Yvonne M R de Punder1, Tim L Th A Jansen1, Annelies E van Ede1, Alfons A den Broeder1, Piet L C M van Riel1, Jaap Fransen2. 1. From the Department of Rheumatology, Radboud University Medical Centre, and the Department of Rheumatology, Sint Maartenskliniek, Nijmegen, the Netherlands.Y.M.R. de Punder, MD; T.L.Th. A. Jansen, MD, PhD; A.E. van Ede, MD, PhD; P.L.C.M. van Riel, MD, PhD, Professor of Rheumatology; J. Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre; A.A. den Broeder, MD, PhD, Department of Rheumatology, Sint Maartenskliniek. 2. From the Department of Rheumatology, Radboud University Medical Centre, and the Department of Rheumatology, Sint Maartenskliniek, Nijmegen, the Netherlands.Y.M.R. de Punder, MD; T.L.Th. A. Jansen, MD, PhD; A.E. van Ede, MD, PhD; P.L.C.M. van Riel, MD, PhD, Professor of Rheumatology; J. Fransen, PhD, Department of Rheumatology, Radboud University Medical Centre; A.A. den Broeder, MD, PhD, Department of Rheumatology, Sint Maartenskliniek. Jaap.Fransen@Radboudumc.nl.
Abstract
OBJECTIVE: To develop a personalized treatment target approach in patients with rheumatoid arthritis (RA) based on baseline risk factors for joint damage progression in combination with disease activity over time. METHODS: Data were used from the Nijmegen early RA cohort. Presence or absence of anticyclic citrullinated peptide antibodies (anti-CCP), high erythrocyte sedimentation rate, and erosions were translated into 4 risk profiles: 0, 1, 2, and 3. Joint damage progression was assessed with the Ratingen score, and disease activity with the original Disease Activity Score (DAS) over 3 years. The probability for joint damage progression was calculated for each risk profile and each DAS category using logistic regression models. The probabilities were translated into personalized disease activity treatment targets. RESULTS: More risk factors at baseline as well as a higher DAS level resulted in a higher probability for joint damage progression in a dose-dependent way. Low DAS corresponded with a probability of 0.0, 0.08, 0.20, and 0.58 in patients with 0, 1, 2, and 3 risk factors, respectively. Moderate DAS corresponded with a probability of 0.06 in patients with 0 risk factors and 0.35 with 1 risk factor. High DAS resulted in a probability of 0.50 with no risk factors present at baseline. CONCLUSION: Presence of anti-CCP, acute-phase response, and erosions at baseline can be used to set individual treatment targets in RA. In patients without these risk factors, a moderate DAS as a target is sufficient, while for patients with all 3 risk factors, a low DAS is not strict enough to limit the risk for joint damage.
OBJECTIVE: To develop a personalized treatment target approach in patients with rheumatoid arthritis (RA) based on baseline risk factors for joint damage progression in combination with disease activity over time. METHODS: Data were used from the Nijmegen early RA cohort. Presence or absence of anticyclic citrullinated peptide antibodies (anti-CCP), high erythrocyte sedimentation rate, and erosions were translated into 4 risk profiles: 0, 1, 2, and 3. Joint damage progression was assessed with the Ratingen score, and disease activity with the original Disease Activity Score (DAS) over 3 years. The probability for joint damage progression was calculated for each risk profile and each DAS category using logistic regression models. The probabilities were translated into personalized disease activity treatment targets. RESULTS: More risk factors at baseline as well as a higher DAS level resulted in a higher probability for joint damage progression in a dose-dependent way. Low DAS corresponded with a probability of 0.0, 0.08, 0.20, and 0.58 in patients with 0, 1, 2, and 3 risk factors, respectively. Moderate DAS corresponded with a probability of 0.06 in patients with 0 risk factors and 0.35 with 1 risk factor. High DAS resulted in a probability of 0.50 with no risk factors present at baseline. CONCLUSION: Presence of anti-CCP, acute-phase response, and erosions at baseline can be used to set individual treatment targets in RA. In patients without these risk factors, a moderate DAS as a target is sufficient, while for patients with all 3 risk factors, a low DAS is not strict enough to limit the risk for joint damage.
Authors: Gwendolyn Vuurberg; Lauren M Wink; Leendert Blankevoort; Daniel Haverkamp; Robert Hemke; Sjoerd Jens; Inger N Sierevelt; Mario Maas; Gino M M J Kerkhoffs Journal: BMC Musculoskelet Disord Date: 2018-07-18 Impact factor: 2.362
Authors: Christopher J Edwards; Patrick Kiely; Subhashini Arthanari; Sandeep Kiri; Julie Mount; Jane Barry; Catherine R Mitchell; Polly Field; Philip G Conaghan Journal: Rheumatol Adv Pract Date: 2019-02-15
Authors: K Doi; H Ito; T Tomizawa; K Murata; M Hashimoto; M Tanaka; K Murakami; K Nishitani; M Azukizawa; A Okahata; M Saito; T Mimori; S Matsuda Journal: Medicine (Baltimore) Date: 2019-11 Impact factor: 1.817
Authors: G Akdemir; I M Markusse; Y P M Goekoop-Ruiterman; G M Steup-Beekman; B A M Grillet; P J S M Kerstens; W F Lems; T W J Huizinga; C F Allaart Journal: Clin Rheumatol Date: 2016-09-28 Impact factor: 2.980