Acquired Hemolytic Anemias
Classification, Etiology, Pathogenesis, and Clinical Manifestations
Definition
Acquired hemolytic anemias are disorders in which red blood cells are destroyed prematurely ( hemolysis ) due to external (non-genetic) factors acting on otherwise normal RBCs.
Classification
I. By site of hemolysis
II. By etiology
Etiology and Pathogenesis
- Immune-Mediated Hemolysis
a) Autoimmune Hemolytic Anemia (AIHA)
Warm AIHA: IgG binds to RBCs at body temperature → Fc receptor-mediated destruction by spleen (extravascular hemolysis ).
Cold AIHA: IgM binds at low temp → activates complement → intravascular hemolysis.
Triggers: Autoimmune diseases (SLE), lymphomas, infections, drugs (e.g., penicillin).
- Mechanical Hemolysis
RBCs are physically destroyed as they pass through narrowed or damaged vessels or artificial surfaces.
Seen in prosthetic valves, microangiopathies like:
- TTP (Thrombotic thrombocytopenic purpura)
- HUS (Hemolytic uremic syndrome)
- DIC (Disseminated intravascular coagulation)
- Infectious Hemolysis
Malaria: Plasmodium invades and lyses RBCs.
Clostridial sepsis: produces toxins (e.g., alpha- toxin) causing direct RBC lysis.
- Chemical and Toxic Agents
Lead poisoning: impairs heme synthesis and causes hemolysis.
Snake venom: contains hemolysins.
- Paroxysmal Nocturnal Hemoglobinuria (PNH)
Acquired mutation in PIGA gene → loss of protective surface proteins (CD55/CD59) on RBCs → increased sensitivity to complement → intravascular hemolysis, especially at night.
Clinical Manifestations
Laboratory Findings
- ↑ Reticulocyte count
- ↑ LDH, ↑ indirect bilirubin
- ↓ Haptoglobin (consumed in intravascular hemolysis )
Peripheral smear: spherocytes, schistocytes, ghost cells (depending on cause)
Positive Coombs test (in AIHA)
Urine hemoglobin / hemosiderin (in intravascular)
Summary Table
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