TAILIEUCHUNG - Chapter 099. Disorders of Hemoglobin (Part 4)

Epidemiology Hemoglobinopathies are especially common in areas in which malaria is endemic. This clustering of hemoglobinopathies is assumed to reflect a selective survival advantage for the abnormal RBC, which presumably provide a less hospitable environment during the obligate RBC stages of the parasitic life cycle. Very young children with αthalassemia are more susceptible to infection with the nonlethal Plasmodium vivax. Thalassemia might then favor a natural protection against infection with the more lethal P. falciparum. Thalassemias are the most common genetic disorders in the world, affecting nearly 200 million people worldwide. About 15% of American blacks are silent carriers for α. | Chapter 099. Disorders of Hemoglobin Part 4 Epidemiology Hemoglobinopathies are especially common in areas in which malaria is endemic. This clustering of hemoglobinopathies is assumed to reflect a selective survival advantage for the abnormal RBC which presumably provide a less hospitable environment during the obligate RBC stages of the parasitic life cycle. Very young children with athalassemia are more susceptible to infection with the nonlethal Plasmodium vivax. Thalassemia might then favor a natural protection against infection with the more lethal P. falciparum. Thalassemias are the most common genetic disorders in the world affecting nearly 200 million people worldwide. About 15 of American blacks are silent carriers for a thalassemia a-thalassemia trait minor occurs in 3 of American blacks and in 1-15 of persons of Mediterranean origin. B-Thalassemia has a 10-15 incidence in individuals from the Mediterranean and Southeast Asia and in American blacks. The number of severe cases of thalassemia in the United States is about 1000. Sickle cell disease is the most common structural hemoglobinopathy occurring in heterozygous form in 8 of American blacks and in homozygous form in 1 in 400. Between 2 and 3 of American blacks carry a hemoglobin C allele. Inheritance and Ontogeny Hemoglobinopathies are autosomal co-dominant traits compound heterozygotes who inherit a different abnormal mutant allele from each parent exhibit composite features of each. For example patients inheriting sickle 0-thalassemia exhibit features of 0-thalassemia and sickle cell anemia. The a-chain is present in HbA HbA2 and HbF a-chain mutations thus cause abnormalities in all three. The a-globin hemoglobinopathies are symptomatic in utero and after birth because normal function of the a-globin gene is required throughout gestation and adult life. In contrast infants with 0-globin hemoglobinopathies tend to be asymptomatic until 3-9 months of age when HbA has largely replaced HbF. .

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