All Itching Is Not Benign; A Case of Refractory Hypereosinophilic Syndrome Treated with Off Label CD52 Inhibitor-Alemtuzumab

INTRODUCTION Usually attributed to allergies or parasites (Seifert et. al Medline 2008) eosinophila is often overlooked. However hypereosinophilia (absolute eosinophil count >1.5 X 109/L on two separate exams one month apart or with pathologic confirmation) can have serious manifestations. When hypereosinophilia is associated with eosinophil-mediated organ damage or dysfunction, a hypereosinophilic syndrome (HES) exists. With an unpredictable course, eosinophilic infiltration commonly affects the skin (eczema), lung (dyspnea), & GIT (gastritis). However life-threatening damage to the CVS (myocarditis) or the CNS may occur. Clinically HES is subdivided into: myeloid variants (M-HES), T lymphocytic variants (L-HES), Familial HES, Idiopathic HES, Organ-restricted, and specific/defined syndromes associated with hypereosinophilia (Roufosse et. al Respiration 2016). Treatment is based upon symptoms and the molecular presence of Fip1-like1-platelet-derived growth factor receptor alpha. If present, patients are initially treated with imatinib mesylate, while those with other types are given a trial of steroids (Cools et. al N Engl J Med 2003). Regrettably complete remissions are rare and long term corticosteroid uses are infamous. Corticosteroid-refractory HES can be fatal with a reported 10 year survival of