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Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can produce them. This destruction, known as hemolysis, can occur in the bloodstream or within organs such as the spleen. Hemolytic anemia can be either inherited or acquired, and it often leads to a variety of health complications, depending on the underlying cause. To understand hemolytic anemia, it is important to first explore the structure and function of red blood cells, the body's primary vehicle for oxygen transport.
Red blood cells (RBCs) are essential for the efficient movement of oxygen from the lungs to tissues throughout the body and the return of carbon dioxide to be exhaled. These cells are disc-shaped and flexible, enabling them to travel through the body’s blood vessels without causing blockages. The lifespan of an RBC is about 120 days, and after this period, they are typically broken down by the spleen. However, in individuals with hemolytic anemia, the destruction of red blood cells occurs at an abnormally high rate, reducing the overall number of healthy RBCs in circulation.
The immune system is often a major contributor to this destruction. In autoimmune hemolytic anemia (AIHA), the body mistakenly identifies its own red blood cells as foreign and attacks them. This immune response can be triggered by infections, medications, or even other autoimmune disorders. There are also genetic forms of hemolytic anemia, such as sickle cell anemia and thalassemia, which are caused by mutations in the genes responsible for producing hemoglobin, the oxygen-carrying component of RBCs. Additionally, hemolytic anemia can be triggered by external factors like toxins, certain medications, or mechanical damage to the red blood cells.
