REFERENCES
- Adams JG, Coleman MB. Structural hemoglobin variants that produce the phenotype of thalassemia. Semin Hematol 1990; 27: 229–238
- Chui DHK, Fucharoen S, Chan V. Hemoglobin H disease: not necessarily a benign disorder. Blood 2003; 101(3)791–800
- Kanavakis E, Papassotiriou I, Karagiorgia M, Vrettou C, Metaxotou-Mavromati A, Stamoulakatou A, Kattamis C, Traeger-Synodinos J. Phenotypic and molecular diversity of Haemoglobin H disease. A Greek experience. Br J Haematol 2000; 111(3)915–923
- Traeger-Synodinos J, Papassotiriou I, Metaxotou-Mavrommati A, Vrettou C, Stamoulakatou A, Kanavakis E. Distinct phenotypic expression associated with a new hyperunstable α globin variant (Hb Heraklion, α1cd37(C2)Pro→0): comparison to other α-thalassemic hemoglobinopathies. Blood Cells Molec Dis 2000; 26(4)276–284
- Waye JS, Eng B, Patterson M, Carcao MD, Chang L, Olivieri NF, Chui DHK. Identification of two new α-thalassemia mutations in exon 2 of the α1-globin gene. Hemoglobin 2001; 25(4)391–396
- Arnon S, Tamary H, Dgany O, Litmanovitz I, Regev R, Bauer S, Dolfin T, Yacobovich J, Wolach B, Jaber L. Hydrops fetalis associated with homozygosity for Hemoglobin Taybe (α 38/39 THR deletion) in newborn triplets. Am J Hematol 2004; 76(3)263–266
- Lorey F, Charoenkwan P, Witkowska HE, Lafferty J, Patterson M, Eng B, Waye JS, Finklestein JZ, Chui DHK. Hb H hydrops foetalis syndrome: a case report and review of literature. Br J Haematol 2001; 115(1)72–78
- Papassotiriou I, Traeger-Synodinos J, Vlachou C, Karagiorga M, Metaxotou A, Kanavakis E, Stamoulakatou A. Rapid and accurate quantitation of Hb Bart's and Hb H using weak cation exchange high performance liquid chromatography: correlation with the α-thalassemia genotype. Hemoglobin 1999; 23(3)203–211
- Carrell RW. Methods of determining hemoglobin instability (unstable hemoglobins). The Hemoglobinopathies. Methods in Hematology, THJ Huisman. Churchill Livingstone, Edinburgh 1986; 15: 109–124
- Dimisianos G, Traeger-Synodinos J, Vrettou C, Papassotiriou I, Kanavakis E. A rare 33 bp in-frame deletion (α63–74 or α64–74 or α65–75) in the α1-globin gene causing α+-thalassemia: a second observation. Hemoglobin 2004; 28(2)137–143
- Traeger-Synodinos J, Kanavakis E, Tzetis M, Kattamis A, Kattamis C. Characterization of nondeletion α-thalassemia mutation in the Greek population. Am J Hematol 1993; 44(3)162–167
- Kanavakis E, Traeger-Synodinos J, Vrettou C, Maragoudaki E, Tzetis M, Kattamis C. Prenatal diagnosis of the thalassemia syndromes by rapid DNA analytical methods. Molec Hum Reprod 1997; 3(6)523–528
- Galacteros F, Girodon E, M'Rad A, Martin J, Goossens M, Jaber L, Cohen IJ, Tamary H, Goshen Y, Zaikov R, Wajcman H. Hb Taybe (α 38 or 39 THR deleted): an α-globin defect, silent in the heterozygous state and producing severe hemolytic anemia in the homozygous. CR Acad Sci Paris, Sci de la Vie/Life Sci 1994; 317(5)437–444
- Bassat B, Simjanovska L, Jaber L, Efremov GD. Hb Taybe: description of genetics and laboratory findings in an Israeli Arab family. Hemoglobin 1998; 22(2)161–166
- Pobedimskaya DD, Molchanova TP, Streichman S, Huisman THJ. Compound heterozygosity for two α-globin gene defects, Hb Taybe (α1; 38 or 39 minus Thr) and a poly A mutation (α2; AATAAA→AATAAG), results in a severe hemolytic anemia. Am J Hematol 1994; 47(3)198–202
- Oron-Karni V, Filon D, Shifrin Y, Fried E, Pogrebijsky G, Oppenheim A, Rund D. Diversity of α-globin mutations and clinical presentation of α-thalassemia in Israel. Am J Hematol 2000; 65(3)198–202