Introduction:
Evans syndrome (ES), a hematological entity described by Evans and colleagues in 1951, is characterized by the presence of Coombs positive hemolytic anemia and immune thrombocytopenia, and less commonly, autoimmune neutropenia [1]. Although the exact pathophysiology of ES remains unknown, immune dysfunction with subsequent production of antibodies targeting the erythrocytes and platelets is a likely mechanism. Glucocorticoids and intravenous immunoglobulin (IVIG) have mostly been used as first-line therapy for ES. Other treatment options include immunosuppressants, blood transfusion, splenectomy, and hematopoietic stem cell transplant [2]. ES has a more variable clinical course as compared to isolated autoimmune hemolytic anemia (AIHA), with more frequent exacerbations and mortality [3]. The co-existence of tuberculosis (TB) with Evans syndrome makes therapy even more challenging.