This is an uncommon anemia that develops when red blood cells are destroyed faster than bone marrow can replace them. The result is a shortage of red blood cells to transport oxygen. Early destruction can result from genetic defects or acquired defects.
Hemolytic Anemia includes any of a group of acute or chronic anemias characterized by shortened survival of mature erythrocytes and the inability of bone marrow to compensate for the decreased life span. They are classified as either inherited (generally due to intrinsic cell defects), or acquired (due to the actions of extrinsic agents such as infectious agents, poisons, physical trauma, or antibodies).
Autoimmune Hemolytic Anemia includes any of a large group of anemias involving autoantibodies against red cell antigens. Some are without a known cause, and others due to autoimmune diseases, hematologic neoplasms, viral infections, or immunodeficiency diseases.
Congenital Nonspherocytic Hemolytic Anemia includes any of a group of inherited anemias characterized by shortened red cell survival, lack of spherocytosis, and normal osmotic fragility associated with erythrocyte membrane defects, multiple intracellular enzyme deficiencies or other defects, or unstable hemoglobins.
Drug-induced Immune Hemolytic Anemia is immune hemolytic anemia induced by drugs, classified by mechanism:
Immune Hemolytic Anemia is an acquired hemolytic anemia in which a hemolytic response is caused by isoantibodies or autoantibodies produced on exposure to drugs, toxins, or other antigens.
Infectious Hemolytic Anemia is due to an incompletely compensated decrease in red blood cell survival secondary to infectious agents, including protozoa (e.g., Plasmodium in malaria), bacteria, and certain viruses.
Other types include Microangiopathic Hemolytic Anemia, Nonspherocytic Hemolytic Anemia, Toxic Hemolytic Anemia (due to toxic agents, including drugs, bacterial lysins, and snake venoms) and Hemolytic Anemia of Newborn.
Genetic defects in the red blood cells' physical or chemical makeup can lead to a rigid or elongated shape. The deformity causes red blood cells to become trapped in the spleen, where most are destroyed before the end of their normal lifespan. More commonly, defective hemoglobin causes red blood cells to develop a crescent (sickle) shape. Sickle cells lodge in small arteries, causing acute pain and blood clots.
Acquired defects can occur when certain infections or the use of antibiotics or anti-inflammatory drugs break down red blood cells. Occasionally, one can acquire a mild form of anemia through an autoimmune process. Some artificial heart valves increase the risk of red blood cell destruction by directly injuring cells.
The patient may need to undergo blood tests, to check the number of young red blood cells and to see if the red blood cells are deformed. If hemolytic anemia is present, there will be a higher number of young red blood cells than normal. One of the tests isolates and identifies the abnormal hemoglobin S, responsible for the sickle shape of the defective red blood cells in sickle cell disease. An enlarged spleen also raises a question of hemolytic anemia.
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