NEW YORK (Reuters Health) - Certain interleukin (IL)-10 promoter polymorphisms are associated with the long-term response to etanercept in patients with rheumatoid arthritis (RA), German researchers report. The findings, Dr. Heiko Schotte told Reuters Health, “might in the future help to select patients that profit from etanercept treatment.”
Dr. Schotte of University Hospital Albert-Schweizer in Munster and colleagues hypothesized that genetically determined differences in IL-10 production might affect the response of RA patients to tumor necrosis factor (TNF) blocking agents such as etanercept.
To investigate, the researchers genotyped 50 patients with active RA who had been treated for up to 4 years with stable doses of etanercept as monotherapy. The results were compared with those in 189 healthy matched controls.
As they report in the April issue of Arthritis and Rheumatism, the team found no association between IL-10 microsatellite polymorphisms and susceptibility to RA. However, when responses based on European League against Rheumatism criteria were compared with polymorphisms, there was an association.
In particular, when the 25 patients with a “good” response were compared with the 17 with a moderate response and the 8 patients with no response, it was found that carriage of the R3 allele or R3-G9 haplotype was associated with a good response.
In patients with a moderate response or no response, the G13 allele and the R2-G13 haplotype predominated.
The R3 allele, the researchers note, may be associated with low IL-10 production. This, they say, has been linked to response to etanercept.
The results could help in understanding “the pathophysiology of rheumatoid arthritis under the specific condition of TNF-antagonization,” Dr. Schotte added.
Source: Ann Rheum Dis 2005;64:575-581. [ Google search on this article ]
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