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Sickle cell disease (SCD), also simply called sickle cell, is a group of hemoglobin-related blood disorders typically inherited. The most common type is known as sickle cell anemia. It results in an abnormality in the oxygen-carrying protein haemoglobin found in red blood cells.
Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene (is heterozygous), but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele (is homozygous).
Sickle cell anemia – most common in those of African, Hispanic, and Mediterranean origin – leads to sickle cell crisis when the circulation of blood vessels is obstructed by sickled red blood cells, causing ischemic injuries. The most common complaint is of pain, and recurrent episodes may cause irreversible organ damage.
Some of these disorders are known by fanciful and cryptic names like sickle-cell anemia, thalassaemia, glucose-6-phosphate dehydrogenase deficiency, ovalocytosis, elliptocytosis and loss of the Gerbich antigen and the Duffy antigen.
The acute chest syndrome is a vaso-occlusive crisis of the pulmonary vasculature commonly seen in people with sickle cell anemia. This condition commonly manifests with a new opacification of the lung(s) on a chest x-ray.
Main symptoms that may appear in anemia The hand of a person with severe anemia (on the left, with ring) compared to one without (on the right) A person with anemia may not have any symptoms, depending on the underlying cause, and no symptoms may be noticed, as the anemia is initially mild, and then the symptoms become worse as the anemia worsens.
Hyperviscosity occurs from pathologic changes of either cellular or protein fractions of the blood such as is found in polycythemias, multiple myeloma (particularly IgA and IgG3), leukemia, monoclonal gammopathies such as Waldenström macroglobulinemia, sickle cell anemia, and sepsis.
Hemoglobin C (abbreviated as HbC) is an abnormal hemoglobin in which glutamic acid residue at the 6th position of the β-globin chain is replaced with a lysine residue due to a point mutation in the HBB gene. [1] People with one copy of the gene for hemoglobin C do not experience symptoms, but can pass the abnormal gene on to their children.
Hemoglobin variants are a part of the normal embryonic and fetal development. They may also be pathologic mutant forms of hemoglobin in a population, caused by variations in genetics. Some well-known hemoglobin variants, such as sickle-cell anemia, are responsible for diseases and are considered hemoglobinopathies.
The underlying causes of hemolytic jaundice, as its name suggests, are disorders associated with hemolysis. Such disorders are manifold and the common causes include: Blood smear of a patient with sickle cell disease. The characteristic sickle-shaped appearance of red blood cells can be observed.
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