Case Presentation: A 10-year-old male from China with prior history of a presumed parasitic infection was admitted for abdominal pain, vomiting, and diarrhea. Ten days prior to admission, he traveled to the United States and developed intermittent abdominal pain associated with non-bloody diarrhea and non-bloody, non-bilious emesis. Review of systems was negative for fever, sick contacts, or introduction of new foods into his diet. Past medical history was significant for mitral regurgitation and a prior hospitalization 1 year ago for similar symptoms with a peripheral eosinophilia. He was diagnosed with eosinophilic enteritis and improved with steroids and praziquantel. On admission, he was afebrile with stable vital signs. Exam was normal, except for a 3/6 systolic murmur and a soft abdomen with mild tenderness to palpation in the bilateral lower quadrants, no guarding or rebound tenderness, or hepatosplenomegaly. CMP was only notable for an albumin of 3.6. CBC revealed an elevated WBC count (14) with a peripheral eosinophilia (34.7% eosinophils). Abdominal XR and Chest XR were normal. ECHO showed moderate mitral valve regurgitation with normal function. An extensive infectious work-up was negative. An EGD/Colonoscopy obtained showed diffuse eosinophilic enteritis. His peripheral leukocytosis and eosinophilia continued to worsen (maximum WBC count of 22.7 with 54.8% eosinophils). He developed fever and chest pain with an elevated troponin level (3.27) and BNP (2510). Repeat ECHO showed low left ventricular systolic functioning and EKG showed diffuse ST segment changes, concerning for eosinophilic myocarditis. Due to worsening peripheral eosinophilia and multi-organ involvement (enteritis and myocarditis), there was a high suspicion for a hypereosinophilia syndrome. Patient was transferred to the ICU for closer monitoring, bone marrow biopsy/aspirate with genetic testing, and initiation of IV methylprednisolone. His clinical symptoms, peripheral eosinophilia, and cardiac markers significantly improved with treatment further supporting a diagnosis of hypereosinophilia syndrome, specifically idiopathic hypereosinophilia syndrome given negative genetic testing
Discussion: In this case, the patient presented with non-specific gastrointestinal symptoms and a peripheral eosinophilia. Due to his symptoms and past history of presumed parasitic infection, initially, the differential diagnosis focused on infectious causes for his hypereosinophilia. However, his worsening peripheral eosinophilia in the setting of end-organ damage significantly increased the index of suspicion for a hypereosinophilia syndrome. As this case demonstrates, it is important to include hypereosinophilia syndromes in your differential for severe hypereosinophilia once secondary causes have been eliminated. If appropriately identified, treatment can lead to dramatic improvement in clinical symptoms and mitigate end-organ damage.
Conclusions: Hypereosinophilia syndromes can present with non-specific symptoms and should be included in the differential diagnosis of severe hypereosinophilia, especially when associated with end-organ damage.