Hemolytic Anemias

Hemolytic anemia is a condition in which red blood cells (erythrocytes) are destroyed (undergo hemolysis) earlier than their normal lifespan of about 100–120 days. As a result, the body cannot produce enough new cells to compensate, leading to anemia.

Hemolytic anemia may be:

• Hereditary – caused by genetic disorders (e.g., thalassemia, hereditary spherocytosis, G6PD deficiency).

• Acquired – develops during life as a result of infections, medications, autoimmune diseases, incompatible blood transfusions, or mechanical damage (e.g., in patients with artificial heart valves).

Hemolytic anemia may develop rapidly or gradually. The most common symptoms include weakness, fatigue, pallor, jaundice (yellowing of the skin and eyes), dark-colored urine, dizziness, confusion, palpitations, tachycardia, splenic and/or liver enlargement, and fever (especially during acute episodes).

The diagnosis is suspected based on symptoms and physical examination, and confirmed by laboratory tests such as:

• Complete blood count (CBC)
• Reticulocyte count (immature red blood cells)
• Bilirubin, LDH, and haptoglobin levels
• Peripheral blood smear (morphology of red blood cells)
• Coombs test (for autoimmune forms)
• Genetic testing, if indicated

Treatment depends on the underlying cause and may include:

• Blood transfusion in cases of severe anemia
• Medications such as corticosteroids, immunosuppressants (e.g., intravenous immunoglobulin, rituximab)
• Splenectomy (surgical removal of the spleen) in some hereditary forms
• Management of infections or discontinuation of causative medications
• Bone marrow transplantation in rare, severe hereditary hemolytic conditions
• Lifestyle adjustments: avoiding infections, cold exposure, and high-risk medications

The disease can often be controlled or cured if the underlying cause is identified in time. Hereditary forms require regular monitoring and, in some cases, long-term treatment.