Acquired hemolytic anemia can be divided into immune and non-immune mediated forms of hemolytic anemia.
Acquired hemolytic anemia | |
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Specialty | Hematology |
Immune edit
Immune mediated hemolytic anaemia (direct Coombs test is positive)[citation needed]
- 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)
- Warm antibody autoimmune hemolytic anemia
- 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)
- Hemolytic disease of the newborn (HDN)
- Drug induced immune mediated hemolytic anemia
- Penicillin (high dose)
- Methyldopa
Non-immune edit
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 anaemia (a specific subtype with causes such as TTP, HUS, DIC and HELLP syndrome)
- Infections (Note: Direct Coombs test is sometimes positive in hemolytic anaemia due to infection)
- Membrane disorders
- Paroxysmal nocturnal hemoglobinuria (rare acquired clonal disorder of red blood cell surface proteins)
- Liver disease
Drug induced hemolysis edit
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:[citation needed]
A total of four mechanisms are usually described, but there is some evidence that these mechanisms may overlap.[1]