%0 Journal Article
%T Applying science in practice: the optimization of biological therapy in rheumatoid arthritis
%A Sofia Ramiro
%A Pedro Machado
%A Jasvinder A Singh
%A Robert B Landew¨¦
%A Jos¨¦ Ant¨®nio P da Silva
%J Arthritis Research & Therapy
%D 2010
%I BioMed Central
%R 10.1186/ar3149
%X The development of specific biological therapies has resulted in a remarkable improvement in the treatment of rheumatoid arthritis (RA) and also in the under-standing of its complex pathogenesis. We better recognize the multitude of cells and biological pathways involved in the disease process. We have also become more aware of the individual variability in disease features and in patterns of response to therapy. A large array of new treatment opportunities is currently under development and soon will be available as new biological agents. While enjoying these fruits of research, rheumatologists face the challenge of defining the best therapeutic plan for patients who have failed classical disease-modifying antirheumatic drugs (DMARDs).It is certainly desirable that our patients feel better and have improved function and acute-phase reactants as measured by response criteria, but the remaining inflammatory activity (status) seems decisive: 'It is good to feel better but it is better to feel good' [1]. Aletaha and colleagues [2] have demonstrated, in a pooled analysis based on data from several clinical trials in RA involving anti-tumor necrosis factor (anti-TNF), that within the ACR50 (American College of Rheumatology 50% improvement criteria) and ACR70 responder groups, the most important determinant of progression is the final disease state and not the relative degree of improvement. In fact, functional ability was best and radiographic progression was lowest in patients who had attained disease remission at 1 year compared with those who had attained only low or moderate disease activity. Further-more, among patients attaining the same disease activity category, physical function and radiographic progression did not differ significantly by the level of response. Even with low disease activity, damage progresses and only sustained remission is capable of abrogating progression of joint destruction [3]. Moreover, optimal disease control is associated with less work
%U http://arthritis-research.com/content/12/6/220