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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 association with kidney and lung infarcts was noted in 1931 by Yater and Mollari and Baird in 1934 respectively. The term sickle-cell trait was coined by Samuel Diggs in Memphis in 1933 to distinguish heterozygotes from those with sickle-cell anaemia. Diggs also reported the association with splenic fibrosis in 1935.
Sickle cell disease, in which a mutation in the globin gene causes the formation of sickle hemoglobin. [2] This disease is marked by the manifestation of chronic compensated hemolytic anemia , with laboratory findings not limited to unconjugated hyperbilirubinemia but also elevated serum lactate dehydrogenase and low serum haptoglobin .
When Hemoglobin O-Arab co-inherits with Hemoglobin S, it produces a syndrome with similarities in severity to sickle cell anaemia, [1] having severe haemolytic anaemia and red cells denser than normal with occurrences of some cells as dense as if contract with sickle cell anaemia. A description with the presence of two variations of β-globin ...
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.
Due to underlying diseases that destroy the spleen (autosplenectomy), e.g. sickle-cell disease. Celiac disease: unknown physiopathology. [6] In a 1970 study, [7] it was the second most common cause of abnormalities of red blood cells linked to hyposplenism, after surgical splenectomy.
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