Abstract
M ost a-thalassemia variants (Table 1) arise from deletions of one or more of the four normal cu-glohin genes ((Y(Y/(Y(Y).‘-~ The more severe cr,-thalassemia syndromes are prevalent only among the populations from Southeast Asia (SEA): Southern China, Burma, Indochina, Thailand, Malaysia, Indonesia, and the Philippines.“.’ Homozygous c-w,-thalassemia (--/--), causes lethal hydrops fetalis with Barts hemoglohinopathy (Fig l), and threatens serious obstetric complications.8-‘0 Triple deletion (--/-a) hemoglobin (Hh) H disease causes a moderate microcytic hemolytic anemia, hut the compound heterozygotes for HhH/Constant Spring (--/(u”“(u) tend to he more severe.‘*““-‘” Heterozygous (pithalassemia (--/a~) double deletions and homozygous (-cu/-cr) single deletion Lu,-thalassemia produce asymptomatic microcytic anemias. Iieterozygous (-(Y/LY(Y) a2-thalassemias overlap both normals and a,-thalassemia heterozygotes. o(~Thalassemia variants occur in many other parts of the world; they significantly alter clinical manifestations of the sickle cell diseases.’
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