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A well-studied case is that of sickle cell anemia in humans, a hereditary disease that damages red blood cells. Sickle cell anemia is caused by the inheritance of an allele (HgbS) of the hemoglobin gene from both parents. In such individuals, the hemoglobin in red blood cells is extremely sensitive to oxygen deprivation, which results in ...
Hakulinen E (March 1990). "The man behind the syndrome. James B Herrick: the discoverer of sickle cell anemia. His first case report received scant interest--only in the 1950s was the role of "moon-crescent" shape considered" [The man behind the syndrome. James B Herrick: the discoverer of sickle cell anemia.
Microcytic anaemia; Microcytosis is the presence of red cells that are smaller than normal. Normal adult red cell has a diameter of 7.2 µm. Microcytes are common seen in with hypochromia in iron-deficiency anaemia, thalassaemia trait, congenital sideroblastic anaemia and sometimes in anaemia of chronic diseases.
Voxelotor has been shown to have disease-modifying potential by increasing hemoglobin levels and decreasing hemolysis indicators in sickle cell patients. [8] It has a safe profile in sickle cell patients and healthy volunteers, without any dose-limiting toxicity. [9] It was developed by Global Blood Therapeutics, a subsidiary of Pfizer. [10]
Diamond–Blackfan anemia (DBA) is a congenital erythroid aplasia that usually presents in infancy. [3] DBA causes low red blood cell counts (), without substantially affecting the other blood components (the platelets and the white blood cells), which are usually normal.
Although their conclusions surrounding the disease are outdated, Doctors Taliaferro and Huck discovered a latent form of sickle cell anemia. Their study on sickle cell anemia was the first of many to occur at Hopkins. In 1940, Irving Sherman, a medical student at Johns Hopkins, correctly identified the deoxygenation of hemoglobin in sickle cell ...
It is possible for a person to have both the gene for hemoglobin S (the form associated with sickle cell anemia) and the gene for hemoglobin C; this state is called hemoglobin SC disease, and is generally more severe than hemoglobin C disease, but milder than sickle cell anemia. [2]
The underlying cause of sickle cell anemia is the synthesis of aberrant hemoglobin, which attaches to other aberrant hemoglobin molecules inside the red blood cell to undergo rigid deformation. [18] Sickle cell anemia symptoms usually appear around the age of six months. They can change over time and differ from person to person.