Kan Y W, Dozy A M, Trecartin R, Todd D
N Engl J Med. 1977 Nov 17;297(20):1081-4. doi: 10.1056/NEJM197711172972002.
The molecular defect that has been demonstrated in alpha-thalassemia is the deletion of the alpha-globin structural genes. Since thalassemias are composed of heterogeneous groups of disorders, other types of defects could also result in alpha-thalassemia. We studied a Chinese family in which analysis of the mode of inheritance of alpha-thalassemia-1 and hemoglobin-H disease suggests a lesion that is not due to structural-gene deletion. Molecular hybridization studies with synthetic radioactive DNA's complementary to alpha-globin mRNA sequences show that in addition to the usual deletion defect, a nondeletion defect produces the phenotype of alpha-thalassemia-1. The combination of the deletion and non-deletion defects results in hemoglobin-H disease and not homozygous alpha-thalassemia associated with hydrops fetalis.
已在α地中海贫血中证实的分子缺陷是α珠蛋白结构基因的缺失。由于地中海贫血由多种异质性疾病组成,其他类型的缺陷也可能导致α地中海贫血。我们研究了一个中国家庭,对该家庭中α地中海贫血-1和血红蛋白H病的遗传方式分析表明,存在一种并非由结构基因缺失引起的病变。用与α珠蛋白mRNA序列互补的合成放射性DNA进行分子杂交研究表明,除了常见的缺失缺陷外,一种非缺失缺陷也会产生α地中海贫血-1的表型。缺失缺陷和非缺失缺陷的组合导致血红蛋白H病,而非与胎儿水肿相关的纯合子α地中海贫血。