The 2009–10 National Health and Nutritional Examination Survey (NHANES) screened 6,684 persons (ages 20–69), and 5,106 were interviewed using a tool specifically designed to survey U.S. adults for the presence of spondyloarthritis.10 It was found that nearly 20% of the U.S. population has chronic low back pain at any given time, and the prevalence of inflammatory low back pain (IBP) was close to 6%. The overall age-adjusted prevalence of axSpA was 0.9% to 1.4% using the Amor and European Spondyloarthropathy Study Group criteria.10 The ASAS classification criteria were not used in the NHANES study because the criteria were not ready when the NHANES study rolled out.
When compared with the recent estimates of the prevalence of rheumatoid arthritis (RA) being 0.6 to 1%, these new NHANES data suggest that axSpA may be at least as prevalent as RA in the U.S. population. However, these numbers are not reflected in a typical U.S. rheumatologist’s office, and most rheumatologists do not see as many axSpA patients as RA patients in their practice. This observation may be a reflection of the referral patterns. In contrast to the RA patients, axSpA patients are probably not referred to rheumatologists and are seen by their primary care providers or chiropractors, or could be evaluated by the orthopedic surgeons and neurosurgeons in spine centers for back pain. Clearly, there is an unmet need for early identification and assessment of these patients because appropriate medical treatment can substantially improve quality of life and avoid unnecessary surgical interventions.
Several studies have shown that the disease burden in nr-axSpA patients, measured by such validated instruments as SF-36 questionnaire or Bath AS disease activity index, is comparable to that of AS.11 This observation combined with the prevalence of axSpA in the U.S. population depicts the true burden of this disease on society.
Genetic Markers
Identification of new genetic markers can inform us about the pathophysiology of axSpA.
More than 90% of Caucasian AS patients are known to be positive for HLA-B27, a major disease-susceptibility gene that contributes 40% of the population-attributable risk for AS in Caucasians. Because it’s a major histocompatibility (MHC) class I molecule involved in antigen presentation, it was originally thought to be presenting an arthritogenic peptide. Failure of finding such a peptide led to alternate theories of how the HLA-B27 molecule could be important in the AS pathogenesis. It’s known the molecule tends to misfold (causing an inflammatory unfolded protein response or UPR) and can form covalent heavy chain homodimers on the cell surface that could be recognized by natural killer cells. More recently, it has been proposed that the HLA-B27 can modulate the human microbiome to create a proinflammatory milieu and development of the disease.12
