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)^{[ 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)
• 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 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)
  • 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:^{[ citation needed]}

• Drug-induced autoimmune hemolytic anemia
• Drug-induced nonautoimmune hemolytic anemia

A total of four mechanisms are usually described, but there is some evidence that these mechanisms may overlap. ^[1]

References

External links