Autoimmune hemolysis: a critical review.
Autoimmune hemolysis is defined as a shortening of erythrocyte lifespan due to antibodies directed against the individuals own red cells. This autoantibody production (by B lymphocytes) is thought to result from deficient activity of suppressor T lymphocytes. The rate of erythrocyte destruction depends on the properties of the autoantibodies and on the activities of the complement and mononuclear phagocyte systems: anemia results when destruction outweighs marrow production. Autoimmune hemolysis, which may be primary or secondary, is classified into "warm," "cold," and "mixed" types. The hemolysis associated with pregnancy. Donath-Landsteiner antibodies, of mixed type, and in children, is treated in detail. Current treatment is with immunosuppressive drugs, surgery, and plasma exchange, though immunomanipulation may become important in the future; blood transfusion may be a life-saving adjunct to other therapy.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000743:Anemia, Hemolytic / Q000150:complications / Q000276:immunology*; D000920:Antibody-Dependent Cell Cytotoxicity; D000938:Antigen-Presenting Cells / Q000276:immunology; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000276:immunology*; D002648:Child; D002675:Child, Preschool; D003165:Complement System Proteins / Q000276:immunology; D004912:Erythrocytes / Q000276:immunology; D006461:Hemolysis; D006801:Humans; D007130:Immunoglobulin Idiotypes / Q000276:immunology; D007223:Infant; D008875:Middle Aged; D009154:Mutation; D009369:Neoplasms / Q000276:immunology; D010586:Phagocytes / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001323:Autoantibodies; D007130:Immunoglobulin Idiotypes; D003165:Complement System Proteins