Microcytic anemia gets its name from the presence of smaller and fewer than normal red blood cells. Macrocytic anemia, on the other hand, occurs when red blood cells are larger than normal. In most cases of microcytic anemia, the red blood cells are hypochromic, meaning they have less color than normal red blood cells. This form of anemia is quite common in teenagers and young children. It may be inherited or acquired, and iron deficiency is the most common cause.
Red blood cells deliver oxygen to all the tissues in the body using an oxygen-carrying protein called hemoglobin. Anemia occurs when the body does not have enough healthy red blood cells and therefore hemoglobin, inhibiting optimal oxygen delivery. Many compounds go into making red blood cells, including iron, folic acid, and vitamin B12, and the cells are primarily produced in the bone marrow. There are many forms of microcytic anemia, but all have the distinguishing characteristic of having smaller than normal red blood cells.
Iron deficiency hypochromic microcytic anemia results from a decreased supply of iron. Anything that reduces the body's iron stores can cause it. When not enough iron is available, the body cannot produce hemoglobin effectively. Less hemoglobin causes the red blood cells to be lighter in color and smaller in size.
Sideroblastic anemia is usually microcytic and hypochromic. In this form of microcytic anemia, the body has adequate iron stores but cannot use them properly, leading to decreased hemoglobin and abnormal red blood cells that are lighter in color and smaller in size. This condition is normally acquired, but it can be inherited. It's most common in infancy and early childhood.
Thalassemias are microcytic anemias that result from the production of defective hemoglobin. There are two forms: alpha and beta. Both are inherited. Alpha-thalassemia appears in families with Southeast Asian, Mediterranean, and African ancestry, while beta-thalassemia is common in people with Indian, Middle Eastern, Southeast Asian, and Mediterranean lineage.
Hereditary spherocytic anemia is a congenital disease associated with microcytic red blood cells. This form of anemia involves the destruction of red blood cells in the spleen. It results from mutations in five different genes, and children with the condition begin showing symptoms between ages 3 and 7. The severity of the symptoms varies.
The symptoms of anemia vary depending on the cause. Some people may have no symptoms at first but develop them as the condition worsens over time. When symptoms do appear, they can include weakness, fatigue, yellowing of the skin, shortness of breath, chest pain, headaches, cold hands and feet, and dizziness.
When diagnosing anemia, physicians usually start with a personal and family health history and a physical exam. Blood tests can confirm a low red blood cell count and hemoglobin levels. The doctor may also order tests to determine the size and shape of the red blood cells. If preliminary tests confirm anemia, the patient may need additional testing to determine the underlying cause.
Treatment of microcytic anemia depends on the cause. For example, iron deficiency anemia requires iron supplements and dietary changes. In cases of acquired microcytic anemia, the cause is identified and the trigger avoided. In severe cases of thalassemia, treatments include folic acid supplements, blood transfusions, and bone marrow transplants, but most cases are mild and do not require treatment.
Prognosis also depends on the type of microcytic anemia. For iron deficiency anemia, the prognosis is good as long as the patient addresses the underlying cause and receives treatment. Severe thalassemia can cause heart failure and early death, but mild cases do not impact the lifespan. Hereditary spherocytosis generally responds well to treatment.
If untreated, severe anemia, including microcytic anemias, can lead to oxygen deficiency in vital organs, causing complications such as heart failure. If hereditary spherocytosisis not caught early, it can cause severe anemia and even gall stones.
When the cause of acquired sideroblastic anemia is identified and treated, symptoms usually resolve; however, those who do not respond to treatment may experience early death related to iron overload from frequent blood transfusions or the development of acute leukemia.
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