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Steinke JW et al. – The LT receptor and synthase promoters have STAT6–binding sites that are engaged by IL–4–induced nuclear extracts and inhibited by aspirin. Assuming that normal monocytes behave like monocytes from patients with aspirin–exacerbated respiratory disease, inhibition of IL–4–STAT6 might explain a mechanism in aspirin desensitization daily treatment, resulting in downregulation of production and responsiveness to cysteinyl leukotrienes. This biologic activity of aspirin likely reflects COX inhibition because it was shared with ketorolac but not sodium salicylate.

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