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Patients with beta thalassemia minor are usually asymptomatic and are often monitored without treatment. [8] Beta thalassemia minor may coexist with other conditions such as chronic hepatitis B , chronic hepatitis C , non-alcoholic fatty liver disease and alcoholic liver disease that, when combined or co-existing, may cause a person to have ...
β thalassemia minor is caused by a β/β o or β/β + genotype. Only one of the two β globin alleles contains a mutation, so β chain production is not terribly compromised and patients may be relatively asymptomatic. Beta thalassemia most often occurs in people of Mediterranean origin.
Beta thalassemia is an inherited genetic mutation in one (Beta thalassemia minor) or both (Beta thalassemia major) of the Beta globin alleles on chromosome 11. The mutant alleles are subdivided into two groups: β0, in which no functional β-globin is made, and β+, in which a small amount of normal β-globin protein is produced.
Normal levels range from 2.1-3.2%, but in the beta-thalassemia disorder, the levels increase to 3.5-6.0%. Additionally, individuals with beta-thalassemia exhibit a high red cell count and low hemoglobin levels. [3] Individuals that express lower levels of hemoglobin A2, have the a 0-thalassemia trait or homozygous gene for a +-thalassemia. [2]
The Mentzer index, described in 1973 by William C. Mentzer, [1] is the MCV divided by the RBC count. It is said to be helpful in differentiating iron deficiency anemia from beta thalassemia trait.
Hb S beta thalassemia is the least common and is experienced in patients who have inherited beta thalassemia hemoglobin from one parent and HbS from the other. [17] In addition, there is sickle cell trait (HbAS) which is defined by having HbA and HbS. This makes the individual heterozygous for sickle cell.
Administration of the gene-editing therapy is complicated, but it cures two rare blood disorders -- sickle cell disease and transfusion-dependent beta thalassemia.
Dietary indicaxanthin has been shown to have protective effects on RBCs in people with beta thalassemia. [26] It has a structure similar to that of amino acids, and is amphiphilic: it is able to bind to cell membranes through charge-related interactions with polar head groups of membrane constituents, as well through adsorption to the lipid ...
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