Ankylosing spondylitis laboratory findings: Difference between revisions

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{{Ankylosing spondylitis}}
{{Ankylosing spondylitis}}
{{CMG}}
{{CMG}} : {{AE}} {{MKK}}
 
==Overview==
==Overview==
[[Image:Ankylosing process.jpg|left|thumb|256px|The ankylosis process.]]
There are no specific [[diagnostic]] [[laboratory]] findings associated with [[ankylosing spondylitis]] (AS). There are certain [[Blood test|blood tests]] that can check for markers of [[inflammation]].Most of the time patients with AS their blood is tested for the [[HLA-B27]] gene, but again most people who are positive for that gene don't have [[ankylosing spondylitis]]. Other laboratory findings consistent with ankylosing spondylitis (AS) include [[Erythrocyte sedimentation rate|ESR]] and [[C-reactive protein|CRP]] levels.
There is no direct test to diagnose AS. A clinical examination and [[X-ray]] studies of the spine, which show characteristic spinal changes and [[Sacroiliac joint|sacroiliitis]], are the major diagnostic tools. A drawback of X-ray diagnosis is that signs and symptoms of AS have usually been established as long as 8-10 years prior to X-ray evident changes occurring on a plain film X-ray, which means a delay of as long as 10 years before adequate therapies can be introduced. An option for more accurate (and much earlier) diagnosis are [[Computed tomography|tomography]] and [[magnetic resonance imaging]] of the sacroiliac joints. The [[Schober's test]] is a useful clinical measure of flexion of the lumbar spine performed during examination.<ref>{{cite journal | author = Thomas E, Silman AJ, Papageorgiou AC, Macfarlane GJ, Croft PR. | title = Association between measures of spinal mobility and low back pain. An analysis of new attenders in primary care. | journal = Spine | volume = 23 | issue = 2 | pages = 343-7 | year = 1998 | id = PMID 9507623}}</ref>


==Laboratory Findings==
==Laboratory Findings<ref name="pmid15082484">{{cite journal |vauthors=Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J |title=How to diagnose axial spondyloarthritis early |journal=Ann. Rheum. Dis. |volume=63 |issue=5 |pages=535–43 |date=May 2004 |pmid=15082484 |pmc=1754994 |doi=10.1136/ard.2003.011247 |url=}}</ref><ref name="pmid12381506">{{cite journal |vauthors=Sieper J, Braun J, Rudwaleit M, Boonen A, Zink A |title=Ankylosing spondylitis: an overview |journal=Ann. Rheum. Dis. |volume=61 Suppl 3 |issue= |pages=iii8–18 |date=December 2002 |pmid=12381506 |pmc=1766729 |doi= |url=}}</ref><ref name="pmid22127957">{{cite journal |vauthors=Poddubnyy D, Haibel H, Listing J, Märker-Hermann E, Zeidler H, Braun J, Sieper J, Rudwaleit M |title=Baseline radiographic damage, elevated acute-phase reactant levels, and cigarette smoking status predict spinal radiographic progression in early axial spondylarthritis |journal=Arthritis Rheum. |volume=64 |issue=5 |pages=1388–98 |date=May 2012 |pmid=22127957 |doi=10.1002/art.33465 |url=}}</ref>==
Increase in
* There are no specific [[diagnostic]] [[laboratory]] findings associated with [[ankylosing spondylitis]](AS) and most the tests are non-specific.
*[[C-Reactive protein|C-reactive protein]] (CRP) and
* [[Human leukocyte antigen]] (HLA)-B27 is positive in most the patients, but not invariably so.<ref name="pmid27586785">{{cite journal |vauthors=de Winter JJ, van Mens LJ, van der Heijde D, Landewé R, Baeten DL |title=Prevalence of peripheral and extra-articular disease in ankylosing spondylitis versus non-radiographic axial spondyloarthritis: a meta-analysis |journal=Arthritis Res. Ther. |volume=18 |issue= |pages=196 |date=September 2016 |pmid=27586785 |pmc=5009714 |doi=10.1186/s13075-016-1093-z |url=}}</ref>
*[[Erythrocyte sedimentation rate]] (ESR).
* laboratory findings consistent with [[Ankylosing spondylitis|ankylosing spondylitis(]]AS) include [[Erythrocyte sedimentation rate|ESR]] and [[C-reactive protein|CRP]] levels.<ref name="pmid19248087">{{cite journal |vauthors=Rudwaleit M, Haibel H, Baraliakos X, Listing J, Märker-Hermann E, Zeidler H, Braun J, Sieper J |title=The early disease stage in axial spondylarthritis: results from the German Spondyloarthritis Inception Cohort |journal=Arthritis Rheum. |volume=60 |issue=3 |pages=717–27 |date=March 2009 |pmid=19248087 |doi=10.1002/art.24483 |url=}}</ref>
* Some patients with active AS are positive for [[normochromic]] [[Normocytic anemia|normocytic]] anemia.
* Some patients with active AS are found to have increased levels of bone-specific [[alkaline phosphatase]].<ref name="pmid258956962">{{cite journal |vauthors=Kang KY, Hong YS, Park SH, Ju JH |title=Increased serum alkaline phosphatase levels correlate with high disease activity and low bone mineral density in patients with axial spondyloarthritis |journal=Semin. Arthritis Rheum. |volume=45 |issue=2 |pages=202–7 |date=October 2015 |pmid=25895696 |doi=10.1016/j.semarthrit.2015.03.002 |url=}}</ref><ref name="pmid19183433">{{cite journal |vauthors=Maksymowych WP |title=What do biomarkers tell us about the pathogenesis of ankylosing spondylitis? |journal=Arthritis Res. Ther. |volume=11 |issue=1 |pages=101 |date=2009 |pmid=19183433 |pmc=2688221 |doi=10.1186/ar2565 |url=}}</ref>
* In some patients with AS serum levels of [[immunoglobulin]] A ([[Immunoglobulin A|IgA]]) are elevated.
* Elevated [[White blood cells|white blood cell]] count mainly [[Polymorphonuclear leukocyte|polymorphonuclear]] leukocytes.


==References==
==References==
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[[Category:Arthritis]]
[[Category:Autoimmune diseases]]

Latest revision as of 03:13, 30 July 2018

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Overview

There are no specific diagnostic laboratory findings associated with ankylosing spondylitis (AS). There are certain blood tests that can check for markers of inflammation.Most of the time patients with AS their blood is tested for the HLA-B27 gene, but again most people who are positive for that gene don't have ankylosing spondylitis. Other laboratory findings consistent with ankylosing spondylitis (AS) include ESR and CRP levels.

Laboratory Findings[1][2][3]

References

  1. ↑ Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J (May 2004). "How to diagnose axial spondyloarthritis early". Ann. Rheum. Dis. 63 (5): 535–43. doi:10.1136/ard.2003.011247. PMC 1754994. PMID 15082484.
  2. ↑ Sieper J, Braun J, Rudwaleit M, Boonen A, Zink A (December 2002). "Ankylosing spondylitis: an overview". Ann. Rheum. Dis. 61 Suppl 3: iii8–18. PMC 1766729. PMID 12381506.
  3. ↑ Poddubnyy D, Haibel H, Listing J, Märker-Hermann E, Zeidler H, Braun J, Sieper J, Rudwaleit M (May 2012). "Baseline radiographic damage, elevated acute-phase reactant levels, and cigarette smoking status predict spinal radiographic progression in early axial spondylarthritis". Arthritis Rheum. 64 (5): 1388–98. doi:10.1002/art.33465. PMID 22127957.
  4. ↑ de Winter JJ, van Mens LJ, van der Heijde D, Landewé R, Baeten DL (September 2016). "Prevalence of peripheral and extra-articular disease in ankylosing spondylitis versus non-radiographic axial spondyloarthritis: a meta-analysis". Arthritis Res. Ther. 18: 196. doi:10.1186/s13075-016-1093-z. PMC 5009714. PMID 27586785.
  5. ↑ Rudwaleit M, Haibel H, Baraliakos X, Listing J, Märker-Hermann E, Zeidler H, Braun J, Sieper J (March 2009). "The early disease stage in axial spondylarthritis: results from the German Spondyloarthritis Inception Cohort". Arthritis Rheum. 60 (3): 717–27. doi:10.1002/art.24483. PMID 19248087.
  6. ↑ Kang KY, Hong YS, Park SH, Ju JH (October 2015). "Increased serum alkaline phosphatase levels correlate with high disease activity and low bone mineral density in patients with axial spondyloarthritis". Semin. Arthritis Rheum. 45 (2): 202–7. doi:10.1016/j.semarthrit.2015.03.002. PMID 25895696.
  7. ↑ Maksymowych WP (2009). "What do biomarkers tell us about the pathogenesis of ankylosing spondylitis?". Arthritis Res. Ther. 11 (1): 101. doi:10.1186/ar2565. PMC 2688221. PMID 19183433.

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