Autoimmune hemolytic anemia

An acquired disorder in which antibodies or complement target red blood cells, causing their premature destruction and resulting anemia.

Warm antibody autoimmune hemolytic anemia: Autoimmune hemolytic anemia in which usually IgG antibodies react most strongly with red cells at body temperature. This common form typically causes splenic removal of antibody-coated red cells.
Hemolysis: The destruction of red blood cells, releasing hemoglobin and shortening their lifespan. It is the red-cell destruction that produces anemia in this disorder.
Corticosteroid: A class of steroid medicines that suppresses inflammation and immune activity. These medicines are commonly initial treatment for warm antibody disease.
Hereditary spherocytosis: An inherited red-cell membrane disorder that produces spherical cells and chronic hemolysis. It can resemble immune hemolysis on a smear but is not antibody-driven.
Cold agglutinin disease: An autoimmune disorder in which cold-reactive antibodies activate complement on red blood cells. This form causes complement-mediated hemolysis, often after exposure to cold.
Anemia: A reduction in the blood's oxygen-carrying capacity, commonly reflected by low hemoglobin concentration. Premature red-cell loss lowers hemoglobin when marrow replacement cannot keep pace.
Rituximab: A monoclonal antibody that depletes B cells expressing the CD20 protein. It can treat autoimmune hemolytic anemia that persists or returns after initial therapy.
Glucose-6-phosphate dehydrogenase deficiency: An inherited enzyme deficiency that makes red cells vulnerable to oxidative damage. Its episodic hemolysis follows oxidative stress rather than immune targeting.
Paroxysmal cold hemoglobinuria: A rare autoimmune hemolytic anemia in which a biphasic antibody lyses red cells after cooling and rewarming. Its distinctive temperature-dependent antibody mechanism differs from other cold-associated forms.
Reticulocyte: An immature red blood cell recently released from bone marrow into circulation. A high reticulocyte count often signals marrow compensation for red-cell destruction.

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