extensive disease. This improvement in pruritus is a clinically important finding, but needs to be supplemented with data on the overall effect of aprepitant on disease activity. This information is especially important as there is some evidence to suggest that aprepitant may have a positive effect on overall disease status given its noted anticancer properties. Furthermore, neurokinin-1 receptor (NK1R), the target of aprepitant, is broadly expressed on immune cells and mediates a variety of endogenous functions. NK1R antagonism may increase natural killer cell cytotoxicity, a mechanism previously suggested as a novel therapeutic mechanism in CTCL. Finally, in many conditions itch severity correlates with disease severity. This is especially true in conditions associated with paraneoplastic pruritus. Future studies examining the chronic use of aprepitant as an antipruritic treatment should also include end points on overall disease severity to examine for antineoplastic effects.
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