Spondyloarthropathy

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.


What is a spondyloarthropathy?

Spondyloarthropathy refers to a group of five seronegative inflammatory rheumatic disorders that are related in disease manifestation and genetic susceptibility [1]. The spondyloarthropathies include:

Spondyloarthropathy is also called spondyloarthritis.

Who gets spondyloarthropathy?

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 prevalence of psoriatic arthritis and reactive arthritis is around 2%. These conditions are less frequently associated with HLA-B27 [2].

What causes spondyloarthropathy?

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 [2]. 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 [3].

What are the clinical features of spondyloarthropathy?

Spondyloarthropathy syndromes are characterised by axial or peripheral arthritis.

  • Patients generally complain of inflammatory back pain in the spine or sacroiliac joints.
  • The onset of back pain is usually before the age of 45 years [2].
  • Peripheral arthritis can affect small and large joints in an asymmetrical pattern.

Patients may also present with:

  • Enthesitis (tenderness at where the tendons and ligaments attach to the bone and heel pain)
  • Tenosynovitis (inflammation and swelling around a tendon)
  • Dactylitis (swelling of the entire digit — the ‘sausage-digit’)
  • Extra-articular manifestations (such as skin rash, inflammatory bowel disease, and uveitis)
  • An immunogenetic association with the HLA-B27 antigen [4,5].

What are the skin conditions associated with spondyloarthropathy?

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 [6].

Skin changes include:

  • Erythematous plaques with a silvery-white scale
  • Nail disease (oil spots, pitting, crumbling)
  • Sterile pustules.
Psoriasis in a patient with ankylosing spondylitis

Enteropathic arthritis can present with:

Mucocutaneous manifestations for reactive arthritis (associated with chlamydia infection) include:

  • Oral ulcers
  • Keratoderma blennorrhagicum (a painless papulosquamous eruption on the palms or soles)
  • Circinate balanitis (vesicles or shallow ulcerations on the glans penis)
  • Nail manifestations with pitting and onycholysis or subungual keratosis [1,5].

What are the complications of spondyloarthropathy?

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 [7].

How is spondyloarthropathy diagnosed?

Spondyloarthropathies are diagnosed according to the Assessment of Spondyloarthritis International Society (ASAS) Classification criteria [8]. 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 [2].

What is the differential diagnosis for spondyloarthropathy?

The differential diagnoses for spondyloarthropathies is based on the distribution of the affected joints.

Axial disease

  • Mechanical back pain — this is usually brief and with a history of a specific injury.
  • Fibromyalgia and myalgia — there is a lack of imaging changes and a minimal response to anti-inflammatory treatment.
  • Vertebral compression fracture — this occurs in patients with low bone mass due to osteoporosis or previous trauma.
  • Osteitis condensans ilii — this is a radiological finding that occurs in multiparous women and involves sclerosis on the iliac part of the sacroiliac joint.
  • Familial Mediterranean fever — patients can develop back pain, peripheral arthritis, and sacroiliitis on imaging. They can be distinguished clinically through their family history of familial Mediterranean fever [2].

Peripheral joint disease

  • Rheumatoid arthritissymmetrical and polyarticular arthritis with radiographic changes, with positive rheumatoid factor and anti-citrullinated peptide antibodies (anti-CCP).
  • Osteoarthritis — symptoms worsen with activity.
  • Behcet syndromeasymmetrical, non-erosive arthritis that is most often described in descendents of residents living along the ancient silk road from eastern Asia to the Mediterranean.
  • Crystalline arthropathy (gout) — typically monoarticular and intensely inflammatory arthritis affecting the lower peripheries.
  • Sarcoidosisacute polyarthritis that usually involves the soft tissue around the joints (periarthritis) in conjunction with erythema nodosum and acute uveitis [7].

What is the treatment for spondyloarthropathy?

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 [9].

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 [9].

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 [5].

What is the outcome for spondyloarthropathy?

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 [10].

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 [11].

Approximately 50% of patients with reactive arthritis can expect symptoms to resolve in the first six months; 30–50% will develop chronic arthritis [12].

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 [5].

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References

  1. Goldman L, Schafer AI. Goldman-Cecil Medicine, 25th edition. ed. 2 volumes (xl, 2722, I108 pages). 2016.
  2. David T Yu MvT, MD, PhD. Overview of the clinical manifestations and classification of spondyloarthritis. UptoDate, Waltham, MA, 19th April 2019; 2018. Available from: https://www.uptodate.com/contents/overview-of-the-clinical-manifestations-and-classification-of-spondyloarthritis
  3. Khan MA. Ankylosing Spondylitis. Cary, United States: Oxford University Press USA - OSO; 2009.
  4. Ehrenfeld M. Spondyloarthropathies. Best Pract Res Clin Rheumatol 2012; 26: 135-45. PubMed
  5. Duba AS, Matthew SD. The Seronegative Spondyloarthropathies. Prim Care 2018; 45: 271–87. PubMed
  6. Habif TP. Clinical dermatology: a color guide to diagnosis and therapy. Fourth edition. ed. xv. 2003.
  7. Yu DT vTA. Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults: UptoDate; 2019. Available from: https://www.uptodate.com/contents/clinical-manifestations-of-axial-spondyloarthritis-ankylosing-spondylitis-and-nonradiographic-axial-spondyloarthritis-in-adults [accessed 15th May, 2019]
  8. Sieper J, Rudwaleit M, Baraliakos X, Brandt J, Braun J, Burgos-Vargas R, et al. The Assessment of SpondyloArthritis international Society (ASAS) handbook: a guide to assess spondyloarthritis. Ann Rheumatic Diseases 2009; 68 (Suppl 2): ii1–44. PubMed
  9. Jameson JL. Harrison's principles of Internal Medicine. Twentieth edition / ed. New York: McGraw-Hill Education; 2018. p. 2 volumes (xli, 3528, I-214 pages).
  10. Chan A GJ. Ankylosing spondylitis [PDF]. London: BMJ publishing group; 2018 [cited 2019]. Available from: https://bestpractice.bmj.com.acs.hcn.com.au/topics/en-gb/366/pdf/366.pdf. [login required].
  11. CJ M. Psoriatic arthritis. London: BMJ publishing group; 2018 [cited 2019]. Available from: https://bestpractice.bmj.com.acs.hcn.com.au/topics/en-gb/524/pdf/524.pdf. [login required].
  12. Carter J. Reactive arthritis London: BMJ publishing group; 2018 [cited 2019]. Available from: https://bestpractice.bmj.com.acs.hcn.com.au/topics/en-gb/597/pdf/597.pdf. [accessed April 27, 2019, login required].

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