany; Klinik für Innere Medizin und Rheumatologie, Klinikum Bielefeld Rosenhöhe, Bielefeld, Germany.
Abstract
OBJECTIVE: To assess the relationship between active inflammation and development of chronic lesions in the spine and sacroiliac (SI)-joints on MRI in early axial spondyloarthritis (SpA) during treatment with etanercept. METHODS: Here, we analyzed the 41 patients of the ESTHER trial, who were treated with etanercept over 3 continuous years and of whom MRIs were available for baseline, year 2, and year 3. MRIs were scored for active inflammation (STIR sequences) and chronic changes (T1 sequence) such as fatty lesions, erosions, and ankylosis in the SI joints and spinal vertebral units (VUs). RESULTS: The mean fatty lesion scores increased between baseline and year 2 both in the spine (1.13 at baseline vs. 1.40 at year 2, p = 0.0254) and in the SI joints (4.76 at baseline vs. 5.46 at year 2, p = 0.27), but we found no further increase of the fatty lesion score between years 2 and 3. New fatty lesions at years 2 and 3 developed nearly exclusively in SI joint quadrants and VUs in which active MRI inflammation was present at baseline. Fatty lesions disappeared only in 3 SI joint quadrants and in none of VUs at years 2 and 3. Erosion and ankylosis scores remained unchanged. CONCLUSION: Our data indicate a relationship between the presence of active MRI inflammation and the new development of fatty lesions. Furthermore, there was no increase of fatty lesions during continuous treatment of axial SpA patients with etanercept after successful suppression of active inflammation. Whether this is predictive of stopping radiographic progression needs to be further investigated.
RCT Entities:
OBJECTIVE: To assess the relationship between active inflammation and development of chronic lesions in the spine and sacroiliac (SI)-joints on MRI in early axial spondyloarthritis (SpA) during treatment with etanercept. METHODS: Here, we analyzed the 41 patients of the ESTHER trial, who were treated with etanercept over 3 continuous years and of whom MRIs were available for baseline, year 2, and year 3. MRIs were scored for active inflammation (STIR sequences) and chronic changes (T1 sequence) such as fatty lesions, erosions, and ankylosis in the SI joints and spinal vertebral units (VUs). RESULTS: The mean fatty lesion scores increased between baseline and year 2 both in the spine (1.13 at baseline vs. 1.40 at year 2, p = 0.0254) and in the SI joints (4.76 at baseline vs. 5.46 at year 2, p = 0.27), but we found no further increase of the fatty lesion score between years 2 and 3. New fatty lesions at years 2 and 3 developed nearly exclusively in SI joint quadrants and VUs in which active MRI inflammation was present at baseline. Fatty lesions disappeared only in 3 SI joint quadrants and in none of VUs at years 2 and 3. Erosion and ankylosis scores remained unchanged. CONCLUSION: Our data indicate a relationship between the presence of active MRI inflammation and the new development of fatty lesions. Furthermore, there was no increase of fatty lesions during continuous treatment of axial SpA patients with etanercept after successful suppression of active inflammation. Whether this is predictive of stopping radiographic progression needs to be further investigated.
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