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Intravascular Erythrophagocytosis

Henry D. Friedman, MD; Robert A. Dracker, MD
JAMA. 1991;265(9):1082. doi:10.1001/jama.1991.03460090030013.
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A previously healthy 8-year-old boy developed severe hemolytic anemia several days after uneventful chickenpox. He presented shortly after cold exposure with a hematocrit of 0.12, hemoglobinuria, and a white blood cell count of 26 × 109/L. His presentation and laboratory findings strongly suggested postinfectious cold agglutinin disease of IgM type.1(pp526-527) The peripheral blood film at admission (Figure) was striking for erythrophagocytosis by 9% of 22 × 109/L segmented neutrophils, erythrocyte agglutination, and a rosette-like arrangement of erythrocytes about segmented neutrophils.

Intravascular erythrophagocytosis appears to serve as an auxiliary means of sequestering and destroying erythrocytes and occurs during excessive opsonization of intravascular erythrocytes1(pp98-101) and when splenic and hepatic macrophages are overwhelmed.2,3 Nonneoplastic diseases associated with intravascular erythrophagocytosis include two types of disorders: (1) those with an abundance of altered erythrocytes (as in sickle cell crisis4 and Heinz-body hemolytic anemia5,6) and (2) those


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