Spondyloarthritis

"SpA" redirects here. For the Italian type of company, see Società per azioni. For other uses, see SPA (disambiguation).
Spondyloarthritis
Other namesSpondyloarthropathy
Bone scintigraphy made with 99mTc demonstrating the highly enhanced tumor borders and the left elbow affected by psoriatic arthritis.
SpecialtyRheumatology Edit this on Wikidata

Spondyloarthritis (SpA), also known as spondyloarthropathy, is a collection of clinical syndromes that are connected by genetic predisposition and clinical manifestations.[1] The best-known clinical subtypes are enteropathic arthritis (EA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), and reactive arthritis (ReA).[2] Spondyloarthritis typically presents with inflammatory back pain and asymmetrical arthritis, primarily affecting the lower limbs, and enthesitis, inflammation at bone-adhering ligaments, tendons, or joint capsules.

Spondyloarthritis is caused by a combination of genetic polymorphisms and environment, with the relative contributions of genes and environment varying across different types.[3] It is associated with ileal inflammation, with an immunological connection between Crohn's disease and ankylosing spondylitis.[4] Reactive arthritis is primarily caused by gastrointestinal pathogens, genitourinary and respiratory infections, and genetic variables.[3] HLA-B27, a polymorphic form of the HLA-B molecule, is found in up to 95% of European spondylitis patients, 70% having reactive arthritis, 60% with psoriatic spondylitis, 25% with peripheral psoriatic arthritis, and 70% with spondylitis associated with inflammatory bowel disease.

The arthritogenic-peptide theory suggests that HLA-B27 displays self-peptides that resemble pathogen-derived peptides to CD8-restricted T cells. Two other theories suggest that HLA-B27's genesis may be autoinflammatory, initiating innate immune responses instead of presenting antigens. The first hypothesis suggests that HLA-B27 heavy chains without β2 microglobulin can form disulphide-linked homodimers, recognized by KIR3DL2 killer immunoglobulin-like receptors. The second hypothesis suggests that the B pocket's Cys 67 residue causes HLA-B27 heavy-chain misfolding, modifying immune cells' cytokine output and reactivity to innate immunological stimuli.[2]

Spondyloarthritis is diagnosed based on clinical factors, including inflammatory back pain, limited spinal mobility, and radiological sacroiliitis, though many patients may not have radiographic evidence of sacroiliitis for up to 10 years. Early diagnosis criteria consider HLA-B27 testing and MRI scanning advancements.[5] Spondyloarthritis is categorized into two groups based on the Assessment of SpondyloArthritis International Society (ASAS) criteria: primarily axial involvement and predominantly peripheral manifestations.[6][7]

Non-steroidal anti-inflammatory drugs (NSAIDs) should be administered first for active axial signs of spondyloarthritis. If NSAIDs are contraindicated or cause side effects, TNF blockers should be used. Traditional disease-modifying antirheumatic drugs (DMARDs) are not advised for patients without peripheral disease signs.[8]

The prevalence of ankylosing spondylitis and spondyloarthritis varies across populations. The incidence of spondyloarthritis was recorded in four investigations, with a range of 0.48/100,000 in Japan to 62.5/100,000 in Spain.[9]

  1. ^ Inman, Robert D. (2012). "The Spondyloarthropathies". Goldman's Cecil Medicine. Elsevier. pp. 1690–1697. doi:10.1016/b978-1-4377-1604-7.00273-6. ISBN 978-1-4377-1604-7.
  2. ^ a b Cite error: The named reference Spondyloarthritis Lancet was invoked but never defined (see the help page).
  3. ^ a b Cite error: The named reference Etiology and Pathogenesis was invoked but never defined (see the help page).
  4. ^ Cite error: The named reference u788 was invoked but never defined (see the help page).
  5. ^ Cite error: The named reference Spondyloarthritis Elsevier was invoked but never defined (see the help page).
  6. ^ Cite error: The named reference ASAS Axial was invoked but never defined (see the help page).
  7. ^ Cite error: The named reference ASAS peripheral was invoked but never defined (see the help page).
  8. ^ Cite error: The named reference New evidence was invoked but never defined (see the help page).
  9. ^ Cite error: The named reference Epidemiology was invoked but never defined (see the help page).