China
Africa
Explore chapters and articles related to this topic
Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
AIHA is caused by an autoantibody to the patient's own red cells. The antibodies are active either at body temperature (37 °C – ‘warm antibody’ = IgG) or at room temperature (15 °C – ‘cold antibody’ = IgM; Table 15.9). Cold antibody AIHA often causes red cell autoagglutination on blood films and is therefore sometimes called cold agglutinin disease. Haemolysis is usually extravascular, resulting from phagocytosis of antibody and/or complement-coated red cells within the spleen and liver.
Immune Hemolytic Anemias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Joseph P. Yoe, Ronald A. Sacher
Autoagglutination of RBCs (berrylike clusters) may occur but are not as conspicuous as with cold complete antibodies. Autoagglutination must be distinguished from rouleaux formation (poker-chip orientation)
Principles of Clinical Pathology
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Niraj K. Tripathi, Jacqueline M. Tarrant
Many drugs have been associated with immune-mediated hemolysis (Packman and Leddy 1995), but drug-induced immune-mediated hemolysis is usually an idiosyncratic phenomenon and difficult to predict. When observed in a nonclinical study, the finding is usually limited to one or two animals and may not be dose-dependent. Immune-mediated hemolysis is typically not observed until a test article has been administered multiple times, and enough time has passed for antibody production to occur. A test article may act as a hapten bound to red cell membrane, or it may elicit an antibody response to itself with resulting antigen-antibody complexes binding to red cell membrane. It is also possible for a test article to alter the ability of the immune system to recognize self, and true autoantibodies may be produced. Complement-mediated intravascular hemolysis is possible, but immune-mediated hemolysis is usually extravascular. Macrophages may engulf the entire affected red cell or remove just the antibody-coated portion of its membrane to produce morphologically distinct spherocytes readily identified in blood smears. Spherocytes and, less commonly, autoagglutination, are the predominant morphologic features of immune-mediated hemolysis. Although a direct antiglobulin test (Coombs’ test) may be attempted to confirm the presence of antibody or complement on red cells, species-specific reagents must be used (Wardrop 2005), and false negatives are not uncommon. With repeated test article administration, immune-mediated hemolytic anemia usually causes severe anemia. However, the regenerative response is robust, and recovery nearly always occurs when dosing is stopped. Rechallenging the animal after recovery is a simple means of confirming the immune-mediated mechanism. Hemolysis and spherocytosis should be evident within 1 or 2 days, with or without autoagglutination. Immune-mediated hemolytic anemia is commonly observed in association with large granular lymphocyte leukemia in older Fischer 344 rats (Stromberg 1985).
Autoimmune hemolytic anemia: causes and consequences
Published in Expert Review of Clinical Immunology, 2022
In mixed AIHA cases [20], which are generally more severe and refractory/relapsing, clinical-laboratory features (monospecific DAT, cold agglutinin titers, autoagglutination, presence of cold agglutinin symptoms) should be evaluated at each relapse to assess the prevailing form (warm versus cold). Glucocorticoids should be given generously, and rituximab considered as an early second line, particularly in the presence of CAD features, while splenectomy is discouraged [4].