Autoimmune hemolytic anemia
- In warm autoimmune hemolytic anemia: immunoglobulin G (IgG) attacks red blood cells (RBCs); patients are usually over age 50; typically treated with corticosteroids and therapies for underlying diseases.
- In chronic cold agglutinin disease: cold-activated immunoglobulin M (IgM) and complement (C3d) coat RBCs and trigger hemolysis; patients usually over age 50; sometimes resolves with cold avoidance; rarely progresses to renal failure.
- The diagnosis of AIHA must meet two criteria: evidence of hemolysis (anemia plus elevated reticulocyte count in the absence of blood loss); and evidence of RBC autoantibodies/complement (usually indicated by a positive direct Coombs test). Note: the direct Coombs test is falsely negative in a small percentage of AIHA.
- Though usually idiopathic, AIHA is commonly associated with infection, autoimmune disease, lymphoproliferative disorders, and some drugs.
- Warm AIHA and cold agglutinin disease are most common among adults over age 50, in whom the diseases are usually chronic and relapsing; PCH, a rare disorder occurring most commonly in children, usually resolves on its own.
- Medical intervention is usually not necessary in the many patients who present with a mild hemolytic anemia; therapy becomes necessary when anemia is significant.
- Treating the cause of autoimmune hemolytic anemia may help treat the condition.
- Cortisone-like drugs suppress the immune response. These drugs usually improve the more common types of autoimmune hemolytic anemia. Other immunosuppressive drugs: Other drugs that suppress the immune system may be used if corticosteroids are not effective. These include azathioprine and cyclophosphamide. Rituximab is another drug that has shown promise in treating this condition.
- Splenectomy: The spleen removes abnormal red cells from the circulation, including those labeled with antibodies. Removing the spleen can preserve those cells and prevent anemia.
- Transfusion: You will need transfusions if your blood gets too anemic.
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