The anti-fibrillar collagen type II (anti-CII) autoantibody is characterised by more intense but transitory inflammation initially, in contraindication to the anti-CCP autoantibody, which confers a bad prognosis with higher disease activity later on.
Anti-CarP autoantibody levels predict for joint damage, but do not correlate with disease activity and quality of life measurements.
The poor prognostic predictors of rapid progressors in RA (thus highlighting them for particular early and aggressive treatment) are:
1) Anti-CCP positivity
2) Joint erosions
3) High disease activity (DAS score)
4) Functional impairment
5) Extra-articular disease (eg vasculitis, uveitis, pneumonitis).
I would add another: inadequate response to initial appropriately aggressive treatment with steroid or targeted therapies. As seen with the anti-fibrillar CII Ab, it is predictive of early but transient high disease activity, but is an overall favorable prognosticator. So having very active inflammation at diagnostic onset is not necessarily damning. It is the persistent inadequate control which translates to functional deterioration that is more telling.