Early treatment of recent-onset rheumatoid arthritis patients impairs the effect of HLA class II antigents on the progression of joint destruction
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KeywordsRheumatoid Arthritis Patient Joint Damage Joint Destruction Sharp Score DMARD Treatment
HLA class II antigens influence disease progression as measured by extend of joint destruction in RA. This effect is supposed to be caused by formation of autoreactive T-cells after presentation of (auto)antigens in the context of HLA class II. To investigate whether in patients with recent-onset RA early DMARD treatment could prevent the involvement of autoreactive T cells, we analyzed the association of HLA class II and joint damage in 110 patients with early RA that were treated according to the pyramid strategy with DMARDs and 98 patients with early RA that were promptly treated with DMARDs at two weeks after the first visit.
DNA isolation, DRB1 typing and subtyping and DQB1 typing were performed. Extend of joint damage was measured by the modified Sharp score of the radiographs of hand and feet.
In the early treatment group the increase in the median Sharp score in the SE+ group was 1.0 to 5.0 in contrast to 1.0 to 3.0 in the SE- group (P > 0.5). However, in the pyramid group the increase in joint damage was 0.0 to 16.0 in the SE+ group in contrast to 0.0 to 5.0 in the SE- group (P < 0.005). On the other hand, in the RF+ group of the early treatment group the increase in joint damage was 1.0 to 6.5 in contrast to 1.0 to 1.0 in the RF- group (P < 0.005). In the pyramid group the increase in joint damage was 0.5 to 17.0 in the RF+ in contrast to 0.0 to 3.0 in the RF- group (P < 0.005).
This study shows that early anti-rheumatic drug treatment abolishes the effect of HLA class II alleles on extend of joint damage in early RA patients.