Acquired hemolytic anemia
Acquired hemolytic anemia can be divided into immune and non-immune mediated forms of hemolytic anemia.
| Acquired hemolytic anemia | |
|---|---|
| Specialty | Hematology |
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)
- 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
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
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:
A total of four mechanisms are usually described, but there is some evidence that these mechanisms may overlap.[1]
References
External links
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