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Warm autoimmune haemolytic anaemia

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A form of autoimmune haemolytic anaemia that involves warm-reacting antibodies causing the pathophysiology


Autoimmune haemolytic anaemia is a form of an acquired haemolytic anaemia. It occurs when the antibodies act against the body's red blood cells. As a result, the red blood cells of a person with a severe automimmune haemolytic anaemia would have a lifespan reduced into just few days from the normal 100-120 days.1 Autoimmune haemolytic anaemia may either be warm or cold depending on the characteristics of the autoantibodies involved. The warm autoimmune haemolytic anaemia occurs in body temperature whereas the cold autoimmune haemolytic anaemia happens in cold temperature (i.e. 28-31 °C). The warm autoimmune haemolytic anaemia is more common than the cold autoimmune haemolytic anaemia. 2

The IgG is the most common type of antibody associated with this condition. This antibody attaches to a red blood cell at 37 °C. The exposed Fc portion of the IgG is then recognized by macrophages and monocytes in the spleen. The macrophages and monocytes take off portions of the red blood cell's membrane, causing the red blood cells to become spherical in shape. The sphere-shaped red blood cells would become trapped in the spleen as a result. This in turn triggers the enlargement of the spleen referred to as splenomegaly.

Warm autoimmune haemolytic anaemia may be caused by intake of certain drugs such as quinidine and alpha methyldopa. It may also be associated with other diseases such as systemic lupus erythematosus, rheumatoid arthritis, and chronic lymphocytic leukemia.

Abbreviation / Acronym: WAIHA


  • warm autoimmune hemolytic anemia

Also called:

  • warm antibody autoimmune haemolytic anaemia

See also:

1 Sawitsky, A. & Ozaeta, P. B. (1970). "Disease-associated autoimmune hemolytic anemia". Bull N Y Acad Med 46 (6): 411–26.
2 Cotran, R. S., Kumar, V., Fausto, N., Nelso F., Robbins, S. L., & Abbas, A. K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. p. 637.