Overview of Spondyloarthropathies: Difference between revisions
No edit summary |
m (Protected "Overview of Spondyloarthropathies" ([Edit=Allow only autoconfirmed users] (indefinite) [Move=Allow only autoconfirmed users] (indefinite))) |
(No difference)
| |
Revision as of 10:45, 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 / Etiology[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]
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.[8]
It affects 0.1 to 1.4% of the population and is predominantly seen in males with a 3.4:1 (male:female) ratio.[9] The onset of symptoms usually occur in patients aged in their 20s and rarely after the age of 45.[9] Less than 5% of cases will develop symptoms after the age of 45.[9] 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).[9]
The most common features of AS are chronic back pain and progressive stiffness.[8] Patients will often present with impaired spinal movement, abnormal posture, buttock and hip pain, peripheral arthritis, enthesitis and dactylitis.[8] The most common extra-articular manifestation of AS is inflammatory bowel disease, acute anterior uveitis and psoriasis.[8]
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.[8]
As with all spondyloarthropathies, the etiology of AS is not fully understood, but research indicates that genetic background, microbial infection, endocrine abnormalities and immune reactions may be significant.[10] As discussed above, there is a correlation between AS and the HLA-B27 gene.[1][8][10]
For more information on AS, please click here.
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Martey C. Overview of Spondyloarthropathies Course. Physioplus, 2020.
- ↑ 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.
- ↑ 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.
- ↑ McGonagle D, Tan AL, Watad A, Helliwell P. Pathophysiology, assessment and treatment of psoriatic dactylitis. Nat Rev Rheumatol. 2019; 15: 113–122.
- ↑ 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.
- ↑ 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.
- ↑ Braun, J., Sieper, J. Early diagnosis of spondyloarthritis. Nat Rev Rheumatol. 2006; 2: 536-45.
- ↑ 8.0 8.1 8.2 8.3 8.4 8.5 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/
- ↑ 9.0 9.1 9.2 9.3 Dean LE, Jones GT, MacDonald AG, Downham C, Sturrock RD, Macfarlane GJ. Global prevalence of ankylosing spondylitis. Rheumatology (Oxford). 2014; 53(4): 650-7.
- ↑ 10.0 10.1 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.
