Because the eosinophils produce end-organ damage through their activation, regardless of the cause of eosinophilia,75 the primary aim of hypereosinophilia management is to reduce the number of eosinophils. The secondary, though no less important, goal is to reduce or correct the already incurred damage. The treatment selected is dictated by the status of the disease at diagnosis and identification of the cause of hypereosinophilia, and consists of nonspecific measures as well as treatment tailored to patients with a particular subcategory of HES.

End-organ damage does not always correlate with the degree of eosinophilia75,87; therefore, assessment of successful therapy should not be limited to monitor ing eosinophil counts, but should also involve regular evaluation of organ status and function (e.g., echocardiograms every 6 months to assess the presence and extent of cardiac disease). The same approach applies to reassessment of the original diagnosis because the evolution of the disease (e.g., clonal evolution in HES) may require timely changes in the management strategy.

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