Frequently Asked Questions:
In AIHA the body destroys RBCs at a greater rate than it can produce new RBCs, eventually leading to anemia (low levels of red blood cells), with symptoms such as fatigue, pale color, rapid heartbeat, and shortness of breath. In severe cases fever, chest pain, fainting, or heart failure may occur. Mild splenomegaly (enlargement of the spleen) is typical.
Warm antibody AIHA refers to the presence of antibodies that react with the red blood cell surface at body temperature. It is the most common form of AIHA, and can be either primary or secondary to an underlying disease such as systemic lupus erythematosus (SLE) or a lymphoproliferative condition such as or chronic lymphocytic leukemia (CLL) or lymphoma.
Some people with AIHA also have a similar condition, immune thrombocytopenia (ITP), in which the body attacks its own platelets—this combination of both conditions is known as Evans syndrome.
- Direct antibody (Coombs) test (DAT) positive for immunoglobulin G (IgG) antibodies. A positive DAT is a key signature of warm antibody AIHA.
- Some or all of the following indicators of active red blood cell destruction/hemolysis: elevated lactate dehydrogenase, decreased haptoglobin, increased indirect bilirubin, and increased reticulocytes (immature red blood cells).
For patients with severe AIHA without a response to other treatments, immunosuppressive agents such as cyclosporine, mycophenolate mofetil, azathioprine, and cyclophosphamide may be used.
Some patients are not effectively treated by any available therapies due to lack of a stable response, or due to severe side effects of treatment.
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