<unk>  is a form of hemolytic anaemia.
Non-immune<unk>  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<unk> s 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<unk> s cause RBC (red blood cell) lysis even in normal individuals. These include dapsone and sulfasalazine.
Non-immune<unk> -induced hemolysis can also arise from<unk> -induced damage to cell volume control mechanisms; for example<unk> s 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<unk> s actions are irreversible cell swelling and lysis (e.g. ouabain at very high doses).
Drug-induced nonautoimmune hemolytic anemia
Drug induced hemolytic anemia
Warm autoimmune hemolytic anemia
Autoimmune hemolytic anemia
Microangiopathic hemolytic anemia
Congenital hemolytic anemia
Non immune hemolytic anemia
Mechanical hemolytic anemia