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Despite the introduction of multiple biological agents for the treatment of rheumatoid arthritis (RA), methotrexate (MTX) remains the initial drug of choice.1 Response to MTX therapy is highly heterogeneous between individuals. An extensive body of work illustrates the complexity of MTX response architecture, which includes genetic polymorphisms, environmental factors and gene-gene interactions.2 Among environmental contributors, elevated body mass index (BMI) has emerged as an important predictor of MTX toxicity.3 Using data from the Treatment of Aggressive Rheumatoid Arthritis (TEAR) trial,4 we present first evidence linking the risk of MTX-associated toxicity to interactions between genotype and BMI.
The TEAR trial, described in previous publications,4 compared two strategies (early intensive …
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