Acquired hemolytic anemia can be divided into immune and non-immune mediated forms of hemolytic anemia. Immune
Immune mediated hemolytic anaemia (direct Coombs test is positive)
Autoimmune hemolytic anemia
Warm antibody autoimmune hemolytic anemia
Idiopathic
Systemic lupus erythematosus (SLE)
Evans syndrome (antiplatelet antibodies and hemolytic antibodies)
Cold antibody autoimmune hemolytic anemia
Idiopathic cold hemagglutinin syndrome
Infectious mononucleosis and mycoplasma (atypical) pneumonia
Paroxysmal cold hemoglobinuria (rare)
Alloimmune hemolytic anemia
Hemolytic disease of the newborn (HDN)
Rh disease (Rh D)
ABO hemolytic disease of the newborn
Anti-Kell hemolytic disease of the newborn
Rhesus c hemolytic disease of the newborn
Rhesus E hemolytic disease of the newborn
Other blood group incompatibility (RhC, Rhe, Kidd, Duffy, MN, P and others)
Alloimmune hemolytic blood transfusion reactions (i.e., from a non-compatible blood type)
Drug induced immune mediated hemolytic anemia
Penicillin (high dose)
Methyldopa

Non-immune
Non-immune mediated hemolytic anemia (direct Coombs test is negative)

Drugs (i.e., some drugs and other ingested substances lead to hemolysis by direct action on RBCs, e.g., ribavirin )
Toxins (e.g., snake venom; plant poisons such as aesculin)
Trauma
Mechanical (from heart valves, extensive vascular surgery, microvascular disease, repeated mechanical vascular trauma)
Microangiopathic hemolytic anemia (a specific subtype with causes such as TTP, HUS, DIC and HELLP syndrome)
Infections (Note: Direct Coombs test is sometimes positive in hemolytic anemia due to infection)
Malaria
Babesiosis
Sepsis
Membrane disorders
Paroxysmal nocturnal hemoglobinuria (rare acquired clonal disorder of red blood cell surface proteins)
Liver disease

Drug induced hemolysis
Drug induced hemolysis has large clinical relevance. It occurs when drugs actively provoke red blood cell destruction. It can be divided in the following manner:
Drug-induced autoimmune hemolytic anemia
Drug-induced nonautoimmune hemolytic anemiaA total of four mechanisms are usually described, but there is some evidence that these mechanisms may overlap. References


== External links ==
Colestyramine (INN) or cholestyramine (USAN) (trade names Questran, Questran Light, Cholybar, Olestyr) is a bile acid sequestrant, which binds bile in the gastrointestinal tract to prevent its reabsorption. It is a strong ion exchange resin, which means it can exchange its chloride anions with anionic bile acids in the gastrointestinal tract and bind them strongly in the resin matrix. The functional group of the anion exchange resin is a quaternary ammonium group attached to an inert styrene-divinylbenzene copolymer. Colestyramine removes bile acids from the body by forming insoluble complexes with bile acids in the intestine, which are then excreted in the feces. As a result of this loss of bile acids, more plasma cholesterol is converted to bile acids in the liver to normalise levels. This conversion of cholesterol into bile acids lowers plasma cholesterol levels. Medical uses
Bile acid sequestrants such as colestyramine were first used to treat hypercholesterolemia, but since the introduction of statins, now have only a minor role for this indication. They can also be used to treat the pruritus, or itching, that often occurs during liver failure and other types of cholestasis where the ability to eliminate bile acids is reduced.Colestyramine is commonly used to treat diarrhea resulting from bile acid malabsorption. It was first used for this in Crohns disease patients who had undergone ileal resection. The terminal portion of the small bowel (ileum) is where bile acids are reabsorbed.