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Salvarani et al recently studied 39 patients with giant cell arteritis (GCA) and found no association with HLA-DRB1*04.1 In contrast, previous immunogenetic studies did show an association between HLA-DRB1*04 and GCA.2 3Rauzy et al, also, reported a significant increase in DRB1*04 frequency in GCA. HLA-DRB1*04 was present in 20 of their 41 patients with GCA (49%) compared with a prevalence of 20% in the control group.4
Likewise, in a series of 53 patients with GCA from north west Spain, we found a significant increase in DRB1*04 frequency (44%v 26% in the controls).5Although Rauzy did not find a correlation between HLA markers and the initial severity of the vasculitis, there are several similarities between their results and ours. Those authors described a relation between HLA-DRB1*04 and corticosteroid resistance. In our series HLA-DRB1*04 was particularly pronounced in those patients with severe visual complications.5 Both higher corticosteroid requirement and severe ischaemic complications imply a worse outcome of the GCA. This supports the idea put forward by Rauzyet al that HLA-DRB1*04 in GCA may be a genetic marker of severity for this form of vasculitis.
In contrast, although Combe et al described an increased frequency of DRB1*04 in their series of 42 patients with GCA, they did not find a significant relation between markers of disease severity and activity of GCA and HLA-DRB1 genes.6These discrepancies may be related to the different ethnic backgrounds of the groups investigated. The importance of HLA-DRB1*04 in the development of more severe GCA needs to be confirmed by further studies of a greater number of patients. An examination of the importance of other class II and non-class II molecules as markers of severity in GCA is also required.
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