Hemolytic (“hemo” means blood, “lytic” means destroying) anemia occurs when red blood cells are being destroyed prematurely. (Normally, the lifespan of RBCs is 120 days. In hemolytic anemia, they have a much shorter lifespan.) And the bone marrow (the soft, spongy tissue inside bones that makes new blood cells) simply can’t keep up with the body’s demand for new cells. This can happen for a variety of reasons. Sometimes, infections or certain medications – such as antibiotics or antiseizure medicines – are to blame.
In a condition known as autoimmune hemolytic anemia, the immune system mistakes RBCs for foreign invaders and begins destroying them. Other children inherit defects in the red blood cells that lead to anemia. Common forms of inherited hemolytic anemia include sickle cell anemia, thalassemia, and glucose-6-phosphate dehydrogenase deficiency.
- Sickle cell anemia is a severe form of anemia found most commonly in people of African heritage, although it can affect those of Caucasian, Saudi Arabian, Indian, and Mediterranean descent. In this condition, the hemoglobin forms long rods when it gives up its oxygen, stretching red blood cells into abnormal sickle shapes. This leads to premature destruction of RBCs, chronically low levels of hemoglobin, and recurring episodes of pain, as well as problems that can affect virtually every other organ system in the body. About 1 out of every 625 African-American children is born with this form of anemia
- Thalassemia, which usually affects people of Mediterranean, African, and Southeast Asian descent, is marked by abnormal and short-lived RBCs. Thalassemia major, also called Cooley’s anemia, is a severe form of anemia in which RBCs are rapidly destroyed and iron is deposited in the skin and vital organs. Thalassemia minor involves only mild anemia and minimal red blood cell changes
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency most commonly affects men of African heritage, although it has been found in many other groups of people. With this condition the RBCs either do not make enough of the enzyme G6PD or the enzyme that is produced is abnormal and doesn’t work well. When someone born with this deficiency has an infection, takes certain medicines, or is exposed to specific substances, the body’s RBCs suffer extra stress. Without adequate G6PD to protect them, many red blood cells are destroyed prematurely.
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