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β thalassemia major (Mediterranean anemia or Cooley anemia) is caused by a β o /β o genotype. No functional β chains are produced, and thus no hemoglobin A can be assembled. This is the most severe form of β-thalassemia. β thalassemia intermedia is caused by a β + /β o or β + /β + genotype. In this form, some hemoglobin A is produced.
The prevalence of Hemoglobin H disease mirrors that of the hemoglobinopathies. As a whole, they are most prevalent in individuals of Asian, African, and Mediterranean decent. [ 5 ] There is a protective effect against malaria for individuals carrying thalassemia genes, which explains the high frequency of thalassemia within the worldwide ...
Alpha thalassemia is has greatest prevalence in populations originating from Southeast Asia, Mediterranean countries, Africa, the Middle East, India, and Central Asia. [7] Having a mild form of alpha thalassemia has been demonstrated to protect against malaria and thus can be an advantage in malaria endemic areas. [12]
"Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013" 2013: May 2014: The Lancet "Population health and burden of disease profile of Iran among 20 countries in the region: from Afghanistan to Qatar and Lebanon" 2010: May 2014
Beta-thalassemia; Other names: Microcytemia, beta type [1] Beta thalassemia genetics, the picture shows one example of how beta thalassemia is inherited. The beta globin gene is located on chromosome 11. A child inherits two beta globin genes (one from each parent). Specialty: Hematology: Types: Thalassemia minor, intermediate and major [2] Causes
Thalassemia prevalence in India is 3-4%, with 10,000 to 12,000 reported thalassemia births taking place every year. It is also estimated that there are 30 million thalassemia carriers in the country. With NAT tested blood, these patients live longer and maintain their quality of life.
Therefore, most transfusion-dependent thalassemia patients can be diagnosed within the first few years of life, which severe anemia, differed growth, jaundice and hepatosplenomegaly can be observed. Parameters for confirmation includes baseline hemoglobin level <7g/dL, enlargement of liver and spleen (>5 cm) and height in the first 10th percentile.
Patient may present with symptomatic anemia or with sickle crises. In the United States and other countries with new-born screening programs, the disease may be identified in neonates. [4] Diagnostic tests include DNA sequencing, hemoglobin electrophoresis, and high-performance liquid chromatography. [5]