OBJECTIVE: To evaluate the clinical usefulness of genomic HLA typing during the first two years of established giant cell arteritis (GCA). METHODS: HLA typing was performed by PCR-SSO in 41 selected white patients with GCA confirmed by biopsy. Patient data were compared with those of a control group of 384 bone marrow donors (relative risk, p value and chi 2 test for each allele). Clinical features at onset and response to treatment over a two year period were evaluated in relation to the genetic pattern. RESULTS: DRB1*04 was significantly increased in the GCA group (frequency of 48.78% compared with 19.79% in controls, p < 0.001). The distribution of the DRB1*04 subtypes in the GCA group was similar to that in controls. No clinical or biological differences were found in association with HLA at the time of diagnosis. Over the two year follow up, nine patients presented resistance to corticosteroid treatment and eight of these (88.88%) had DRB1*04 (p < 0.001). CONCLUSIONS: GCA seems to be associated with HLA DRB1*04 (regardless of the subtype) and this association appears to be accompanied by corticosteroid resistance, suggesting that genomic typing may be useful to identify patients eligible for early alternative treatment to corticosteroid drugs.
OBJECTIVE: To evaluate the clinical usefulness of genomic HLA typing during the first two years of established giant cell arteritis (GCA). METHODS: HLA typing was performed by PCR-SSO in 41 selected white patients with GCA confirmed by biopsy. Patient data were compared with those of a control group of 384 bone marrow donors (relative risk, p value and chi 2 test for each allele). Clinical features at onset and response to treatment over a two year period were evaluated in relation to the genetic pattern. RESULTS:DRB1*04 was significantly increased in the GCA group (frequency of 48.78% compared with 19.79% in controls, p < 0.001). The distribution of the DRB1*04 subtypes in the GCA group was similar to that in controls. No clinical or biological differences were found in association with HLA at the time of diagnosis. Over the two year follow up, nine patients presented resistance to corticosteroid treatment and eight of these (88.88%) had DRB1*04 (p < 0.001). CONCLUSIONS: GCA seems to be associated with HLA DRB1*04 (regardless of the subtype) and this association appears to be accompanied by corticosteroid resistance, suggesting that genomic typing may be useful to identify patients eligible for early alternative treatment to corticosteroid drugs.
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