Chasing Eosinophils and Troponins in Healthy Woman: A Rare Case of Hypereosinophilic Syndrome with Pulmonary and Cardiac Involvement.

Case Presentation: A 44-year-old Nigerian woman with no medical history and recent travel to Mexico presents with cough for 4 weeks, fever, and malaise. She initially presented to urgent care with respiratory complaints, was diagnosed with pneumonia and given azithromycin. Her symptoms did not improve and she went to the ED. Vitals were notable for tachycardia, no hypoxia. Labs were significant for a WBC of 22 with 48% eosinophils and 33% PMN’s. CT PE study was negative but showed multifocal pneumonia. She was started on ceftriaxone. Her troponin was elevated on admission and peaked at 2.89. Her EKG showed no ischemic changes, TTE was normal and cardiac MRI showed late gadolinium enhancement and a small pericardial effusion. Her differential at this time remained broad. She was initially treated for community acquired pneumonia with an asthma exacerbation; however, given her travel there was concern for parasitic infection such as strongyloides, schistosoma or coccidiodes, as well as hypereosinphilic syndrome (HES) with pulmonary and cardiac involvement. A bronchoscopy BAL was performed which grew pseudomonas with 92% eosinophils. Bone marrow biopsy showed hypercellular (60-70%) marrow composed of predominantly eosinophils at all stages of maturation consistent with HES. She was started on steroids and her leukocytosis improved to 14.2 with 17% eosinophils. Strongyloides antibody was 0.16, therefore it could not be completely ruled out. Other parasitic and helminthic studies were negative.

Discussion: HES is a rare disease defined as persistent absolute eosinophil count of > 15,000 cells/uL with eosinophilia-mediated organ damage. There are 3 categories of HES: primary (clonal), secondary (reactive), or idiopathic (unknown). Primary occurs in the setting of neoplasm, secondary by parasitic infections and certain solid tumors. The patient’s travel history placed her at risk for parasitic infections and that could not be ruled out as the cause for HES. She demonstrated both pulmonary and cardiac eosinophilia mediated organ involvement and she was treated with high dose prednisone. In HES, necrotizing myocarditis occurs in 3 stages, with MRI findings occurring in stage III. Treatment for HES is high dose glucocorticosteroid in patients with extreme hypereosinophilia (HE) and life-threatening complications such as concern for HE- induced organ damage. It is important to rule out strongyloides before prednisone is given because corticosteroid treatment may cause fatal disseminated strongyloidiasis. Because strongyloides could not be ruled out in our patient, a decision was made to administer empiric ivermectin 200mcg/kg daily for 2 days concurrently with prednisone.

Conclusions: The finding of HE and hypertroponinemia necessitated an expansion of the differential for this patient. We were able to rule out other causes of eosinophilia and establish a diagnosis of HES with pulmonary and cardiac involvement. She improved clinically with eosinophil reduction following appropriate treatment with steroids.