Vitamin B12 deficiency and metabolism-mediated thrombotic microangiopathy (MM-TMA)

Waleed Sabry, Mohamed Elemary, Thierry Burnouf, Jerard Seghatchian, Hadi Goubran

研究成果: 雜誌貢獻回顧型文獻

摘要

Thrombotic microangiopathies (TMA) are characterized by microangiopathic hemolytic anemia, thrombocytopenia and organ damage resulting from mechanical factors, accumulation of the ultra-large von Willebrand factor multimers or complement-mediated abnormalities. Severe acquired vitamin B12 (Cobalamin - Cbl) deficiency or congenital defective Cbl metabolism could lead to a picture that mimics TMA. The later has been termed metabolism-mediated TMA (MM- TMA). This confusing picture is mediated partly by the large red cell fragmentation coupled with reduced platelet production in the absence of vitamin B12 and partly by the accumulated byproducts and metabolites that induce endothelial injury and hence organ damage. Expensive and complicated treatment for TMA is often initiated on an empiric basis, pending the results of confirmatory tests. In contrast, vitamin B12 Pseudo-TMA and MM-TMA could be treated with proper vitamin B12 supplementation. It is therefore important to identify these disorders promptly. The recent availability of a validated scoring system such as the PLASMIC score uses simple clinical and laboratory parameters. As it incorporates the mean corpuscular volume in its laboratory parameters, this helps in the identification of pseudo and MM-TMA. Perhaps some minor modification of this scoring system by changing the parameters of hemolysis to include reticulocytosis and rather than and/or other hemolytic parameters could even help refine this identification.

原文英語
文章編號102717
期刊Transfusion and Apheresis Science
DOIs
出版狀態接受/付印 - 一月 1 2020

指紋

Thrombotic Microangiopathies
Vitamin B 12 Deficiency
Vitamin B 12
Reticulocytosis
Erythrocyte Indices
Hemolytic Anemia
von Willebrand Factor
Hemolysis
Thrombocytopenia
Blood Platelets
Wounds and Injuries

ASJC Scopus subject areas

  • Hematology

引用此文

Vitamin B12 deficiency and metabolism-mediated thrombotic microangiopathy (MM-TMA). / Sabry, Waleed; Elemary, Mohamed; Burnouf, Thierry; Seghatchian, Jerard; Goubran, Hadi.

於: Transfusion and Apheresis Science, 01.01.2020.

研究成果: 雜誌貢獻回顧型文獻

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AB - Thrombotic microangiopathies (TMA) are characterized by microangiopathic hemolytic anemia, thrombocytopenia and organ damage resulting from mechanical factors, accumulation of the ultra-large von Willebrand factor multimers or complement-mediated abnormalities. Severe acquired vitamin B12 (Cobalamin - Cbl) deficiency or congenital defective Cbl metabolism could lead to a picture that mimics TMA. The later has been termed metabolism-mediated TMA (MM- TMA). This confusing picture is mediated partly by the large red cell fragmentation coupled with reduced platelet production in the absence of vitamin B12 and partly by the accumulated byproducts and metabolites that induce endothelial injury and hence organ damage. Expensive and complicated treatment for TMA is often initiated on an empiric basis, pending the results of confirmatory tests. In contrast, vitamin B12 Pseudo-TMA and MM-TMA could be treated with proper vitamin B12 supplementation. It is therefore important to identify these disorders promptly. The recent availability of a validated scoring system such as the PLASMIC score uses simple clinical and laboratory parameters. As it incorporates the mean corpuscular volume in its laboratory parameters, this helps in the identification of pseudo and MM-TMA. Perhaps some minor modification of this scoring system by changing the parameters of hemolysis to include reticulocytosis and rather than and/or other hemolytic parameters could even help refine this identification.

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