Case Presentation:
A 73 year-old female presented with significant lethargy and orthostasis with progressive generalized weakness over one week. The patient related that she had experienced increasing fatigue over one year, but that it had acutely worsened in the last two weeks. Upon admission, her vital signs were blood pressure 114/47 mm Hg, heart rate 77 bpm, temperature 97.8 F, and respiratory rate 18 bpm. Her exam was notable for conjunctival pallor, scleral icterus, and normal neurological exam. Her laboratory evaluation was significant for hemoglobin 3.9 g/dL, MCV 122, LDH 4095 U/L, undetectable haptoglobin, and unconjugated hyperbilirubinemia. There was initially concern for an autoimmune hemolytic anemia, DIC, or TTP. She was given one dose of corticosteroids. Further laboratory findings revealed an inappropriately low reticulocyte index, a negative direct antiglobulin test, very low serum B12 of 30 (normal range 210-1033), elevated methylmalonic acid and homocysteine and normal serum folate. A peripheral smear confirmed significant megaloblastic anemia without evidence for DIC/TTP. Given the findings of severe B12 deficiency, further evaluation revealed elevated parietal cell IgG Ab level. The patient improved significantly with transfusion and vitamin B12 replacement. The patient’s hemoglobin, functional status and exercise tolerance markedly improved over the course of her admission. She was followed by her primary physician and our hematology service for treatment of her significant B12 deficiency due to pernicious anemia and three months post discharge, her hemoglobin had normalized and all of her symptoms had resolved.
Discussion:
Pernicious anemia is the most common cause of symptomatic vitamin B12 deficiency in the developed world. Patients most often present with insidious symptoms of anemia with pallor and lethargy. Further manifestations can include paresthesias, ataxia, and glossitis. It is a disease that is most often identified as an outpatient, so we felt it was important to bring to the attention of hospitalists. Hemolysis in B12 deficiency related megaloblastic anemia is classically ascribed to intramedullary destruction of erythrocytes and ineffective erythropoiesis. This unique case illustrates that B12 deficiency should be in the differential in patients with severe anemia with significant hemolysis. It also highlights the importance of a thorough evaluation of new onset, severely symptomatic anemia and the connection between hemolysis and severe B12 deficiency as the inciting etiology.
Conclusions:
Severe vitamin B12 deficiency from pernicious anemia can manifest as a severe, symptomatic anemia with features of hemolysis. Workup for both anemia and hemolysis by inpatient physicians must include this disease process in the differential in the appropriate clinical setting.