<unk>  is typically an asymptomatic<unk> opathy, which is caused by an autosomal recessive genetic mutation. The Hb<unk>  variant, consisting of two normal alpha globin chains (HBA) and two delta-beta globin fusion chains which occurs due to a "crossover" between the delta (HBD) and beta globin (HBB) gene loci during meiosis and was first identified in the<unk>  family, an Italian-American family, in 1958. There are three varieties of Hb<unk> , Washington (Hb<unk>  Washington, AKA Hb<unk>  Boston or Hb<unk>  Washington-Boston), Baltimore (Hb<unk>  Baltimore) and Hollandia (Hb Hollandia). All three varieties show similar electrophoretic and chromatographic properties and hematological findings bear close resemblance to those of the beta-thalassemia trait; a blood disorder that reduces the production of the iron-containing protein<unk>  which carries oxygen to cells and which may cause anemia. The homozygous state for Hb<unk>  is rare. Patients of Balkan descent tend to have the most severe presentation of symptoms including severe anemia during the first five years of life. They also presented with significant splenomegaly, hepatomegaly, and skeletal abnormalities identical to those of homozygous beta-thalassemia. The amount of Hb<unk>  in the patients blood ranged from 8 to 30%, the remainder being fetal<unk>  (Hb F) which is present in minute quantities (typically<1 percent) in the red blood cells of adults. Known as F- cells they are present in a small proportion of overall RBCs. Homozygous Hb<unk>  is similar to beta-thalassemia major; however, the clinical course is variable. Patients with this condition typically present with severe anemia during the first two years of life. The heterozygote form is mildly anemic (Hb 11–13 g/dl) but presents with a significant hypochromia (deficiency of<unk>  in the red blood cells) and microcytosis.
Hemoglobin Lepore syndrome
Freeman–Sheldon syndrome
3-M syndrome
Sick cell syndrome
Beta thalassemia
Hughes–Stovin syndrome
Fryns-Aftimos syndrome
Diamond–Blackfan anemia