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Erosive osteoarthritis (EOA) is an important subtype of OA, characterised by an aggressive clinical course in perimenopausal women.1 Pain, swelling, redness, warmth and limited function of the digital joints are commonly found in most patients. Erosions (sharp marginal defects, central “crumbling” erosion, “gull-wing” deformity) are an essential hallmark for diagnosis. EOA eventually leads to joint deformity and ankylosis and is an important cause of disability, usually compared to the handicap caused by rheumatoid arthritis.
There are currently no guidelines on the best therapeutic approach in EOA, and treatments usually recommended for patients who do not have EOA (paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), intra-articular injection of corticosteroids, chondroitin sulfate) or physiotherapy are frequently disappointing.
Recent research has highlighted the role of interleukin(IL) 1 in disease progression. Proinflammatory cytokines such as IL1β and, to a lesser extent, tumour necrosis factor α, play a key role in the destruction of the cartilage matrix in OA.2 The IL1 receptor antagonist, anakinra, inhibits the effect of IL1 by blocking its interaction with cell surface receptors.3
This study describes three cases of aggressive EOA treated successfully with anakinra.
Patients with severe EOA, who had failed conventional treatment and had important disability, were treated with a 100 mg daily subcutaneous injection of anakinra. A diagnosis of rheumatoid arthritis was excluded prior to treatment (positive rheumatoid factor and anti-cyclic citrullinated peptide (CCP); erythrocyte sedimentation rate (ESR) >10 mm). Evaluation of pain level using a visual analogue scale (VAS), of patient assessment of global handicap on the VAS and of NSAID therapy was performed at baseline and 3 months after initiation of anakinra.
Three postmenopausal women (patient 1 was 59, patient 2 was 70 and patient 3 was 52), with a history of severe EOA (patient 1: 11, patient 2: 13, patient 3: 12) and who had failed conventional therapy, were treated. At baseline, all patients had important radiographic erosions, a high level of pain on VAS (patient 1: 9/10, patient 2: 8, patient 3: 7.5) and global handicap VAS (patient 1: 8/10, patient 2: 8, patient 3: 5) despite conventional treatment (100% NSAID therapy). After 3 months, there was an improvement in all parameters: pain VAS decreased by 70.2% (patient 1: 88.9%, patient 2: 75%, patient 3: 46.7%), global handicap VAS decreased by 47.5% (patient 1: 62.5%, patient 2: 50%, patient 3: 30%), and NSAIDs were withdrawn in all patients (fig 1). The subcutaneous injections of anakinra were well tolerated.
IL1 is a key factor in the pathogenesis of EOA and anakinra may be able to slow down the disease progression of OA by modulating IL1. Although this study is limited by the lack of disease specific measures of hand function and pain such as the Functional Index For Hand Osteoarthritis (FIHOA), Australian Canadian Osteoarthritis Hand Index (AUSCAN) and Score for the Assessment and Quantification of Chronic Rheumatoid Affections of the Hands (SACRAH), it nevertheless demonstrates a good response to anakinra using a VAS for pain and global handicap. Furthermore, anakinra was well tolerated in all three patients with severe EOA. Placebo-controlled studies are now required to confirm the efficacy of anakinra in a larger number of patients.
Competing interests: None declared.
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