Page 59 - THE EVOLUTION OF EARLY ARTHRITIS AND CARDIOVASCULAR RISK Samina A. Turk

HOW DOES ESTABLISHED RHEUMATOID ARTHRITIS DEVELOP
UA, PAST AND PRESENT
The term “UA” suggests that the condition in the patient concerned is in a stage of transition from an unspecified type of arthritis toward either RA, another arthritis- 3 associated diagnosis, or spontaneous remission. The incidence of UA ranges from 41
(in Finland) to 149 (in Sweden) per 100.000 adults, and 13-54% of these patients will eventually develop RA, according to the 1987 ACR criteria(61). In the past, the transition
from UA to RA was equivalent to fulfilling the 1987 ACR criteria for RA(62) after a phase
with arthritis in which these criteria were not yet fulfilled. In practice, this mainly
applied to the progression from oligoarthritis to polyarthritis and/or the development
of erosive disease, as other elements of the criteria set such as RF or nodules do not
often appear in early arthritis, if not present at the first presentation(63). Therefore, the transition from UA to RA could be viewed as the development of a more severe arthritis
in inadequately controlled early RA, which made this an outcome of interest. The main
predictor of the transition was the ACPA status of the patient(64).
The 2010 ACR/EULAR criteria for RA aim to increase sensitivity in early disease(65), which is mainly achieved by a focus on small joint involvement and serology. Thus, a patient with one swollen finger joint of 6 weeks duration and a high-titer ACPA will already classify as RA. The consequence is that the subgroup of UA in early arthritis patients is strongly reduced, and it is now composed mainly of seronegative (oligo-) arthritis. On average, these “2010 UA” patients will have a milder and more heterogeneous disease than “1987 UA” patients(66). Although both the 1987 and 2010 criteria for RA are classification and not diagnostic criteria, the 2010 criteria were specifically developed for use in early disease, and they reflect the trend among clinicians to diagnose RA earlier and even in the presence of only a few involved joints.
Just as was the case with 1987 UA patients, a part of 2010 UA patients will remit and a part will go on to have a severe disease course. In a recent study of three early arthritis cohorts, the Leiden prediction rule (developed to predict 1987 RA in 1987 UA patients) and the ACPA status failed to predict the development of 2010 RA in 2010 UA patients(67). New biomarkers are needed that can help to detect the 2010 UA patients at high risk of disease progression, so that they may be considered for more aggressive therapy than the remaining UA patients, for whom symptomatic treatment may be sufficient. An example is anti-CarP antibodies, which were shown to predict radiographic damage in early ACPA-negative RA patients(68). Next to blood-based biomarkers, imaging modalities such as ultrasound or magnetic resonance imaging (MRI) may prove to be useful in this respect(69, 70).
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