Abstract

INTRODUCTION: Eosinophilic gastroenteritis (EGE) is a rare inflammatory disorder characterized by eosinophilic infiltration of the gastrointestinal (GI) tract. The pathogenesis remains largely unknown but several studies have suggested involvement of IL-5+ Th2 cells and cytokines IL-3, IL-5, and granulocyte macrophage-colony stimulating factor. EGE usually manifests with non-specific GI symptoms as well as, in some cases, severe iron-deficiency anemia. A secondary hypogammaglobinemia is not an established complication of EGE, but can be a consequence of iron-deficiency anemia. We present an active duty patient with EGE, found to have severe iron-deficiency anemia with low IgG level and loss of immune titer to MMR, Rubeola and Varicella. CASE DESCRIPTION/METHODS: A 25-year-old active duty soldier presented to emergency room with dyspnea and fatigue and was incidentally found to be severely anemic (Hemoglobin: 6.3g/dL, MCV: 62.7fL, and Ferritin: 2.86ng/mL) with absolute eosinophil (Abs Eo) of 1.0 × 10(9)/L. She received blood transfusion and was started on enteral iron therapy, as well as, work-up for eosinophilia to include malignancy, infection, and autoimmune/vasculitis etiologies. At 6 month follow-up, hemoglobin normalized to 15.2g/dL but eosinophilia persisted, reaching as high as 2.44 × 10(9)/L. As part of the work-up, immunoglobin was obtained which showed low IgG (328mg/dL), but normal levels of IgA, IgM, and IgE. She was also noted to have lost titer to MMR, Rubeola, and Varicella (though having had previously received all appropriate vaccinations in 2015 for military service). During primary immunodeficiency work-up, she was placed on inhaled fluticasone by pulmonology for presumed diagnosis of eosinophilic asthma (PFTs were normal). Patient clinically improved with subsequent lab showing improvement in IgG level and down-trending eosinophil counts. She was re-vaccinated and developed appropriate level of immune titers to all the vaccines. DISCUSSION: EGE is a rare inflammatory disorder of GI tract with non-specific GI symptoms. While secondary hypogammaglobinemia is not an established complication of EGE, our case raises the question of whether patients diagnosed with EoE or EGE should additionally be screened for secondary hypogammaglobinemia and/or associated loss of immune titers to vaccines.

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