SP0004 How to Assess Disease Activity and Severity in Clinical Practice

Psoriatic Arthritis (PsA) is a complex multisystem disease with involvement of synovial structures, entheseal sites, spine, and skin and nails all common features. The extended clinical phenotype has recently received some attention with obesity, hypertension, Type 2 Diabetes Mellitus, hypercholesterolemia and metabolic syndrome all found more frequently in PsA as compared to controls. An excess of cardiovascular-related events including early mortality is a likely consequence. Radiographic change is also heterogeneous with features including erosive disease and osteolysis and also new bone formation, sacroiliitis and ankylosis. Disease activity measures in PsA have either focused on joint or skin disease or have been borrowed from rheumatoid arthritis. The Psoriatic Arthritis Response Criteria (PsARC) was developed as a specific PsA response measure but the measure is dichotomous and poorly discriminates responders from placebo. More recently, a number of composite disease activity measures have been proposed. These measures are designed to capture disease activity across all of the involved domains; as not all domains are active in all individuals with PsA and as there may be a differential treatment response, ideally it should also be possible to access disease activity and response in individual domains as well. The individual composite measures and their relative performance in clinical trial data to date will be presented and discussed. Measuring disease severity may well relate to disease activity but this is yet to be clearly demonstrated. There would be little argument with the statement that patients with the arthritis mutilans phenotype have severe disease but there are many patients with polyarticular disease and high inflammatory markers who do not develop this severe phenotype. Severe disease whether it is defined on the basis of radiographic change, severe skin/nail disease, some of the cardiovascular risk factors such as presence of the metabolic syndrome or even some composite score requires further study in order to identify as early as possible risk factors which predict its development. Some recent results based on analysis of detailed clinical and genetic data will be presented. If risk factors are modifiable or if early treatment intervention for patients with potentially severe disease can bring about a change in outcome, then some progress for PsA patients will have been made. Disclosure of Interest O. Fitzgerald Grant/research support from: Pfizer, Abbott, BMS, Roche, Merck