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Inflammatory arthritis is present in
The typical presentation of lupus arthritis is a symmetric polyarthritis that preferentially involves the small joints over the large joints although any joint may be affected. The duration of the joint symptoms is variable, ranging from hours to weeks to months. Swelling of the joint as a consequence of joint fluid or synovial proliferation can be present although the swelling is often not as prominent as it is with rheumatoid arthritis (RA). Physical examination may reveal tender joints
While sacroiliitis is typically thought of as a manifestation of the seronegative spondyloarthropathies, it has been reported in SLE [8], [9], [10]. Although one study reported an approximate 50% prevalence of SI joint involvement based on X-rays or bone scans, it has been suggested that this number is too high [11]. Its true prevalence in SLE is unclear.
There have also been rare reports of cervical spine involvement with subluxation [12], [13]. Atlanto–axial subluxation, ranging from 3.5 to 7.0 mm, was seen in 5 of 59 unselected lupus patients (8.5%) and was associated with Jaccoud's arthropathy, longer disease duration, chronic renal failure and increased serum parathyroid hormone levels [14].
While the majority of lupus patients with arthritis have a non-deforming course, patients can occasionally develop deformities, which could be erosive or nonerosive. Jaccoud's arthropathy, which was initially described in rheumatic fever, is a variant of lupus arthritis resulting from ligament laxity and joint subluxation. Significant deformity occurs that can mimic RA; however, on X-ray, erosions are characteristically absent and physical examination reveals reducible joint deformity. The
Occasionally, patients who fulfil American College of Rheumatology Criteria for SLE will have erosive changes on X-rays, most commonly in the hands. These patients have often been called “rhupus” although no agreed-upon definition for this overlap condition exists [26], [27]. The prevalence of lupus/RA overlap is estimated to be 0.01–2% and has been associated with the presence of anti-CCP antibodies in some studies [28], [29], [30] although another study found the prevalence of anti-CCP in
In addition to the ligament laxity that is seen with Jaccoud's arthropathy, tendinopathies also occur in SLE. They can manifest as tendonitis, tenosynovitis or tendon rupture. Tenosynovitis of the hand was noted in 44% of SLE patients in an ultrasound study [32]. In one study comparing hand magnetic resonance imaging (MRI) findings, the overall tenosynovitis in SLE was nearly indistinguishable from RA [33]. Tendon rupture is a rare complication of SLE. The tendons that are more commonly
SLE synovial membrane biopsies in one study demonstrated nonspecific changes including vascular changes of congestion, oedema, proliferation of small blood vessels, perivascular mononuclear cell infiltration and surface fibrin deposits, which was more intense than in other rheumatologic conditions; there was also less synovial lining cell hyperplasia and fewer infiltrative mononuclear cells seen than in RA [41]. Labowitz and Schumacher described similar changes in seven SLE patients, noting
A variety of X-ray findings in SLE joint examinations have been described, including soft tissue swelling, peri-articular osteoporosis, acral sclerosis, soft tissue calcification, cystic bone lesions (41% in one series) [43], joint subluxations as seen with Jaccoud's arthropathy and occasionally, erosions [44]. In one study, lupus MRI findings in the hand, including tenosynovitis, were nearly indistinguishable from early RA except that RA patients had more bone marrow oedema of the MCP joints
When evaluating the lupus patient who presents with joint pain, alternative explanations other than lupus-related arthritis need to be considered. Infection either as a septic joint or as osteomyelitis can cause an acute arthritis that is frequently monoarticular but can be polyarticular or chronic, especially with atypical infections such as fungal and mycobacterial in the setting of an immunocompromised patient. AVN appears to be a risk factor for septic arthritis in SLE, with a variety of
AVN, also called osteonecrosis, aseptic necrosis and ischaemic bone, was first reported to occur in SLE by Dubois and Cozen in 1960 [51]. Interestingly, this correlates with the institution of corticosteroid therapy in the 1950s and its presumed pathogenic contributions. AVN has subsequently been reported by numerous others with an incidence in lupus cohorts of 4–16% [4], [51], [52], [53] In addition to its association with SLE, AVN has a variety of other risk factors that have not necessarily
The goals of treatment for lupus arthritis include decreasing inflammation, decreasing pain, improving quality of life and minimising toxicities. Given the episodic and limited nature of arthritis flares in some lupus patients, intermittent salicylates and nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used. The prevalence of NSAID use for the treatment in SLE in one cohort was approximately 75% [69]. Randomised trials of NSAIDs in SLE are very limited and recommendations in
There are three anti-malarial agents – hydroxychloroquine, quinacrine and chloroquine – that have been used in the treatment of SLE. A variety of mechanisms have been attributed to the efficacy of anti-malarial therapy. These include alterations in the lysosome pH, which in itself has different effects, alterations in antigen presentation, a decrease in the production of cytokines such as interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and interferon-γ (IFN-γ), alterations in
Low-dose glucocorticoids have been a mainstay in the management of SLE. Randomised trials of corticosteroid therapy, specifically for the treatment of the arthritis manifestations, are not available. Their efficacy is inferred through the positive results in randomised trials of lupus nephritis in combination with clinical experience. They are most commonly used in lower doses of 10 mg (prednisone equivalent) or less for the shortest duration possible to avoid steroid complications such as
Immunosuppressive therapy is often added for refractory arthritis or steroid-sparing effects. Methotrexate, a folate antagonist, has both immunosuppressive and anti-inflammatory effects [78]. Metabolites are predominantly renally excreted so its use in lupus must be judicious. Several studies have evaluated its efficacy in the treatment of lupus arthritis. Carneiro and Sato performed a 6-month double-blind, placebo-controlled RCT of 41 patients with SLE using methotrexate at 15–20 mg weekly [79]
Patients with SLE frequently suffer from an inflammatory arthritis, which typically manifests as a polyarticular arthritis, more likely to affect small joints and with less prominent synovitis than is seen in RA. A variety of medications are effective in the treatment of lupus arthritis; however, identifying therapies that are more targeted to the joint symptoms and have fewer side effects and risks are long-term goals for lupus research. Inflammatory arthritis is present inPractice points