We describe the characteristics and outcome of inflammatory arthritis in patients with myelodysplastic syndrome (MDS) in a French multicenter retrospective study.
Twenty-two patients with MDS (median age, 77.5 yr [interquartile range, 69–81]; 10 women) were included. Inflammatory arthritis presented as polyarthritis in 17 cases (77%) and with symmetric involvement in 15 cases (68%). At diagnosis, the median disease activity score 28 based on C-reactive protein (DAS28-CRP) was 4.5 [2–6.5]. Two patients had anti-citrullinated protein antibodies (ACPAs), and 1 had radiologic erosions. The median time between the diagnoses of arthritis and MDS was 10 months [6–42], with a median articular symptom duration of 3 months [2–8]. The diagnosis of both diseases was concomitant in 6 cases (27%); arthritis preceded MDS in 12 cases (55%), and occurred after MDS in 4 (18%). While the number of swollen and tender joints significantly decreased during follow-up, as did the median DAS28-CRP (from 4.3 [3.8–4.6] at baseline to 2.9 [1.75–3.3]; p < 0.05), CRP remained elevated (CRP >20 mg/L) in 8 patients (42%). Nevertheless, radiographic progression and new ACPA positivity were not observed during a median follow-up of 29 months [9–76]. While most of the patients were treated with steroids (n = 16) for arthritis, additional treatment was administered in only 4 patients (hydroxychloroquine, n = 2; sulfasalazine [Salazopyrin] and etanercept, n = 1, respectively). Eleven patients died during follow-up from acute myeloid leukemia (n = 5); infections (n = 3); or cerebral bleeding, cardiorespiratory failure, or undetermined cause (n = 1, respectively).
Inflammatory arthritis associated with MDS can have various presentations and is often seronegative and nonerosive. Steroids alone are the most common treatment in MDS-associated arthritis, but that treatment is insufficient to control arthritis. Steroid-sparing strategies need to be identified.
From the Service de médecine interne (AM, EG, OF), Université Paris 13, AP-HP, Hôpital Jean Verdier, Bondy; Service d’hématologie clinique (TB, PF), Université Paris 13, AP-HP, Avicenne, Bobigny; Service de médecine interne (OD), Université Rennes 1, Hôpital Universitaire de Rennes, Rennes; Service de rhumatologie (GF), Université Sorbonne Paris Cité, Université Paris 13, Li2P, EA4222, Hôpital Avicenne, Bobigny; Centre Investigation Clinique Biothérapie CBT-506 & Service de rhumatologie (ET), CHU Besançon, Besançon; Service de médecine interne (LR), CHU de Bordeaux, Bordeaux; Service de rhumatologie (MO), CH Romilly/Seine; Service de médecine interne (BG), Hôpital de La Rochelle, La Rochelle; Service de médecine interne et gériatrique (BDW), CHU Nîmes, Nîmes; Service de médecine interne (A-LB), CH Douai, Douai; Service de rhumatologie (J-MZ), CH Croix Saint Simon, Paris; Service de médecine interne (DL), CHU Lille, Université Lille II, Lille; Service de médecine interne (GD), Hôpital de Rochefort, Rochefort; Service de médecine interne (SM), CHG Albi, Albi; and Service d’hématologie clinique (CR), Hôpital Saint-Vincent de Paul, UC Lille, Univ Nord de France, Lille; France.
Presented at the 2012 American College of Rheumatology Congress, Washington, DC.
The authors have no funding or conflicts of interest to disclose.
Reprints: Arsène Mekinian, MD, Service de Médecine Interne, Université Paris 13, AP-HP, Hôpital Jean Verdier, 93140 Bondy, France (e-mail: firstname.lastname@example.org).
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