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Proliferative sickle retinopathy is the most severe ocular complication of sickle cell disease. Even though PSCR begins in the first decade of life, the condition remains asymptomatic and unnoticed until visual symptoms occur due to vitreous hemorrhage or retinal detachment.
A similar relationship exists between malaria and sickle-cell disease. One theory to explain this is that cells infected with the Plasmodium parasite are cleared more rapidly by the spleen . This phenomenon might give G6PD deficiency carriers an evolutionary advantage by increasing their fitness in malarial endemic environments.
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.
The discovery that hemoglobin F alleviated the symptoms of sickle cell disease occurred in 1948. Janet Watson observed that red blood cells from infants with the disease took longer to sickle and did not deform as much compared to their mother's cells, which carried the disease trait.
A single point mutation in this polypeptide chain, which is 147 amino acids long, results in the disease known as Sickle Cell Anemia. [18] Sickle-cell anemia is an autosomal recessive disorder that affects 1 in 500 African Americans, and is one of the most common blood disorders in the United States. [17]
With HbS, there can be mild sickle cell trait but no symptoms. [13] [14] Hemoglobin O-Arab causes sickle cell disease in heterozygous (HbS/HbO) individuals. However, the symptomatic anemia is mild and is not life-threatening. It is even milder than in heterozygous sickle cell trait (HbS/HbA). [15] A case of sickle cell retinopathy is documented ...
Scientists at Weill Cornell Medical College have developed a gene therapy strategy that could feasibly treat both beta-thalassemia and sickle cell disease. The technology is based on delivery of a lentiviral vector carrying both the human β-globin gene and an ankyrin insulator to improve gene transcription and translation, and boost levels of ...
Tay–Sachs disease is a genetic disorder that results in the destruction of nerve cells in the brain and spinal cord. [1] The most common form is infantile Tay–Sachs disease, which becomes apparent around the age of three to six months of age, with the baby losing the ability to turn over, sit, or crawl. [1]