| Literature DB >> 30451654 |
Xenofon Baraliakos1, Philip G Conaghan2,3, Maria-Antonietta D'Agostino4,5, Walter Maksymowych6, Esperanza Naredo7, Mikkel Ostergaard8,9, Georg Schett10, Paul Emery2,3.
Abstract
Imaging is increasingly used in the routine management of rheumatic diseases as well as in the clinical trials of these disorders. This viewpoint, authored by a group of international imaging experts following two meetings dedicated to imaging in rheumatology, reports a consensus about the current knowledge and addresses where further research should be focused based on the views of the international imaging experts and discussion of the evidence with attending imaging practitioners. The goal was to maximize the potential of imaging to improve the clinical management of four rheumatic diseases. These rheumatic diseases include rheumatoid arthritis, psoriatic arthritis, axial spondyloarthritis, and osteoarthritis.Entities:
Year: 2019 PMID: 30451654 PMCID: PMC6459329 DOI: 10.5152/eurjrheum.2018.18121
Source DB: PubMed Journal: Eur J Rheumatol ISSN: 2147-9720
US and MRI in RA (current knowledge)
| What is known? |
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US and MRI are more sensitive than clinical examination for identifying minimal synovitis and can aid diagnosis when there is diagnostic doubt. US- and MRI-detected inflammation can predict progression to clinical RA from undifferentiated inflammatory arthritis and for ACPA-positive, non-specific symptoms. Subclinical synovitis detected by US and MRI predicts subsequent damage and flare, even when clinical remission is present. US and MRI may be used to predict treatment response and be useful in monitoring disease activity. MRI is more responsive to change in joint damage than CR and can assist in monitoring of disease progression. MRI is more sensitive than clinical examination and can detect bone marrow edema, which is a strong predictor of subsequent radiographic progression in early RA. |
Clinical practice research agenda for US and MRI in RA
| What is unknown and should be known? |
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What is the optimal set of joints to be scanned by US, and how frequently can clinical examination be enhanced? What is the optimal selection of joints and timing of MRI for the assessment of diagnosis and prognosis in RA? What are the thresholds of abnormality of imaging-detected inflammation to guide intervention? What are further data on MRI diagnostic value for patients not fulfilling the American College of Rheumatology/EULAR 2010 classification criteria? What is the role of MRI in predicting response to therapy and in defining remission? What is the cost-effectiveness of using US in diagnosis, treatment monitoring, and remission and of MRI in clinical practice? What is the added value of US in a tight control regimen in established RA? |
Clinical trials in RA (research agenda)
| What is unknown and should be known? |
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What is the value of MRI-detected damage as an endpoint in RA clinical trials? Which data are required to support regulatory acceptance of MRI structural outcome and inflammatory outcome measures relevant for new drug development/approval? Can tenosynovitis scoring be added to RAMRIS, and what value does this offer? What is the added value of further trials based on MRI assessment of the joints other than the hand, in which most studies have been conducted? What cutoff values for clinical remission assessed by MRI and US (and their correlation) should be used in clinical trials? |
US and MRI in PsA (current knowledge)
| What is known? |
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US visualizes the peripheral joints and entheses and is better than clinical examination in detecting entheseal abnormality. US studies have shown significant subclinical enthesitis and synovitis in patients with psoriasis without arthritis. US-detected subclinical enthesitis in psoriasis may differ from subclinical enthesitis in PsA (patients with PsA having more power Doppler). Baseline enthesitis and persistent synovitis or enthesitis by US after 6 months of therapy predicts subsequent structural damage. DAPSA and Boolean definitions of remission appear to be the best predictors of US remission. MRI visualizes all relevant inflammatory and structural pathologies of PsA and is more sensitive to inflammatory and destructive changes than X-ray and clinical examination. Whole-body MRI can assess inflammation and structural damage by detecting multisite enthesitis, peripheral synovitis, and tenosynovitis and axial involvement. |
Research agenda for US and MRI in PsA
| What is unknown and should be known? |
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What is the role of US- or MRI-detected subclinical enthesitis as predictor for the development of PsA in patients with psoriasis? What are the optimal joint sets for screening/diagnostic investigation by US/MRI? What is the predictive value of US monitoring compared with clinical/laboratory monitoring? What is the predictive capability of US-detected inflammatory patterns in PsA therapy response? What is the prognostic value of subclinical US/MRI abnormalities in PsA remission? What is the predictive value of MRI findings for therapeutic response and subsequent damage progression in PsA? What is the optimal MRI monitoring strategy in PsA clinical trials? What is the utility of novel MRI techniques (whole-body MRI, dynamic MRI, and other quantitative methods) in PsA clinical trials and practice? How can dactylitis and enthesitis be better defined by MRI, and how should these features be assessed in PsA clinical practice? |
Imaging axial SpA (current knowledge)
| What is known? |
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CR of the SIJs should, generally, be the first imaging method to diagnose sacroiliitis as part of axial SpA. MRI should be used if diagnosis of axial SpA cannot be established based on clinical features and CR. CR detects new bone formation and is important for long-term monitoring of structural damage. MRI allows early detection and monitoring of inflammation and structural damage in the sacroiliac joints and the spine. CR detects syndesmophytes, which are predictive of new development of syndesmophytes. MRI predicts the development of new radiographic syndesmophytes. MRI-detected inflammation (bone marrow edema) is a predictor of good clinical response to anti-TNF-alpha treatment in addition to elevated CRP. |
Imaging axial SpA (research agenda)
| What is unknown/should be known? |
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What is the potential role of very early intervention, prediction, and identification of patients likely to progress early? What is the significance of fat metaplasia as a lead indicator of radiographic progression? What is the role of MRI in defining remission in treat-to-target strategies, and is subclinical inflammation on MRI of prognostic significance? What is the predictive potential of MRI lesions with respect to new bone formation? What is the validation of MRI lesions as lead indicators of radiographic progression in the spine? What is the interaction of different types of inflammatory and structural lesions detected by MRI and CR to predict disease progression? What are more rational clinical trial study designs for disease modification (disease duration <10 years, patients selected for disease progression, positive CRP, presence of MRI inflammation, and baseline presence of definite syndesmophyte)? |
Imaging OA (research agenda)
| What is unknown/should be known? |
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What is the added value of imaging (any modality) to clinical or differential diagnosis? What is the cost-effectiveness of imaging in OA clinical practice? Can imaging identify subgroups/phenotypes to enable targeted treatment? Is the use of imaging to measure therapy response of clinical benefit? Can imaging features predict therapy response to specific therapies? What are the benefits of imaging in less studied OA sites, such as the foot and shoulder? What is the added value of weight-bearing versus non-weight-bearing X-rays? Can imaging guidance be developed to improve the efficacy of treatments? |