[Toward a non-empirical treatment for rheumatoid arthritis based on its molecular pathology]

Rheumatoid arthritis (RA) is a chronic, disabbling disease that affects individuals during the productive years of their lives. Modern treatment for RA includes the so called "biologic" therapy, which is based on recombinant proteins that modify the biologic processes. These agents have potent therapeutic effects and different mechanisms of action. Nevertheless, therapeutic failure still prevails. Treatment that prevents disability in RA must be started in an early manner, before the development of complications and, ideally, with a minimum possibility of therapeutic failure. As yet, there are no clinical or laboratory criteria to identify those patients with a higher probability of responding to particular types of therapy, delaying control of RA ad affecting the prevention of incapacity. Research into gene diversity through single-nucleotide polymorphisms (SNPs) by means of microarray systems, allows the detailed analysis of gene factors associated to a given disease. SNPs have been recently applied to the study of RA, where the major polymorphisms associated to RA occur primarily in genes that code for proteins related to the initiation of an immune response and/or the control of cellular activity in the immune system, in addition to genes related to tissue repair. The specific meaning of these findings is in its initial stages of research. On the other hand, proteomics relate to the analysis of protein expression profiles at multiple levels. Both types of studies will contribute to the knowledge of patterns of gene expression in RA compared to the general population, and will allow an understanding of the pathogenesis of RA. Moreover, proteomic and genomic profiles can be employed to designs probes that identify individuals with the risk of developing RA, individually predict the response to different therapeutic modalities (pharmacogenomics) and for the follow-up of the biologic response to therapy.