Current Concepts In Treating RA | Arthritis Information

Rheumatoid arthritis (RA) affects more than two million adults in the United States.¹ In the past decade, the advent of tumor necrosis factor inhibitors for the treatment of RA has ushered in a new era of targeted biologic modalities. We have seen a shift to more aggressive therapy involving earlier treatment and the use of multiple medications in combination. Although the long-term effects of new treatment approaches are not yet fully known, early results appear favorable.
       A substantial proportion of patients with inflammatory arthritis of short duration have remission and only some patients with persistent disease will go on to develop RA.² Therefore, it is important to determine genetic, clinical, serological or radiographic markers that allow clinicians to identify patients with early disease destined for RA so they can provide appropriately targeted therapy.
       Functional alterations in cytokine regulation can predict and affect destructive disease among patients with early disease. In a genetic analysis to establish prognostic markers, Prots et al., showed that the 150V IL4R single-nucleotide polymorphism may be a candidate marker for early radiographic bone erosions in patients with RA.³ Khanna et al., showed that the TNFA-308 polymorphism is associated with significantly higher radiographic progression in a cohort of early seropositive RA patients.⁴
       Markers of inflammation or osteoclast activation can also provide information on the likelihood of joint destruction among patients with early disease. Aside from an elevated baseline erythrocyte sedimentation rate, researchers have recently shown that the osteoprotegrin/RANKL ratio is inversely related to bone destruction among patients with RA who have not been previously treated with disease modifying antirheumatic drug (DMARD) therapy.^5,6 When it comes to serological findings, antibodies to citrullinated peptides (anti-CCP) serve as specific disease markers whose appearance in the blood can predate the onset of symptoms.⁷
       The presence of anti-CCP2 antibodies during the first three years of RA diagnosis has been associated with more radiographic progression of disease and may also predict damage by bone marrow edema on MRI views of the hands of patients with early RA.^8,9 In regard to radiologic studies, ultrasound can show synovitis as well as cortical bone lesions not visible on plain films while MRI can demonstrate local areas of bone edema, which frequently progress to erosions demonstrated by plain radiographs.
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