How is beta-thalassemia characterized?

How is beta-thalassemia characterized?

• A. Excess production of alpha globin chains
• B. A reduction in beta globin chain production
• C. High levels of vitamin K
• D. Increased red blood cell size

Answer: (B)

Beta-thalassemia is characterized by a reduction in the production of beta globin chains, which are essential components of hemoglobin in red blood cells. This decreased synthesis leads to an imbalance in globin chain production, resulting in an excess of alpha globin chains relative to beta globin chains. The accumulation of unpaired alpha chains causes damage to red blood cell precursors in the bone marrow and leads to ineffective erythropoiesis, contributing to anemia. This condition can lead to various clinical manifestations, including fatigue, pallor, splenomegaly, and complications related to iron overload due to increased intestinal absorption of iron as a compensatory mechanism for the anemia. Management often involves regular blood transfusions, iron chelation therapy, and sometimes hematopoietic stem cell transplantation. In contrast, the other options do not accurately represent the defining characteristics of beta-thalassemia. For example, excessive production of alpha globin chains occurs as a consequence of reduced beta chains, rather than being a primary characteristic of the disease. Similarly, high levels of vitamin K are not directly related to beta-thalassemia, and increased red blood cell size is typically associated with other conditions, such as macrocytic anemia, rather than the micro

Beta-thalassemia is characterized by a reduction in the production of beta globin chains, which are essential components of hemoglobin in red blood cells. This decreased synthesis leads to an imbalance in globin chain production, resulting in an excess of alpha globin chains relative to beta globin chains. The accumulation of unpaired alpha chains causes damage to red blood cell precursors in the bone marrow and leads to ineffective erythropoiesis, contributing to anemia.

This condition can lead to various clinical manifestations, including fatigue, pallor, splenomegaly, and complications related to iron overload due to increased intestinal absorption of iron as a compensatory mechanism for the anemia. Management often involves regular blood transfusions, iron chelation therapy, and sometimes hematopoietic stem cell transplantation.

In contrast, the other options do not accurately represent the defining characteristics of beta-thalassemia. For example, excessive production of alpha globin chains occurs as a consequence of reduced beta chains, rather than being a primary characteristic of the disease. Similarly, high levels of vitamin K are not directly related to beta-thalassemia, and increased red blood cell size is typically associated with other conditions, such as macrocytic anemia, rather than the micro