title: Personalized medicine in rheumatoid arthritis: is the glass half full or half empty?
abstract: The care of patients with rheumatoid arthritis (RA) has been revolutionized since the 1990s. Strict monitoring and disease control based on measurement of signs and symptoms towards a target of low disease activity have improved outcome of patients enormously. As a result of treatment strategies based upon individualized measurement of disease activity, the clinical view of RA has changed from a destructive autoimmune disease (with a median joint damage of >10 Sharp units per year) to a condition in which significant damage can be prevented in the majority of patients. Moreover, a large number of targeted therapies (tumour necrosis factor, IL6, CD80/CD86 and CD20 inhibitors) have become available to better treat the underlying disease process. However, identification of the underlying pathways that drive the disease process in an individual patient has been relatively unsuccessful, implying that no predictive factors have been identified to guide the choice of a specific treatment. Distinct subsets of RA patients have been identified, based on the presence or absence of anticitrullinated protein antibodies (ACPAs). These two subsets are associated with different environmental and genetic risk factors, histology and disease outcome (a more destructive disease course with more persistent joint inflammation is observed when ACPAs are present). Therefore, it is recommended that treatment should be guided towards a more consistently low level of disease activity in the presence of ACPAs than in the absence of the antibodies.
authors.affiliation: Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: T W J
authors.initials: TWJ
authors.lastname: Huizinga
mesh_terms: D000465:Algorithms; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000628:therapy*; D001323:Autoantibodies / Q000097:blood*; D018122:B7-1 Antigen / Q000037:antagonists & inhibitors; D051940:B7-2 Antigen / Q000037:antagonists & inhibitors; D002956:Citrulline / Q000276:immunology; D019317:Evidence-Based Medicine; D006801:Humans; D000069285:Infliximab; D057285:Precision Medicine; D012307:Risk Factors; D000069283:Rituximab; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D000093242:Interleukin-6 Inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D018501:Antirheumatic Agents; D001323:Autoantibodies; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D002956:Citrulline; D000069285:Infliximab; D000069283:Rituximab; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors
keywords: arthritis; autoantibodies; autoimmune diseases; rheumatoid; treat to target; treatment strategies