TREATMENT OF ASTHMA MIGHT HAVE DELAYED END-ORGAN DAMAGE IN THE PATIENT WITH LYMPHOCYTIC HYPEREOSINOPHILIC SYNDROME

Abstract

<h3>Introduction</h3> Hypereosinophilic syndrome (HES) is characterized by an absolute eosinophil count (AEC) > 1,500 and organ damage or dysfunction attributable to tissue eosinophilia. <h3>Case Description</h3> This 71-year-old patient with a 12-year history of asthma was treated with inhaled and variable daily doses of oral corticosteroids for four years. Without the risk factors for cardiovascular disease, he suddenly developed stroke symptoms. His brain MRI revealed multiple scattered patchy foci of acute cortical matter ischemia, and he was diagnosed with an acute cerebrovascular accident. He also had elevated troponin and underwent cardiac catheterization with stent placement to a proximal LAD and mid-LAD lesion. Four months later, he came for an allergy evaluation because of "elevated white cells" and "food allergy." However, he had an increased AEC of 3,800 and clinically irrelevant IgE to the tolerated foods. His medical record revealed that over the last four years, his AEC fluctuated between 374 and 8,730. Therefore, we initiated an evaluation for suspected HES, eosinophilic granulomatosis with polyangiitis, and, less likely, parasitoses. Molecular studies revealed a clonal population of lymphocytes with T-cell receptor gene γ and β rearrangement consistent with a diagnosis of lymphoid variant HES. Other laboratory findings are in figure 1. <h3>Discussion</h3> A common occurrence of eosinophilia in the patients with asthma might lower the index of suspicion of HES. However, this patient's very high AEC should have prompted an investigation earlier. His HES presented as multifocal ischemic brain and cardiac infarcts. This presentation was likely delayed by treating the patient's asthma with systemic corticosteroids.