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Genetic Variants and Therapeutic Response to Anti–TNF-α Agents in Juvenile Idiopathic Arthritis

J uvenile idiopathic arthritis (JIA) is an heterogeneous rheumato- logic condition that affects children and adolescents with onset before 16 years of age. The disease is characterized by persistent joint inflammation that, if not adequately treated, can lead to in-creasing disability and serious impairment in the quality of life. In the last decades, the introduction of tumor necrosis factor α (TNF- α ) blocking agents has considerably improved the outcome of patients affected by JIA. 1 However, approximately a third of children have been described as nonresponder to biologic drugs, especially those with the polyarticular and the systemic onset sub-types. The pathophysiologic mechanism underlying these failures is still a matter of research. Among the proposed hypotheses, drug immunogenicity and/or issues related to bioavailability, pharma- cokinetics, and pharmacodynamics are the most corroborated. 2 Some demographic and clinical factors such as sex, age at onset, disease subtype, and the length of time between symptom onset and either diagnosis or treatment were identified as putative pre- dictors of response, but, alone, they are not sufficient to reliably guide clinical decision-making. 3 To date, the treatment selection continues to rely on a “ trial-and-error ” approach, trying different therapies until a drug that induces low disease activity or remission is identified. Consequently, in the recent years, most scientific ef-forts have involved development of biomarkers able to predict therapeutic inefficacy or substantial adverse effects with the ul-timate result of the optimization of patient outcomes. 3 In this context, pharmacogenomics helps to identify and characterize the genetic contribution to interindividual variability in drug response. Promising genetic markers include variants at a single po- sition,