Pseudo-Thrombotic Microangiopathy Secondary to Vitamin B12 Deficiency

Author:

Morrissey Dylan1,Sun Yuheng1,Koilpillai Sarina1,Kropf Jacqueline1,Carlan Steve J.2ORCID

Affiliation:

1. Department of Internal Medicine, Orlando Regional Healthcare, Orlando, Florida, USA

2. Division of Academic Affairs and Research, Orlando Regional Healthcare, Orlando, Florida, USA

Abstract

Background. Clinical B12 deficiency with hematological or neurological manifestations is rare. An unusual manifestation of B12 deficiency is pseudo-thrombotic microangiopathy (TMA), which is characterized by hemolytic anemia, thrombocytopenia, and schistocytosis and only occurs in 2.5% of those with B12 deficiency. Pseudo-TMA is misdiagnosed as thrombotic thrombocytopenic purpura (TTP) in 40% of cases, resulting in misguided treatment including plasmapheresis. Case. A 44-year-old Hispanic presented with 3 weeks of progressively worsening non-radiating chest pain, fatigue, and shortness of breath (SOB). Laboratory findings revealed severe pancytopenia and macrocytosis with a hemoglobin of 5.4 g/dL, mean corpuscular volume of 116.3 fL, and vitamin B12 low at 149 pg/mL. She was diagnosed with pseudo-TMA and after starting 1000 micrograms of parenteral vitamin B12 injections daily and discontinuing plasmapheresis and steroid administration, she improved. Conclusion. Failure to recognize pseudo-TMA often results in unnecessary treatment with plasmapheresis and delays appropriate treatment with vitamin B12 supplementation. It is therefore extremely important to consider pseudo-TMA as a differential diagnosis in patients that present with hemolytic anemia, thrombocytopenia, and schistocytosis.

Publisher

Hindawi Limited

Subject

General Medicine

Reference6 articles.

1. Vitamin B12 deficiency

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3. Kyaw Zin Thein, and Thein Hlaing Oo. Vitamin B12 deficiency-related pseudo-thrombotic microangiopathy might be misdiagnosed and treated with plasma product therapy: review of the literature and analysis of the reported cases;A. M. Tun;Blood,2017

4. Neurologic and neurodevelopmental phenotypes in young children with early-treated combined methylmalonic acidemia and homocystinuria, cobalamin C type

5. Et Tu, B12? Cobalamin Deficiency Masquerading As Pseudo-Thrombotic Microangiopathy

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