The question was raised again as to whether Anti-CCP positive/negative Rheumatoid disease is different. One postulation is that proteins become citrillunated (by smoking for example) and subjects with the shared epitope variants of DR4 then develop anti-CCP antibodies. The Prompt study from yesterday showed that MTX had no impact on the evolution of anti-CCP negative undifferentiated arthritis to RA, but in anti-ccp positive UA MTX significantly reduced the evolution to RA. Treatment with anti-BLys antibodies was also less effective in CCP negative RA.
Much talk about the best use of DMARDs...use early in adequate doses (dare I say aggressive doses?), monitor frequently and adjust to control disease (as in the TICORA study). Consider checking anti-CCP status in RF negative inflammatory arthrtis.
Treatment of refractory RA (ie failed MTX and one anti-TNF)
Optimise DMARD: dose to 25mg/week, change PO to SubCut, use a split dose (more on that later)
Optimise Anti-TNF: dose, frequency
Switch TNF: more useful for secondary failures (ie worked initially) than primary failures
Use another biologic: Abatacept, Rituximab.
Just a short note for now since my internet connection is about to run out of money.
PS split dose MTX: taking some in the evening and some next morning may improve bioavailability of higher doses (above 15mg) but the evidence is limited. Worth a try if all else fails though.
MJM
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