Overview of Spondyloarthropathies: Difference between revisions

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Between 17 and 39 percent of patients with IBD develop rheumatic manifestations. Between two and 16 percent of IBD patients develop EnA in the axial skeleton. The prevalence of sacroiliitis in this population is between 12 and 20 percent of patients.<ref name=":7" />
Between 17 and 39 percent of patients with IBD develop rheumatic manifestations. Between two and 16 percent of IBD patients develop EnA in the axial skeleton. The prevalence of sacroiliitis in this population is between 12 and 20 percent of patients.<ref name=":7" />
{{#ev:youtube|6rCvEdhw9qQ}}<ref>Kevin Mangum. 100P - Enteropathic Arthropathy. Available from: https://www.youtube.com/watch?v=6rCvEdhw9qQ [last accessed 8/11/2020]</ref>


Like other spondyloarthropathies, there is an association with the HLA-B27 gene, ranging from 3.9 to 18.9 percent, but the pathogenesis is not fully understood.<ref name=":7" /> However, it has been observed that joint inflammation occurs in patients who are genetically predisposed and who have bacterial gut infections. This, therefore, suggests that there is some relationship between inflammation of the gut mucosa and arthritis.<ref name=":7" />
Like other spondyloarthropathies, there is an association with the HLA-B27 gene, ranging from 3.9 to 18.9 percent, but the pathogenesis is not fully understood.<ref name=":7" /> However, it has been observed that joint inflammation occurs in patients who are genetically predisposed and who have bacterial gut infections. This, therefore, suggests that there is some relationship between inflammation of the gut mucosa and arthritis.<ref name=":7" />

Revision as of 11:47, 8 November 2020

Introduction[edit | edit source]

Spondyloarthropathy (or Spondyloarthritis) is an umbrella term for a group of inflammatory rheumatic diseases.[1][2] Spondyloarthropathies are progressive and painful. They often involve the axial skeleton (i.e. the spine and the sacroiliac joints), but can also affect the peripheral skeleton.[1] They are associated with enthesitis (inflammation of the site where tendons / ligaments insert into bone[3]) and dactylitis (i.e. diffuse swelling of the fingers[4]). Other areas affected include the heart, eyes, lungs, skin, gut and genitourinary tract.[2]

There are five types of Spondyloarthritis:[1]

  • Ankylosing Spondylitis (also known as Bechterew's disease or Marie-Strumpell disease)
  • Psoriatic Arthritis
  • Reactive Arthritis (formerly called Reiter's syndrome)
  • Enteropathic Arthritis
  • Undifferentiated spondyloarthropathy

Epidemiology / Aetiology[edit | edit source]

Symptoms associated with spondyloarthropathy typically start before the age of 45.[1] They affect men slightly more than women with a 1,1:1 ratio and men are younger at diagnosis than women.[5] Unlike other rheumatic diseases like Rheumatoid Arthritis, spondyloarthropathies are seronegative for rheumatoid factor.[6]

The etiology and pathogenesis of spondyloarthropathies have not been determined, but the research suggests that there are various environmental triggers, as well as a significant genetic component.[2]

In particular, spondyloarthropathies have been found to share genetic links with the HLA-B27 gene.[1][7] 90 percent of patients presenting with axial spondyloarthritis have this gene. However, it is important to note that having this gene is not, in itself, diagnostic of spondyloarthropathy as five to ten percent of patients who are HLA-B27+ do not go on to develop these conditions.[1]

[8]

Characteristics / Clinical Presentation[edit | edit source]

The symptoms of spondyloarthropathies are varied and as many individuals present with back pain, it is important to be able to distinguish between mechanical and inflammatory back pain. The specific features of each type of spondyloarthropathy are discussed below.

Ankylosing Spondylitis[edit | edit source]

Ankylosing spondylitis (AS) is a seronegative spondyloarthritis of the spine and pelvis. AS affects the axial skeleton, as well as the peripheral joints, digits and entheses.[9]

It affects 0.1 to 1.4% of the population and is predominantly seen in males with a 3.4:1 (male:female) ratio.[10] The onset of symptoms usually occur in patients aged in their 20s and rarely after the age of 45.[10] Less than 5% of cases will develop symptoms after the age of 45.[10] AS is more prevalent within Europe (mean 23.8 per 10,000) and Asia (mean 16.7 per 10,000) than within Latin America (mean 10.2 per 10,000).[10]

The most common features of AS are chronic back pain and progressive stiffness.[9] Patients will often present with impaired spinal movement, abnormal posture, buttock and hip pain, peripheral arthritis, enthesitis and dactylitis.[9] The most common extra-articular manifestation of AS is inflammatory bowel disease, acute anterior uveitis and psoriasis.[9]

AS has been linked to an increased risk of cardiovascular disease, potentially due to the systemic inflammation associated with this condition. Because AS results in diminished chest wall expansion and decreased spinal mobility, it can lead to a restrictive pulmonary pattern in patients with AS. These individuals are also more prone to vertebral fragility fractures, atlantoaxial subluxation, spinal cord injury and, occasionally, cauda equina syndrome.[9]

[11]

As with all spondyloarthropathies, the aetiology of AS is not fully understood, but research indicates that genetic background, microbial infection, endocrine abnormalities and immune reactions may be significant.[12] As discussed above, there is a correlation between AS and the HLA-B27 gene.[1][9][12]

For more information on AS, please click here.

Psoriatic Arthritis[edit | edit source]

Psoriatic Arthritis (PsA) is a chronic, immune-mediated inflammatory joint disease that is associated with psoriasis.[13] Individuals present with joint and entheses inflammation in both the axial skeleton and peripheral joints. It affects multiple organs, including the skin and is associated with increased risk of mortality from cardiovascular disease.[13][14]

There is a wide variation in annual incidence of psoriatic arthritis, ranging from 0.1 to 23.1 cases per 100,000. Prevalence rates also vary between countries, as does the mean age at diagnosis (40.7 to 52.0 years).[15]

Hallmark features of PsA are:[15]

  • The presence of psoriasis
  • Inflammatory arthritis
  • Absence of serological tests for rheumatoid arthritis

Between 60 and 70 percent of patients will develop psoriasis prior to PsA. However, in 15 to 20 percent of patients, symptoms of arthritis develop first. For some individuals (15 to 20 percent), psoriasis and arthritis will begin within a year of each other.[15]

For more information on PsA, please click here.

[16]

Enteropathic Arthritis[edit | edit source]

Enteropathic Arthritis (EnA) is a spondyloarthropathy that occurs in patients who also have inflammatory bowel disease (IBD) and / or other gastrointestinal disease, such as ulcerative colitis and Crohn’s disease.[17]

There is no gold standard test for EnA, so diagnosis generally relies on medical history and physical examination.[17] Typically, patients who have IBD and then go on to develop inflammatory back pain and / or synovitis (predominantly in the lower limbs) are diagnosed as having spondyloarthropathy.[17] Women are more likely to have peripheral joint involvement, whereas men are more likely to experience axial skeleton symptoms.[17]

Between 17 and 39 percent of patients with IBD develop rheumatic manifestations. Between two and 16 percent of IBD patients develop EnA in the axial skeleton. The prevalence of sacroiliitis in this population is between 12 and 20 percent of patients.[17]

Like other spondyloarthropathies, there is an association with the HLA-B27 gene, ranging from 3.9 to 18.9 percent, but the pathogenesis is not fully understood.[17] However, it has been observed that joint inflammation occurs in patients who are genetically predisposed and who have bacterial gut infections. This, therefore, suggests that there is some relationship between inflammation of the gut mucosa and arthritis.[17]

For more information on EnA, please click here.

Reactive Arthritis[edit | edit source]

Reactive arthritis (ReA) is a seronegative spondyloarthritis, which occurs after an extra-articular infection, typically of the gastrointestinal or genitourinary tract.[18][19] It is associated with inflammatory back pain, oligoarthritis (“a chronic inflammatory arthritis of unknown origin that begins before the age of 16 and lasts for at least 6 weeks”[20]), and extra-articular symptoms.[19] It tends to develop after at least one and at most three to six weeks after a urogenital or gastrointestinal infection.[19][21]

A classic triad of symptoms have been identified, which are:[22]

  • Arthritis
  • Urethritis
  • Conjunctivitis

Dermatological manifestations (such as keratoderma blennorrhagicum, circinate balanitis, ulcerative vulvitis, nail changes, and oral lesions) can occur,[22] and it can also affect the heart and eyes, although symptom severity is varied.[19]

ReA is more common in men[22] and typically affects young adults.[19] Its exact pathophysiology is not yet understood, but it appears likely that infectious and immune factors are involved.[22] Again, those affected are more likely to carry the HLA-B27 gene.[19]

[23]

Clinical symptoms can be distinguished from septic arthritis. Key signs of septic arthritis are:[19]

  • Fever
  • Systemic signs of infection
  • Monoarthritis

For more information, please click here.

Undifferentiated Spondyloarthropathy[edit | edit source]

The diagnosis undifferentiated spondyloarthropathy is used in cases where individuals exhibit features of spondyloarthropathy, but they do not fit into any of the conditions discussed above.[24]

Summary[edit | edit source]

Spondyloarthropathy is an umbrella term that encompasses five inflammatory rheumatic diseases. These conditions can impact multiple areas of the body, as well as other organs.

While the specific aetiology remains unknown, current research suggests a strong genetic component, as well as specific environmental triggers.

References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Martey C. Overview of Spondyloarthropathies Course. Physioplus, 2020.
  2. ↑ 2.0 2.1 2.2 Ehrenfeld M, Infection and spondyloarthropathies. In: Shoenfeld Y, Agmon-Levin N, Rose NR editors. Infection and autoimmunity. Elsevier B.V. 2015. p745-57.
  3. ↑ Schett G, Lories R, D'Agostino M, Elewaut D, Krikham B, Soriano ER et al. Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol. 2017; 13: 731–741.
  4. ↑ McGonagle D, Tan AL, Watad A, Helliwell P. Pathophysiology, assessment and treatment of psoriatic dactylitis. Nat Rev Rheumatol. 2019; 15: 113–122.
  5. ↑ Alzate M, Vargas F, Ramirez F, et alSAT0414 Differences in clinical presentation by gender in colombian patients with spondyloarthropathies. Annals of the Rheumatic Diseases 2017;76(2): 928.
  6. ↑ Navallas M, Ares J, Beltrán B, Lisbona MP, Maymó J, Solano A. Sacroiliitis associated with axial spondyloarthropathy: new concepts and latest trends. Radiographics. 2013 Jul-Aug;33(4):933-56.
  7. ↑ Braun, J., Sieper, J. Early diagnosis of spondyloarthritis. Nat Rev Rheumatol. 2006; 2: 536-45.
  8. ↑ USME Spondyloarthropathy Available from: https://www.youtube.com/watch?v=1Fgi7whO7NQ (last accessed 8.11.2020)
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 Wenker KJ, Quint JM. Ankylosing Spondylitis. [Updated 2020 Jul 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470173/
  10. ↑ 10.0 10.1 10.2 10.3 Dean LE, Jones GT, MacDonald AG, Downham C, Sturrock RD, Macfarlane GJ. Global prevalence of ankylosing spondylitis. Rheumatology (Oxford). 2014; 53(4): 650-7.
  11. ↑ Zero To Finals. Ankylosing Spondylitis: Visual Explanation for Students. Available from https://www.youtube.com/watch?v=a23A3nAaO0E [last accessed: 8/11/2020]
  12. ↑ 12.0 12.1 Watad A, Bridgewood C, Russell T, Marzo-Ortega H, Cuthbert R, McGonagle D. The Early Phases of Ankylosing Spondylitis: Emerging Insights From Clinical and Basic Science. Front Immunol. 2018. 16;9: 2668-75.
  13. ↑ 13.0 13.1 Veale DJ, Fearon U. The pathogenesis of psoriatic arthritis. Lancet. 2018; 391(10136): 2273-2284.
  14. ↑ Van den Bosch F, Coates L. Clinical management of psoriatic arthritis. Lancet. 2018; 391(10136): 2285-2294.
  15. ↑ 15.0 15.1 15.2 Kerschbaumer A, Fenzl KH, Erlacher L, Aletaha D. An overview of psoriatic arthritis - epidemiology, clinical features, pathophysiology and novel treatment targets. Wien Klin Wochenschr. 2016; 128(21-22): 791-795.
  16. ↑ Zero To Finals. Psoriatic Arthritis. Available from: https://www.youtube.com/watch?v=fQCU7rQbovk [last accessed 8/11/2020]
  17. ↑ 17.0 17.1 17.2 17.3 17.4 17.5 17.6 Peluso R, Di Minno MN, Iervolino S, et al. Enteropathic spondyloarthritis: from diagnosis to treatment. Clin Dev Immunol. 2013; 2013: 631408.
  18. ↑ Courcoul A, Brinster A, Decullier E, Larbre JP, Piperno M, Pradat E et al. A bicentre retrospective study of features and outcomes of patients with reactive arthritis. Joint Bone Spine. 2018; 85(2): 201-205.
  19. ↑ 19.0 19.1 19.2 19.3 19.4 19.5 19.6 Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmun Rev. 2014; 13(4-5): 546-9. 
  20. ↑ Petty RE, Cassidy JT. Oligoarthritis. In: Cassidy JT, Petty RE, Laxer RM, Lindsley CB editors. Textbook of Pediatric Rheumatology. Philadelphia: Saunders, 2011. p262-71.
  21. ↑ Ono K, Kishimoto M, Shimasaki T, Uchida H, Kurai D, Deshpande GA et al. Reactive arthritis after COVID-19 infection. RMD Open 2020; 6: e001350.
  22. ↑ 22.0 22.1 22.2 22.3 Wu IB, Schwartz RA. Reiter's syndrome: the classic triad and more. J Am Acad Dermatol. 2008; 59(1): 113-21.
  23. ↑ Zero To Finals. Reactive Arthritis: Visual Explanation for Students. Available from: https://www.youtube.com/watch?v=snjGL2x6Eus [last accessed 8/11/2020]
  24. ↑ Chou CT, Lin KC, Wei JCC, Tsai WC, Ho HH, Hwang CM et al. Study of undifferentiated spondyloarthropathy among first-degree relatives of ankylosing spondylitis probands. Rheumatology. 2005; 44(5): 662-5.
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