Common Immune Markers in Ankylosing Spondylitis
The most clinically relevant immune markers in ankylosing spondylitis are HLA-B27 (positive in 74-89% of patients), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), though none of these should be used alone to rule out the disease. 1
HLA-B27: The Primary Genetic Marker
HLA-B27 is the strongest immune marker associated with ankylosing spondylitis, present in 74% to 89% of patients with axial spondyloarthritis. 1 However, this marker must be interpreted carefully:
HLA-B27 should function as a screening parameter rather than a definitive diagnostic test, with only 30-40% of patients with chronic back pain and positive HLA-B27 ultimately receiving an AS diagnosis. 2, 3
Approximately 10% of AS cases are HLA-B27 negative, meaning a negative test cannot exclude the diagnosis. 3
The test only needs to be performed once in a patient's lifetime using molecular methods that detect the HLA-B27 genotype directly. 3
HLA-B27 positivity increases the likelihood of peripheral spondyloarthritis, but should be combined with clinical criteria for referral decisions. 1, 2
Inflammatory Markers: CRP and ESR
C-reactive protein and erythrocyte sedimentation rate are the standard inflammatory markers monitored in AS, though they have significant limitations:
Spondyloarthritis should NOT be ruled out based solely on normal CRP or ESR values, as these can be normal even in active disease. 1
CRP and ESR should be monitored regularly alongside validated AS disease activity measures to assess treatment response and disease progression. 1
These markers provide additional information when combined with MRI findings for monitoring disease activity in axial spondyloarthritis. 1
Critical Clinical Pitfall
The single most important pitfall is ruling out spondyloarthritis based on negative laboratory results alone. 1 The diagnosis cannot be excluded based on:
- Negative HLA-B27 testing
- Normal C-reactive protein levels
- Normal erythrocyte sedimentation rate
All three markers must be interpreted within the clinical context of inflammatory back pain characteristics, imaging findings, and extra-articular manifestations. 1, 2