Hemoglobin failure, or abnormal hemoglobin (such as that of sickle-cell disease). The ability of each hemoglobin molecule to carry oxygen is normally modified by altered blood pH or CO, causing an altered oxygen–hemoglobin dissociation curve. However, it can also be pathologically altered in, e.g., carbon monoxide poisoning. Decrease of hemoglobin, with or without an absolute decrease of red blood cells, leads to symptoms of anemia. Anemia has many different causes, although iron deficiency and its resultant iron deficiency anemia are the most common causes in the Western world. As absence of iron decreases heme synthesis, red blood cells in iron deficiency
Fetal hemoglobin is encoded on chromosome 11, as is the beta subunit. There are two similar copies of the gamma subunit gene: γG which has a glycine at position 136, and γA which has an alanine. The gene that codes for the alpha subunit is located on chromosome 16 and is also present in duplicate. When fetal hemoglobin production is switched off after birth, normal children begin producing adult hemoglobin (HbA). Children with sickle-cell disease instead begin producing a defective form of hemoglobin called hemoglobin S which aggregates together and forms filaments that cause red blood cells to change their shape from