PROLONGED BLOOD HYPEREOSINOPHILIA AND EOSINOPHILIC ENTEROCOLITIS FROM PINWORM INFECTION ASSOCIATED WITH IGA AND IGE DEFICIENCY

Abstract

<h3>Introduction</h3> Pinworm (<i>Enterobius vermicularis</i>) infection is generally considered a benign infection without systemic symptoms. However, severe infections can cause gastrointestinal inflammation, blood eosinophilia and systemic symptoms. What factors contribute to severe disease remains unclear. We present a case of pinworm infection causing prolonged blood hypereosinophilia and eosinophilic enterocolitis in a patient with severe combined IgA and IgE deficiency. <h3>Case Description</h3> A 16-year-old, non-atopic female presented at age 10 with intermittent low-grade fevers, abdominal pain and blood eosinophilia (AEC 3100 cells/mcL). Etiology was undetermined. As her abdominal pain continued, she was diagnosed with IBS; her blood hypereosinophilia persisted and remained unexplained. At age 15, she developed recurrent episodes of abdominal pain, non-bloody watery diarrhea and intermittent emesis. Evaluation revealed severe blood eosinophilia (AEC 6200 cells/mcL), elevated fecal calprotectin (95 mcg/gm) and gastrointestinal (esophagus, stomach, small and large intestine) eosinophilic inflammation. Direct endoscopic visualization, stool and serology testing for parasites were negative. Immunologic evaluation revealed mildly decreased IgG (621 mg/dL), undetectable IgE, low IgA (14.5 mg/dL) and normal IgM. Eosinophilia etiology remained undetermined; she was diagnosed with hypereosinophilic syndrome and treated with mepolizumab (anti–IL-5), which improved her blood eosinophilia but not her symptoms. Repeat EGD/colonoscopy (after 6 months) showed improved gastrointestinal eosinophilia but was notable for direct visualization of pinworms. Mepolizumab was discontinued. Albendazole completely resolved her symptoms; blood eosinophilia and IgG normalized, but IgA and IgE remained undetectable. <h3>Discussion</h3> Pinworms can cause persistent gastrointestinal disease and severe blood hypereosinophilia. We postulate that mucosal immunodeficiency secondary to IgA and IgE deficiency contributed to this presentation.