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The most common antibody isotype involved in warm antibody AIHA is IgG, though sometimes IgA is found. The IgG antibodies attach to a red blood cell, leaving their F C portion exposed with maximal reactivity at 37 °C (versus cold antibody induced hemolytic anemia whose antibodies only bind red blood cells at low body temperatures, typically 28–31 °C).
AIHA is a relatively rare condition, with an incidence of 5–10 cases per 1 million persons per year in the warm-antibody type and 0.45 to 1.9 cases per 1 million persons per year in the cold-antibody type. [4] Autoimmune hemolysis might be a precursor of later onset systemic lupus erythematosus. [5]
AIHA can be classified as warm autoimmune hemolytic anemia or cold autoimmune hemolytic anemia, which includes cold agglutinin disease and paroxysmal cold hemoglobinuria. These classifications are based on the characteristics of the autoantibodies involved in the pathogenesis of the disease.
Mixed warm and cold AIHA runs a chronic course with severe intermittent exacerbations, such as serious anemia, and is treated by blood transfusion. Successful therapeutic options for the treatment of hemolysis associated with mixed AIHA are limited but increasing. [5] [non-primary source needed] [6] [better source needed]
[2] Usual onset: Hours to months (various types of hypersensitivities reactions)of the initial drug exposure. [1] Causes: Antimicrobials, nonsteroidal anti-inflammatory drugs, antineoplastic drugs, and other drugs. [3] Diagnostic method: Blood tests, blood smear, and Direct antiglobulin testing [4] Differential diagnosis: Warm antibody ...
Secondary cold agglutinin syndrome occurs when autoantibodies bind to red blood cells, rendering them subject to attack by the complement system. [17] It is a result of an underlying condition potentially associated with either monoclonal cold-reacting autoantibodies or polyclonal cold-reacting autoantibodies [16] predominantly caused by infection or lymphoproliferative disorders. [16]
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