Epidemiology

HLA-B27 is present in about 90% of patients who have AS.[18] The prevalence of HLA-B27 varies among ethnic communities in the US, with 7.5% of non-Hispanic white, 4.6% of Mexican-American, and 1.1% of non-Hispanic black people being HLA-B27 positive.[19] HLA-B27 contribution to the total genetic risk for ankylosing spondylitis (AS) is, however, relatively modest (approximately 20%).[20][21]

Global prevalence of AS ranges from 9 to 30 people per 10,000 in the general population.[22] The mean AS prevalence per 10,000 people (from 36 eligible studies) has been estimated as 23.8 in Europe, 16.7 in Asia, 31.9 in North America, and 10.2 in Latin America. Additional estimates, weighted by study size, were calculated as 18.6, 18.0, and 12.2 for Europe, Asia, and Latin America, respectively.[23] Survey data (2009-2010) suggest an overall age-adjusted prevalence of definite and probable spondylarthritis of 0.9% in the US.[24]

Low prevalence rates of AS have been reported in Japan and Greece.[25][26] Prevalence rates of 0.37%, 0.3%, and 0.86% have been reported in Italy, France, and Germany, respectively.[27][28][29]

Incidence rates vary between 0.4 per 100,000 in Iceland to 15 per 100,000 in Canada.[30] In the US, an annual incidence rate of 7.3 per 100,000 person-years has been reported.[31]

AS commonly presents in the second decade of life.[32] Men are more frequently affected than women (2.5:1).[33][34][35] Early use of magnetic resonance imaging has resulted in increased detection of AS, and reduced male-to-female prevalence (1.21 prevalence ratio) has been reported in one study.[36]

There is a delay in diagnosis of about 8 years between symptom-onset and diagnosis, often leading to worse clinical outcomes.[16][37] Juvenile-onset AS has greater peripheral joint involvement and is associated with a worse clinical outcome.[16][37] Approximately 9% to 21% of AS cases in white populations have a juvenile onset.[16]

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