IGHE and Alzheimer disease: Although the mechanism of action in play for AD is elusive, a possible alteration in tissue-bound IgE or alterations in the levels of auto-reactive IgE have been suggested and recently demonstrated.79, 80, 81 Nevertheless, the removal of circulating inflammatory mediators, such as eosinophil, eosinophil cationic protein, soluble interleukin-2 receptor and soluble E-selectin, with non-IgE specific extracorporeal apheresis cannot be ruled out as a possible mechanism of clinical efficacy.82