Hemolytic anemia causes: Difference between revisions
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* Antibodies against RBC membrane such as seen in [[autoimmune hemolytic anemia]], [[alloimmune hemolytic anemia]], delayed [hemolytic] transfusion reaction, some drug-induced hemolytic anemias) | * Antibodies against RBC membrane such as seen in [[autoimmune hemolytic anemia]], [[alloimmune hemolytic anemia]], delayed [hemolytic] transfusion reaction, some drug-induced hemolytic anemias) | ||
* RBC destructions secondary to trauma as seen in valvular malfunctioning, [[disseminated intravascular coagulation]], [[thrombotic thrombocytopenic purpura]] and [[hemolytic uremic syndrome]] | * RBC destructions secondary to trauma as seen in valvular malfunctioning, [[disseminated intravascular coagulation]], [[thrombotic thrombocytopenic purpura]] and [[hemolytic uremic syndrome]] | ||
* Infections - [[malaria]], [[babesiosis]], [[clostridium perfringens]] | |||
* Oxidative stress such as aniline dyes, [[dapsone]], [[pyridium]] in normal patients or with [[G6PD deficiency]], congenital [[methemoglobinemia]], or unstable hemoglobin variants. | |||
* [[Hypersplenism]] | * [[Hypersplenism]] | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 18:34, 25 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
It has numerous possible causes, ranging from relatively harmless to life-threatening.
Causes
Common Causes
- Hemolytic anemia occurs when the bone marrow is unable to increase production to make up for the premature destruction of red blood cells.
- If the bone marrow is able to keep up with the early destruction, anemia does not occur (this is sometimes called compensated hemolysis).
- There are many types of hemolytic anemia, which are classified by the reason for the premature destruction of red blood cells. The defect may be in the red blood cell itself (intrinsic factors), or outside the red blood cell (extrinsic factors).
Intrinsic or Intracorpuscular
- Commonly hereditary in nature exceptions, paroxysmal nocturnal hemoglobinuria and acquired alpha thalassemia
- Occurs secondary to abnormalities in RBC components such as hemoglobin, RBC membranes (alpha or beta globin chains in thalassemia, hereditary spherocytosis, paroxysmal nocturnal hemoglobinuria), glycolysis, and reducing power of the RBC.
Extrinsic factors
- Commonly acquired in nature
- Antibodies against RBC membrane such as seen in autoimmune hemolytic anemia, alloimmune hemolytic anemia, delayed [hemolytic] transfusion reaction, some drug-induced hemolytic anemias)
- RBC destructions secondary to trauma as seen in valvular malfunctioning, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura and hemolytic uremic syndrome
- Infections - malaria, babesiosis, clostridium perfringens
- Oxidative stress such as aniline dyes, dapsone, pyridium in normal patients or with G6PD deficiency, congenital methemoglobinemia, or unstable hemoglobin variants.
- Hypersplenism