Hemophilia Research Paper

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Hemophilia, also spelled as Haemophilia is a rare inherited genetic bleeding disorder. People with this condition or hemophiliacs doesn’t bleed any faster than normal, slowing down their clotting. This is because their blood lacks sufficient clotting proteins, which helps stop bleeding process following a blood draw, injury, or surgery. There are two major types of this disorder __ Hemophilia A, also known as classic hemophilia or factor VIII deficiency and Hemophilia B, also known as Christmas disease or factor IX deficiency. Severe cases of hemophilia include internal bleeding in organs, joints, muscles and even brain which could lead to acute complications. Milder forms of hemophilia does not necessary spontaneous bleeding and the condition …show more content…

Males receive X from the mother, Y from the father whereas females receives two Xs, one from each parent. Hemophilia is an X-linked or sex-linked recessive disorder where the faulty gene is located on the X chromosome. Therefore, the son inherits the defective gene from the mother and is likely to have the disease. Since the daughter inherits two Xs, it is not very likely for her to show the trait since the disorder is recessive but they will still be the carrier of hemophilia gene. In rare cases, some carriers can experience bleeding symptoms if their clotting factors are moderately decreased. In unusual situations, some people can develop hemophilia later in life which can be resolved through treatments. The affect group involves middle-aged or elderly people, or young women who have recently given birth or are in the later stages of …show more content…

Since the development of inhibitory antibodies to factor VIII is the most serious complication of replacement therapy in hemophilia A, activation of the innate immune system during exposure to this protein(in dexamethasone) contributes to prevent those inhibitors. Results shows that transient dexamethasone treatment during initial factor VIII exposure reduced the incidence of anti-factor VIII immunoglobulin G in both a conventional hemophilia A mouse and a hemophilia A mouse model. The mice that did not develop anti-factor VIII immunoglobulin G after initial exposure were less likely to develop a response after

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