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We read with great interest the article by Sakurai and Hashizume¹ that reported a rare case involving the deterioration of rheumatoid arthritis (RA) after the administration of troglitazone, since peroxisome proliferator–activated receptors (PPARs) are a current topic in medicine. We would like to add a few comments in regard to this interesting case report. The authors stated that "the in vivo antiinflammatory [sic] effect of troglitazone is yet to be elucidated." Indeed, synthetic thiazolidinediones, as well as the natural ligand 15-deoxy-^12,14-prostaglandin J₂, are expected to have anti-inflammatory properties, because PPAR- reduces monocyte secretion of interleukin 1, interleukin 6, and tumor necrosis factor .² PPAR- activation actually inhibits the activation of nuclear factor B, activation protein 1, and signal transducer and activator of transcription activities, 3 important factors that regulate cytokine gene expression by binding to their promoters.³ However, the potential weakness of studies that suggest the correlation . . . [Full Text of this Article]

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