Hemolytic anemia pathophysiology: Difference between revisions
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Non-immune drug-induced hemolysis can also arise from drug-induced damage to cell volume control mechanisms; for example drugs can directly or indirectly impair regulatory volume decrease mechanisms, which become activated during [[hypotonic]] RBC swelling to return the cell to a normal volume. The consequence of the drugs actions are irreversible cell swelling and lysis (e.g. [[ouabain]] at very high doses). | Non-immune drug-induced hemolysis can also arise from drug-induced damage to cell volume control mechanisms; for example drugs can directly or indirectly impair regulatory volume decrease mechanisms, which become activated during [[hypotonic]] RBC swelling to return the cell to a normal volume. The consequence of the drugs actions are irreversible cell swelling and lysis (e.g. [[ouabain]] at very high doses). | ||
==Compensatory response== | |||
Hemolytic anemia causes a compensatory increases of erythropoetin that in turn causes an increase in reticulocyte percentage and absolute reticulocyte count. This results in increased hemoglobin and RBC production. This response is manifested initially by an increase in the reticulocyte percentage and absolute reticulocyte count, followed by an increase in hemoglobin concentration. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 13:53, 25 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Drugs play a large role in the mechanism of hemolytic anemia. The mechanistic actions of drug induced hemolysis are described below.
Drug Induced Hemolysis
Drug induced hemolysis has large clinical relevance. It occurs when drugs actively provoke red cell destruction.
Immune
Penicillin in high doses can induce immune mediated hemolysis via the hapten mechanism in which antibodies are targeted against the combination of penicillin in association with red blood cells. Complement is activated by the attached antibody leading to the removal of red blood cells by the spleen.
The drug itself can be targeted by the immune system, e.g. by IgE in a Type I hypersensitivity reaction to penicillin, rarely leading to anaphylaxis.
Non-immune
Non-immune drug induced hemolysis can occur via oxidative mechanisms. This is particularly likely to occur when there is an enzyme deficiency in the antioxidant defence system of the red blood cells. An example is where antimalarial oxidant drugs like primaquine damage red blood cells in Glucose-6-phosphate dehydrogenase deficiency in which the red blood cells are more susceptible to oxidative stress due to reduced NADPH production consequent to the enzyme deficiency.
Some drugs cause RBC (red blood cell) lysis even in normal individuals. These include dapsone and sulfasalazine.
Non-immune drug-induced hemolysis can also arise from drug-induced damage to cell volume control mechanisms; for example drugs can directly or indirectly impair regulatory volume decrease mechanisms, which become activated during hypotonic RBC swelling to return the cell to a normal volume. The consequence of the drugs actions are irreversible cell swelling and lysis (e.g. ouabain at very high doses).
Compensatory response
Hemolytic anemia causes a compensatory increases of erythropoetin that in turn causes an increase in reticulocyte percentage and absolute reticulocyte count. This results in increased hemoglobin and RBC production. This response is manifested initially by an increase in the reticulocyte percentage and absolute reticulocyte count, followed by an increase in hemoglobin concentration.