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Histopathological evidence for macrophage activation driving post‐transfusion hyperhaemolysis syndrome
Author(s) -
Win Nay,
Lucas Sebastian,
Hebballi Sangam,
McKernan Angela,
Hamilton Rosie,
Robinson Ivan,
Chen Frederick
Publication year - 2019
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.15925
Subject(s) - phagocytosis , macrophage , macrophage activation syndrome , haemolysis , pathogenesis , bystander effect , medicine , immunology , complication , antibody , red blood cell , blood transfusion , biology , biochemistry , arthritis , in vitro
Summary Post‐transfusion hyperhaemolysis syndrome ( PTHS ) is a rare life‐threatening transfusion complication reported mainly in sickle cell patients. Its pathogenesis is poorly understood. Antibody‐mediated haemolysis and bystander effect have been proposed as putative mechanisms, but in half of cases, red cell antibodies are undetectable, and PTHS develops despite transfusion of cross‐matched compatible RBC . An alternate hypothesis proposes activated macrophages as the main drivers of red cell destruction through direct phagocytosis. We report the histopathological findings of two patients with PTHS showing extensive macrophage expansion and erythrophagocytosis, supportive of macrophage activation driving PTHS . This supports a possible role for novel therapies that target macrophage activation.