Johns Hopkins Arthritis Center
Antibodies against citrullinated proteins have emerged as powerful diagnostic and prognostic tools in RA that may contribute to the initiation phases of the disease. The enzymes that catalyze the citrullination process, known as peptidyl argenine deiminases (or PADs), may also be involved in the initiation and propagation steps of the RA disease process. Additionally, autoimmunity to these catalysts may identify a subset of RA patients with unique disease phenotypes.
Anti-B cell therapy with rituximab has been shown to be safe and beneficial for RA treatment. Rituximab is approved and marketed for the treatment of RA in patients who have failed other therapies. Ocrelizumab, a fully human monoclonal antibody against CD20, may have less immunogenicity and less complement activation than rituximab which, theoretically, may reduce [...]
On July 29, 2008, the Arthritis Advisory Board of the FDA reviewed the new Biologics License Application for tocilizumab, which will be marketed under the trade name Actemra, as presented by the manufacturer, Hoffmann-La Roche. After reviewing the efficacy and safety data from multiple Phase III studies, the Board recommended the approval of the biologic [...]
Type II collagen is abundant in the joint and is a major target of immune-mediated damage in RA. As suggested in studies of experimental animals, induction of immune tolerance at the level of the cartilage may be a way of reducing the signs and symptoms of RA and prevent joint destruction. However, whether oral administration of Type II collagen is an efficacious treatment for humans with established active RA has not been established.
Increasing the dose of infliximab and, in some cases, adalimumab can result in improved efficacy in RA patients with inadequate responses to initial dosing. However, whether increasing the dose of etanercept can also result in clinical improvement has not been studied.
