Hemoglobin D | |
---|---|
Specialty | Hematology |
Symptoms | HbD/HbA asymptomatic; HbD/HbD mild hemolytic anemia; HbD/HbS sickle cell anemia; HbD/Hb-thalassemia thalassemia |
Causes | Point mutation in HBB gene |
Treatment | Not required |
Hemoglobin D (HbD) is a variant of hemoglobin, a protein complex that makes up red blood cells. Based on the locations of the original identification, it has been known by several names such as hemoglobin D-Los Angeles, hemoglobin D-Punjab,[1] D-North Carolina, D-Portugal, D-Oak Ridge, and D-Chicago.[2] Hemoglobin D-Los Angeles was the first type identified by Harvey Itano in 1951, and was subsequently discovered that hemoglobin D-Punjab is the most abundant type that is common in the Sikhs of Punjab (of both Pakistan and India) and of Gujarat.[3]
Unlike normal adult human hemoglobin (HbA) which has glutamic acid at its 121 amino acid position, it has glutamine instead.[4] The single amino acid substitution can cause various blood diseases, from fatal genetic anemia to mild hemolytic anemia, an abnormal destruction of red blood cells.[5] Depending on the type of genetic inheritance, it can produce four different conditions:[4] heterozygous (inherited in only one of the chromosome 11) HbD trait, HbD-thalassemia, HbS-D (sickle cell) disease, and, very rarely, homozygous (inherited in both chromosome 11) HbD disease.[6] It is the fourth hemoglobin type discovered after HbA, HbC and HbS;[1] the third hemoglobin variant identified after HbC and HbS;[2] and the fourth most common hemoglobin variant after HbC, HbS, and HbO.[5]