Author: Dr Belinda Lai, Intern, Western Local Health District, New South Wales, Australia. DermNet NZ Editor in Chief: Adjunct A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell. May 2019.
Spondyloarthropathy refers to a group of five seronegative inflammatory rheumatic disorders that are related in disease manifestation and genetic susceptibility . The spondyloarthropathies include:
Spondyloarthropathy is also called spondyloarthritis.
Ankylosing spondylitis affects 0.1–1.4% of Caucasians. It is three times as common in males as in females. Ankylosing spondylitis has a strong familial component. About 95% of affected individuals carry the tissue antigen HLA-B27.
The exact aetiology and pathology of spondyloarthropathies are undetermined. There is clear evidence that genetic background and environmental factors trigger pro-inflammatory cytokines, and these lead to an increased susceptibility to spondyloarthropathies . There is a close link between ankylosing spondylitis and psoriasis and with Crohn disease. This link suggests that the pathogenesis of ankylosing spondylitis involves an immune reaction with the gut or the skin which may be influenced by microbial responses .
Spondyloarthropathy syndromes are characterised by axial or peripheral arthritis.
Patients may also present with:
Psoriatic arthritis is strongly associated with chronic plaque psoriasis. Psoriatic arthritis more commonly develops after psoriasis, but arthritis can precede or accompany the skin disease. Patients with psoriatic arthritis usually have a family history of psoriasis and are more likely to have nail psoriasis than patients with psoriasis that do not have psoriatic arthritis .
Skin changes include:
Enteropathic arthritis can present with:
Mucocutaneous manifestations for reactive arthritis (associated with chlamydia infection) include:
Complications of axial spondyloarthritis include reduced bone mineral density, fractures, neurological manifestations, and renal disease. Low bone mineral density is commonly seen within the first ten years of the disease. Spinal fractures can result in spinal cord injuries or spinal nerve compression.
Rarely, glomerulopathy, immunoglobulin A (IgA) nephropathy, and renal amyloidosis occur in ankylosing spondylitis .
Spondyloarthropathies are diagnosed according to the Assessment of Spondyloarthritis International Society (ASAS) Classification criteria . These criteria only apply to patients < 40 years old or those with inflammatory back pain for > 3 months. The criteria consider imaging, HLA-B27, and the features of spondyloarthropathy.
Imaging typically includes plain radiographs and magnetic resonance imaging (MRI). Sacroiliitis on plain radiography is specific for spondyloarthropathies. It may take several years before sacroiliitis is observed on imaging.
Laboratory evaluation should include full blood count, complete metabolic panel, and erythrocyte sedimentation rate or C-reactive protein. The ESR and CRP are elevated in about 50% of patients. Increased levels of CRP are a good predictor of radiographic progression and better response to tumour necrosis factor (TNF) inhibitors .
The differential diagnoses for spondyloarthropathies is based on the distribution of the affected joints.
The goal of treatment for spondyloarthropathies is to improve function, decrease pain, and decrease complications. Management should include lifestyle interventions such as an exercise program to maintain posture, strength, and range of movement. Patients should also be monitored for osteoporosis and encouraged to cease smoking.
Non-steroidal anti-inflammatory drugs (NSAIDs) are considered to be the first line treatment for axial ankylosing spondylitis. They are quite effective and reduce pain, tenderness, and stiffness in 80% of patients. Patients who do not respond to NSAIDs may benefit from anti-tumour necrosis factor (anti-TNF-alpha) therapy, such as infliximab, etanercept, or adalimumab. These can reduce the spinal and peripheral joint inflammation of ankylosing spondylitis and control extra-articular symptoms.
Disease-modifying anti-rheumatic drugs (DMARDs) include sulfasalazine and methotrexate. Intra-articular corticosteroid injections have a modest benefit for peripheral arthritis .
Treatment for psoriatic arthritis targets the joints and skin lesions. Anti-TNF-alpha therapy has radicalised the treatment for psoriatic arthritis, with significant improvement in symptoms and delay in progression of the disease. Secukinumab, an anti-IL-17A monoclonal antibody, is effective at treating psoriasis and psoriatic arthritis.
Management of reactive arthritis involves assessing and treating an active infection. Chlamydial infections should be treated with antibiotics. No evidence supports the use of antibiotics for treatment of urogenital or enteric forms of reactive arthritis. High-dose NSAIDs are also used to treat patients with reactive arthritis. Indomethacin 50–75 mg twice daily is commonly used. Persistent reactive arthritis may respond to DMARDs, such as sulfasalazine, azathioprine, or methotrexate .
Enteropathic arthritis is also treated with NSAIDs and cyclooxygenase-2 inhibitors, but these can cause flare-ups of inflammatory bowel disease. DMARDs are beneficial for gastrointestinal and joint involvement. Anti-TNF agents can be used if traditional DMARDs fail; however, there have been rare cases of inflammatory bowel diseases precipitated by etanercept. Total colectomy of the affected colon does not improve axial involvement in inflammatory bowel disease .
The progression of ankylosing spondylitis is highly variable. It may result in the fusion of sacroiliac joints and the vertebral column, also known as a ‘bamboo spine’. Patients who have frequent occurrences of iritis, hip involvement at presentation, peripheral joint involvement, and high inflammatory markers at baseline tend to have a poorer prognosis .
At least 20% of patients with psoriatic arthritis will develop severe and disabling disease. Up to 7% of patients may require joint surgery, with the most common being hip arthroplasty .
Approximately 50% of patients with reactive arthritis can expect symptoms to resolve in the first six months; 30–50% will develop chronic arthritis .
The prognosis of enteropathic arthritis is determined by the severity of the underlying bowel disease. Patients with well-controlled inflammatory bowel disease rarely develop severe enteropathic arthritis .
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