Abstract Introduction Vitamin B12 deficiency is typically characterized by macrocytic anemia and neuropsychiatric manifestations. In severe cases, pancytopenia, ineffective erythropoiesis, and intramedullary hemolysis can produce clinical features indistinguishable from thrombotic thrombocytopenic purpura (TTP). Early recognition is essential to avoid unnecessary plasma exchange and intensive care utilization. We present a rare case of vitamin B12-induced thrombotic microangiopathy (TMA )initially misdiagnosed and treated as TTP. Case Presentation A 38-year-old female with unknown past medical history presented with two weeks of diarrhea and progressive weakness. On arrival, she was tachycardic and tachypneic. Laboratory studies showed hemoglobin 2 g/dL, hematocrit 6.3%, WBC 14.7 × 10³/µL, and platelets 55 × 10³/µL. Serum creatinine was 1.26 mg/dL, bicarbonate 10 mmol/L, and lactic acid 25 mmol/L. HIV and hepatitis panels were negative. Peripheral smear before transfusion revealed red cell clumping with few schistocytes. She was admitted to the MICU for severe anemia and metabolic acidosis and received three units of packed red blood cells. Given the hemolytic picture with thrombocytopenia, TTP was suspected. The PLASMIC score was 5, indicating intermediate risk, and plasma exchange therapy with high-dose corticosteroids was initiated. ADAMTS13 activity later returned at 0.36, making TTP unlikely. Hemolysis labs showed LDH 4500 U/L, haptoglobin 10 mg/dL, and indirect hyperbilirubinemia. Folate was normal, but vitamin B12 was severely reduced at 68 pg/mL. Methylmalonic acid and homocysteine levels were elevated. Despite three sessions of plasma exchange, hematologic recovery was minimal until vitamin B12 supplementation was initiated. After seven doses of intramuscular vitamin B12, platelet count improved to 117 × 10³/µL. Cardiology was consulted for new left ventricular dysfunction (EF 25-30%) attributed to type II myocardial injury from severe anemia. Psychiatry evaluated acute delirium and suicidal ideation; collateral history revealed schizophrenia. The cytopenias were linked to severe vitamin B12 deficiency causing ineffective erythropoiesis and intramedullary hemolysis. Discussion Severe vitamin B12 deficiency can cause thrombotic microangiopathy through ineffective erythropoiesis and intramedullary hemolysis, leading to profound anemia and thrombocytopenia. Because TTP is a medical emergency, the two can appear identical. Elevated methylmalonic acid and homocysteine levels help confirm the diagnosis. The ADAMTS13 level of 0.36 in this case, though reduced, was not severely deficient, prompting reassessment. Prompt vitamin B12 replacement results in rapid hematologic recovery. Clinicians should maintain a high index of suspicion for vitamin B12 deficiency when TMA features create diagnostic uncertainty. This abstract is funded by: None
Sheikh et al. (Fri,) studied this question.