Rationale of using different biological therapies in rheumatoid arthritis

The cure of diseases or at least an abatement of symptoms are the core aims of therapeutic medicine, and we might soon witness the transition from today's abatement to tomorrow's cure with regard to the quality of disease remission in the field of rheumatic conditions, with rheumatoid arthritis (RA) as one of the most frequent entities. At present, achieving complete remission is the ultimate aim, at least for patients with recently diagnosed, early RA. The reduction of clinical disease activity below a disease activity score of 2.6 when evaluating the 28 relevant joints (DAS28), as well as the exclusion of still remaining clinically silent synovial inflammation, are considered to be the principal goals of current rheumatologic treatment concepts [1]. In cases with longer histories and at later stages of disease, however, the cutoff level for individually acceptable residual disease activity might have to be further defined together with the patient, and on the basis of this, individual stage -adapted medication evaluated continuously in close agreement with the patient [1,2].Past pharmacologic options used to induce remission from RA included chrysotherapy, which became the first established 'gold' standard. In 1928, Jacques Forestier had already started to use gold salts therapeutically in France, assuming an infectious factor in RA, which was in the tradition of Robert Koch's evaluation of gold compounds against pure cultures of Mycobacterium tuberculosis [3]. Gold salts, however, were just one drug amongst a growing number of long-acting, remission-inducing agents showing only slow action in decreasing the inflammatory activity of RA. Owing to this mode of action, they have been termed 'second-line' medication, also known as disease-modifying anti-rheumatic drugs (DMARDs); apart from gold salts, these also include medications such as azathioprine, chloroquine and hydroxychloroquine (HQ), cyclosporin A (CsA), cyclophosphamide, lefluno-mide (LEF), methotrexate (MT