Etiopathogenesis, clinical features, and management of hemolytic anemias
Pathophysiology and immune mechanisms of autoimmune hemolytic anemia
Autoimmune hemolytic anemia (AIHA) is an immune-mediated disorder leading to red blood cell destruction. Its management involves corticosteroids, immunosuppressants, and splenectomy in severe cases.
Etiopathogenesis, Clinical Features, and Management of Hemolytic Anemias
Pathophysiology and Immune Mechanisms of Autoimmune Hemolytic Anemia
Autoimmune hemolytic anemia (AIHA) is characterized by the destruction of red blood cells due to autoantibodies targeting erythrocyte surface antigens. The pathogenesis involves the dysregulation of the immune system, leading to an inappropriate attack on self-antigens.
Etiopathogenesis
AIHA can be classified into warm and cold antibody types. Warm AIHA is primarily mediated by IgG antibodies, while cold AIHA involves IgM antibodies that activate complement-mediated hemolysis.
Clinical Features
- Pallor and fatigue due to anemia
- Jaundice resulting from increased bilirubin levels
- Splenomegaly due to increased RBC destruction
- Possible hemoglobinuria in severe cases
Diagnostic Approaches
Diagnostic workup includes peripheral blood smear, direct Coombs test (DAT), reticulocyte count, and hemoglobin electrophoresis.
Management Strategies
The primary management involves corticosteroids as first-line therapy. Other options include immunosuppressants, rituximab, and in refractory cases, splenectomy may be considered.
Conclusion
Understanding the pathophysiology of AIHA allows for effective treatment strategies, minimizing complications and improving patient outcomes.
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