From the Friedrich-Alexander-University Erlangen-Nuremberg (FAU), Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen, Erlangen, Germany; St. Vincent Hospital, Vinforce Study Group, Medical University of Vienna, Vienna, Austria; Institutio de Rheumatologia, São Paolo, Brazil; University of Würzburg, Internal Medicine 2, Würzburg; University Medical Center Freiburg, Rheumatology and Clinical Immunology, Freiburg; Rheumatology Clinical Practice Erlangen, Erlangen; Rheumatology Practice and Department of Internal Medicine 2, Clinic Burghausen, Burghausen; Asklepios Medical Center, Department of Rheumatology and clinical Immunology, Bad Abbach; Rheumatology Practice Bamberg, Bamberg; Rheumatology Practice Bayreuth, Bayreuth; University of Heidelberg, Medicine 5, Heidelberg; Rheumatology Practice Nuremberg, Nuremberg; Schlosspark Klinik, Internal Medicine/Rheumatology, Berlin; University of Tübingen, Centre for Interdisciplinary Clinical Immunology, Tübingen; Praxiszentrum St. Bonifatius, Munich, Germany.
M. Hagen, BSc, CandMed, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; M. Englbrecht, PhD, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; J. Haschka, MD, St. Vincent Hospital, Vinforce Study Group, Medical University of Vienna; M. Reiser, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; A. Kleyer, MD, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; A. Hueber, MD, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; B. Manger, MD, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; C. Figueiredo, MD, Institutio de Rheumatologia; J. Fogagnolo Cobra, MD, Institutio de Rheumatologia; H.P. Tony, MD, University of Würzburg, Internal Medicine 2; S. Finzel, MD, University Medical Center Freiburg, Rheumatology and Clinical Immunology; S. Kleinert, MD, Rheumatology Clinical Practice Erlangen; J. Wendler, MD, Rheumatology Clinical Practice Erlangen; F. Schuch, MD, Rheumatology Clinical Practice Erlangen; M. Ronneberger, MD, Rheumatology Clinical Practice Erlangen; M. Feuchtenberger, MD, Rheumatology Practice and Department of Internal Medicine 2, Clinic Burghausen; M. Fleck, MD, Asklepios Medical Center, Department of Rheumatology and clinical Immunology; K. Manger, MD, Rheumatology Practice Bamberg; W. Ochs, MD, Rheumatology Practice Bayreuth; H.M. Lorenz, MD, University of Heidelberg, Medicine 5; H. Nüsslein, MD, Rheumatology Practice Nuremberg; R. Alten, MD, Schlosspark Klinik, Internal Medicine/Rheumatology; J. Henes, MD, University of Tübingen, Centre for Interdisciplinary Clinical Immunology; K. Krüger, MD, Praxiszentrum St. Bonifatius; G. Schett, MD, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen; J. Rech, MD, FAU, Department of Internal Medicine 3 - Rheumatology and Immunology, Universitätsklinikum Erlangen.
J Rheumatol. 2019 May;46(5):460-466. doi: 10.3899/jrheum.180028. Epub 2018 Dec 1.
To analyze the effect of a risk-stratified disease-modifying antirheumatic drug (DMARD)-tapering algorithm based on multibiomarker disease activity (MBDA) score and anticitrullinated protein antibodies (ACPA) on direct treatment costs for patients with rheumatoid arthritis (RA) in sustained remission.
The study was a posthoc retrospective analysis of direct treatment costs for 146 patients with RA in sustained remission tapering and stopping DMARD treatment, in the prospective randomized RETRO study. MBDA scores and ACPA status were determined in baseline samples of patients continuing DMARD (arm 1), tapering their dose by 50% (arm 2), or stopping after tapering (arm 3). Patients were followed over 1 year, and direct treatment costs were evaluated every 3 months. MBDA and ACPA status were used as predictors creating a risk-stratified tapering algorithm based on relapse rates.
RA patients with a low MBDA score (< 30 units) and negative ACPA showed the lowest relapse risk (19%), while double-positive patients showed high relapse risk (61%). In ACPA-negative and MBDA-negative (< 30 units), and ACPA or MBDA single-positive (> 30 units) groups, DMARD tapering appears feasible. Considering only patients without flare, direct costs for synthetic and biologic DMARD in the ACPA/MBDA-negative and single positive groups (n = 41) would have been €372,245.16 for full-dose treatment over 1 year. Tapering and stopping DMARD in this low-risk relapse group allowed a reduction of €219,712.03 of DMARD costs. Average reduction of DMARD costs per patient was €5358.83.
Combining MBDA score and ACPA status at baseline may allow risk stratification for successful DMARD tapering and cost-effective use of biologic DMARD in patients in deep remission as defined by the 28-joint count Disease Activity Score using erythrocyte sedimentation rate.
分析基于多生物标志物疾病活动（MBDA）评分和抗瓜氨酸蛋白抗体（ACPA）的风险分层疾病修正抗风湿药物（DMARD）逐渐减少算法对处于持续缓解的类风湿关节炎（RA）患者直接治疗成本的影响。
本研究是对持续缓解的 146 例 RA 患者进行的回顾性分析，他们正在逐渐减少并停止 DMARD 治疗，这是前瞻性随机 RETRO 研究的一部分。在继续使用 DMARD 的患者（第 1 组）、减少剂量 50%（第 2 组）或减少后停药（第 3 组）的基线样本中确定了 MBDA 评分和 ACPA 状态。患者随访 1 年，每 3 个月评估一次直接治疗费用。MBDA 和 ACPA 状态被用作预测因子，根据复发率创建风险分层逐渐减少算法。
MBDA 评分（<30 分）和 ACPA 阴性的 RA 患者复发风险最低（19%），而双阳性患者复发风险最高（61%）。在 ACPA 阴性和 MBDA 阴性（<30 分）、ACPA 或 MBDA 单阳性（>30 分）的组中，DMARD 逐渐减少似乎是可行的。仅考虑无发作的患者，在 ACPA/MBDA 阴性和单阳性组（n=41）中，合成和生物 DMARD 的直接成本在 1 年内全剂量治疗将为€372,245.16。在复发风险低的组中逐渐减少和停止 DMARD 治疗可减少 DMARD 治疗费用€219,712.03。每位患者平均减少 DMARD 治疗费用为€5358.83。
在基线时结合 MBDA 评分和 ACPA 状态可对成功 DMARD 逐渐减少进行风险分层，并在通过红细胞沉降率定义的 28 关节计数疾病活动评分达到深度缓解的患者中，以具有成本效益的方式使用生物 DMARD。
