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August 01, 2015  
EDUCATION CENTER: Clinical Overview

Clinical Overview
Definition
Symptoms Diagnosis and Treatment

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  • Thalassemia

    Clinical Overview
    Thalassemia, from the Greek meaning “blood from the sea,” is the term used to describe a group of genetic blood disorders. Thalassemia is caused by a defect in the body’s normal rate of production of hemoglobin, the oxygen-bearing part of your red blood cells. Two major types of thalassemia exist: thalassemia minor and thalassemia major, also called Cooley’s Anemia. Thalassemia minor is more common and mild than thalassemia major, which can be a serious medical condition.

    More than 300,000 people worldwide have thalassemia. It is regarded as the most common inherited genetic blood disorder in the world. In addition, more than 2 million Americans are carriers of the thalassemia trait. Thalassemia is found most often among people of Italian, Greek, Chinese, Southeast Asian, and Middle Eastern backgrounds.

    Two parents who both carry the same thalassemia genetic trait have a 25 percent chance of having a child born with thalassemia.

    Hemoglobin comprises two proteins, alpha and beta globins. If you cannot properly produce one of the two due to your genetic disposition, your red blood cells cannot form and carry sufficient oxygen throughout your system. The condition that results is thalassemia, a type of anemia that lasts a lifetime.

    Thalassemia minor is defined by a lack of beta protein. People with this condition carry the genetic trait for thalassemia and usually experience no health problems due to the disease, other than mild anemia. In many cases, it is diagnosed as iron-deficient anemia. However, treating it with iron supplements will have no effect.

    Thalassemia major, Cooley’s Anemia, is the most severe form of thalassemia known. The patient suffers from a complete lack of beta protein in the hemoglobin, which results in a life-threatening anemia. Patients with Cooley’s Anemia require lifelong medical care.

    Last updated: Feb-23-07

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