Abstract
Most individuals with vitamin B12 deficiency present with anemia, fatigue, and neurologic disturbances such as paresthesia and loss of sensory function if chronic. However, in severe states, it may manifest as hemolytic anemia, thrombocytopenia, schistocytosis, elevated lactate dehydrogenase, and low reticulocyte production. This phenomenon is known as pseudo-thrombotic microangiopathy (TMA), and is most commonly due to pernicious anemia. The overlap in clinical presentation with primary TMA creates a challenge in the diagnosis and management of pseudo-TMA. Primary TMA, particularly thrombotic thrombocytopenic purpura, is emergently managed with plasma exchange and may require admission to an intensive care unit due to high risk of mortality. In contrast, pseudo-TMA does not respond to plasma exchange and instead is treated with vitamin B12 supplementation. Patients with this atypical presentation of B12 deficiency may receive unnecessary, costly, and potentially harmful therapy. We present the case of a patient with pseudo-TMA in the setting of pernicious anemia.