HLA-B alleles and complotypes in Mexican patients with seronegative spondyloarthropathies.

Vargas‐Alarcón, Gilberto; Garcia, A. Sanchez; Bahena, Susana; Melín-Aldana, Héctor; Andrade, Felipe; Ibañez-De-Kasep, Graciela; Alcocer‐Varela, Jorge; Alarcón‐Segovia, Donato; Granados, Julio

doi:10.1136/ard.53.11.755

Cited by 23 publications

(9 citation statements)

References 28 publications

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“…In contrast, we could not confirm the association between SpA or AS with HLA-DR8 and B39 reported in previous studies. 15 16 Differences between these studies may be due to the number of patients studied, case selection, and tissue typing techniques. In this study the inclusion of a cohort of patients seen by a single group of investigators and the use of DNA based genotyping methods certainly reduced selection bias and the rate of false positive and negative results.…”

Section: Discussionmentioning

confidence: 99%

Effect of HLA-B and HLA-DR genes on susceptibility to and severity of spondyloarthropathies in Mexican patients

Vargas‐Alarcón

Londoño²,

Hernández-Pacheco³

et al. 2002

Annals of the Rheumatic Diseases

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Objective: To investigate the role of HLA-B and HLA-DR genes as contributors to genetic susceptibility and clinical expression of the spondyloarthropathies (SpA) , OR=28.7), HLA-DR1 (pC=0.045, OR=2.77), and HLA-B15 (p=0.034, pC=NS, OR=2.04) alleles in the whole group were found. HLA-B27 strength of association (OR) was 41.4 in AS; 20.9 in undifferentiated SpA; 27.2 in reactive arthritis. HLA-DR1 and HLA-B15 were increased in undifferentiated SpA (pC=0.045, OR=2.98 and p=0.004, pC=NS, OR=2.75). By analysing 58 HLA-B27 negative patients it was found that HLA-B15 and HLA-DR1 associations with SpA were independent of HLA-B27; increased frequencies of HLA-B15 were found in the whole SpA group and in patients with undifferentiated SpA (pC=0.03, OR=3.09 and pC<0.01, OR=3.77) and of HLA-DR1 in the latter (p=0.04, pC=NS, OR=3.15). HLA-B27 positive patients were younger than HLA-B27 negative patients at onset (p=0.03), but HLA-DR1 positive patients were older than HLA-DR1 negative patients (p=0.03). Bath indices for disease activity and functioning were higher in HLA-B27 positive patients (p=0.006 and p=0.004 v HLA-B27 negative patients). In contrast, neither HLA-DR1 nor HLA-B15 influenced these indices. Conclusion: Apart from HLA-B27, there is a significant association of HLA-DR1 and HLA-B15 with SpA in Mexicans which is independent of B27. HLA-B27 is associated with younger age at onset and increased disease severity and HLA-DR1 with older age at onset. The strength of HLA-B15, HLA-B27, and HLA-DR1 associations varied in different forms of SpA.T he spondyloarthropathies (SpA) are a heterogeneous group of diseases characterised by axial as well as peripheral enthesitis and arthritis and less commonly by a range of extra-articular manifestations. SpA are strongly linked to genetic factors and in some patients to infections with arthritogenic bacteria. Their presentation and clinical course seem, additionally, influenced by ethnicity, age at onset, and sex.

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Section: Discussionmentioning

confidence: 99%

Effect of HLA-B and HLA-DR genes on susceptibility to and severity of spondyloarthropathies in Mexican patients

Vargas‐Alarcón

Londoño²,

Hernández-Pacheco³

et al. 2002

Annals of the Rheumatic Diseases

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“…13 This association was subsequently confirmed in 284 UK patients with AS,14 as well as in HLA-B27-negative Taiwanese patients with AS15 and in African American patients with AS (Zhang et al , unpublished data). However, it was not seen in Mexican Mestizos with SpA 16. Other MHC alleles have also been implicated, but definitive associations with these have been confounded by linkage to HLA-B27.…”

Section: Other Genes Implicated In Susceptibility To Asmentioning

confidence: 95%

The genetic basis of spondyloarthritis

Reveille

2011

Annals of the Rheumatic Diseases

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Modern technological innovations have advanced our understanding of the genetic basis of spondyloarthritis. In ankylosing spondylitis (AS), where the major histocompatibility complex (MHC) accounts for nearly half of the predisposition, most comes from HLA-B27, for which 65 subtypes are now recognised, although other genes are also at work including HLA-B60 (B*40:01). Other genes have been identified, including those involved in peptide editing for loading onto class I MHC molecules (ERAP1) and cytokine genes such as interleukin 1A (IL-1A) and those involved in the Th17 network (IL-23R, an association seen primarily in Caucasians) and others. In acute anterior uveitis, these associations are also seen as well as a region on chromosome 9p and genes whose confirmation is under way. Psoriasis and psoriatic arthritis fall into this disease spectrum, with the largest region of susceptibility coming from the MHC (most likely HLA-C, ie, C*06:02 although additional influences are also being implicated), and most of the other genetic susceptibility coming from genes involved in cytokine production, specifically genes in the Th17 pathway (IL-12B, IL-23A and IL-23R, the latter, like in AS, not seen in Asians), genes in the nuclear factor κB pathway (TNFAIP3 and TNIP1) and genes in the Th2 pathway (IL-4 and IL-13). Given that more than half of patients with AS have evidence on colonoscopy of at least occult inflammatory bowel disease (IBD), it is not surprising that shared genetic influences are operative. In IBD, genes important in the innate immune response (NOD2), autophagy (ATG6L1) and regulation of the IL-23 pathway (IL-23R) play a role in disease susceptibility.

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“…Both alleles were strongly increased in HLA-B27 negative patients (Wei, et al, 2004). Although all this replications confirming the relationship between HLA-B60 and AS, the same was not seen in Mexican Mestizos where, instead, HLA-B49 was identified as significantly increased in patients with AS (Vargas-Alarcón, et al, 1994).…”

Section: Introductionmentioning

confidence: 50%