Ankylosing Spondylitis Research Today is a free monthly online journal that collates and summarizes the latest research about Ankylosing Spondylitis, including details on diagnosis, treatment, symptoms, causes. | ||||||||
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Distribution of HLA-B27 subtypes in ankylosing spondylitis in an Israeli population.Alaez C, Gazit E, Ibarrola B, Yaron M, Livneh A, Avishai O, Gorodezky C Department of Immunology and Immunogenetics, Instituto de Diagnóstico y Referencia Epidemiológicos, InDRE, SSA, Mexico. BACKGROUND: The aim of this study was to investigate the contribution of the B27 subtypes to ankylosing spondylitis (AS) expression in a group of Jewish patients from Israel and to compare their distribution with that found in Mexican Mestizo patients. Several HLA-B27 alleles have been clearly associated with AS. Among them, B( *)2705 and B( *)2702 are involved in susceptibility in different populations worldwide. The aim of this study was to investigate the associated subtypes in Israel and to compare the results with Mexican Mestizos, who have Semitic genes as part of their ancestry. METHODS: This is a case/control study that included a group of 24 HLA-B27+ Israeli patients with AS and 51 B27+ healthy subjects, most of them Ashkenazi Jews. The B27 subtypes were characterized using a PCR-SSP method. RESULTS: Only B( *)2702 and B( *)2705 alleles were present in AS patients. However, their allele frequency was not significantly different from that found in the control group, probably because of the small sample size: B( *)2702 (patients 62.5% vs. controls 41.2%, OR = 2.31) and B( *)2705 (patients 37.5% vs. controls 50.9%). Two additional alleles were present only in the controls in low frequency: B( *)2707(5.9%) and B( *)2701(1.9%). It is clear that the major susceptibility allele in Ashkenazi Jews from Israel is B( *)2702. CONCLUSIONS: The only allele conferring risk to AS expression in Israeli Jews was B( *)2702, as was previously described in Mexican Mestizos. Populations of Mediterranean ancestry, such as Latin Americans, should be further explored to understand the contribution of ethnicity to the etiopathogenesis of AS. Published 9 April 2007 in Arch Med Res, 38(4): 452-5.
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