What Are The Causes Of Hemophilia – Recent evidence has shown that B hemangiomas are less severe than A hemangiomas in the clinic, suggesting the need to discuss more therapeutic options for various hemangiomas.
“Hemophilia B is not more severe than hemophilia A in the clinic: further evidence,” in Transfusion.
What Are The Causes Of Hemophilia
Hemophilia is an inherited, genetic disease that affects the body’s platelets, the process that stops bleeding. The disease can present in two forms, hemangioma A or B, respectively, and may be caused by genetic mutations in the genes encoding factors VIII (FVIII) and IX (FIX).
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The prevalence of hemangioma is 1 in 5,000 men in the general population, and hemangioma is 1 in 40,000. Moderate hemangioma is characterized by plasma factors between 1-5 IU/dL. and more than 5 IU/dL indicates mild atherosclerosis
People with mild hemophilia may bleed profusely after surgery, tooth extraction, or major trauma. People with mild anemia bleed after minor trauma, while people with severe anemia bleed spontaneously or due to minor trauma.
As a result, severe arthrosis can include life-threatening symptoms such as arteriosclerosis (pain in one joint and swelling caused by bleeding into the joint). soft tissue bleeding retroperitoneal (the anatomic space in the abdominal cavity, the membrane that lines the abdominal cavity) and intracerebral hemorrhage and postoperative hemorrhage;
Hemophilia A and B are generally considered clinically distinct, and the authors of this study demonstrate that severe hemophilia B may be clinically more severe than hemophilia B.
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One of the highlights is the genetic mutation, which is known to be the most important factor in the severity of atherosclerosis: the type of mutation: in severe aneurysm A (80%), null mutations occur, but silent mutations are common. B in severe atherosclerosis (about 60%). Here, the authors present a study establishing an association between non-null mutations in severe hemangioma and a milder clinical phenotype.
Another point made by the authors is that a recent report showed that patients with anemia B had a higher rate of ischemic stroke (HSS) than patients with hemophilia B, and a Canadian study found that patients with hemophilia B had less than those with anemia. It will be. Patients. Patients with hemophilia A, another Italian study, found that patients with hemophilia A had lower bleeding and World Federation of Hemophilia ultrasonography scores.
Clinical trials examining long-acting FVIII and FIX products also found lower bleeding rates (annualized bleeding rate, ABR) over 12 years in patients with B-cell disease.
There is evidence to suggest that patients with B hematuria use fewer FIX-based transplants per year.
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The authors believe that, although it is not yet clear, increasing evidence suggests that severe aneurysm B may be clinically more severe than aneurysm A. FIX is missing
Patricia Inacio, PhD Patricia received her PhD in Cell Biology from Universidad Nova de Lisboa in Portugal and has conducted several research projects and collaborations for European institutions. He also worked as a postdoctoral research assistant in the Department of Microbiology and Immunology at Columbia University, New York, for which he received a Luso-American Foundation for Development (FLAD) award. Hemophilia is a genetic disease that affects the blood cells. The two most common forms are hemangioma A and hemangioma B. Although the causes are different, the main effect is the same: hemangiomas bleed longer than normal people.
Untreated strokes are dangerous. This puts people at risk of spontaneous bleeding, which is difficult to stop.
There is no cure for hemangiomas, but there are effective treatments for hemangiomas, and when hemangiomas are detected early and treated appropriately, long-term health outcomes are usually excellent. Anemia is also possible without a family history. Blood tests are done in newborns and later in people with bleeding problems.
Bleeding Disorders Deficiency Of Any Of The Clotting Factors Leads To Excessive Bleeding Most Common And Important Bleeding Disorders Are Due Vitamin K.
Factor VIII and factor IX are two of the 13 coagulation factors in blood that form a signaling chain. A cut or other injury triggers a signal that results in the formation of a hard clot that seals the wound and stops bleeding. If factor VIII or factor IX is not working, the blood does not clot properly
Haemophilia A and B are caused by mutations in two different genes: For A blood cells, the affected gene is F8 For B blood cells, F9 Both genes code for a protein called coagulation factor VIII (eight) on the X chromosome. Protein Coagulation Factor FX Code (Nine).
Factor VIII, factor IX, and other coagulation factors become proteins in the blood. After injury, the sleep factor is activated in the area through a chain reaction, the factors together signal. In the final step, the signal binds the protein and the blood cell together, forming a blood clot sealed with the blood cell. The bleeding stops and healing begins
Because the F8 and F9 genes are on the X chromosome, the syndrome is inherited differently in males and females (see Inheritance). As long as a person has one working copy (allele) of the F8 and F9 genes, they have normal blood.
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People with hemophilia only have a null allele of the F8 or F9 gene, meaning they lose the coagulation factor VIII or IX protein. Either way, the clotting factor signaling chain is interrupted or weakened, in some cases the protein is less than normal, in others none at all. Blood Does Not Clot Without blood clots, the wound does not seal and the person continues to bleed
Bleeding disorders due to other clotting factors such as I, II, V, VII, X, XI, XII, and XIII also occur. These cases are extremely rare, mainly because the genes for these proteins are not on the sex chromosome, but on their own. Only one affected allele is needed to cause A or B (at least for males) anemia, but it usually takes two to cause defects in other coagulation factors. This disorder affects men and women equally. For more information, visit the National Vascular Foundation
Because the F8 and F9 genes are on the X chromosome, they are different from males and females. Boys inherit only one X chromosome from their mother and girls inherit one X chromosome from each parent
In terms of genetic disorders, anemia follows an X-linked recessive pattern of inheritance. Boys with hemangioma inherit a single, inactive allele of F8 or F9 from their mother. It takes two dysfunctional alleles for a girl to have hemangioma, and she inherits it from her mother (she’s usually a carrier). A daughter’s second defective allele comes from her father, who has sperm that has the disease or causes the new mutation.
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In terms of proteins, clotting factors are made from each individual’s allele.
Hemophilia was once common in European royalty, with Queen Victoria of Great Britain carrying blood type B and passing it on to many of her children.
Girls and boys inherit different numbers of X chromosomes Parents get one X chromosome from each parent Boys inherit only one X chromosome from their mother
Proteins VIII and IX are made primarily in the liver and remain inactive in blood tissues until they are activated by injury
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The F8 and F9 genes are mainly activated in liver cells, while F8 is also activated in cells in the spleen and lymph nodes
Hepatocytes make most of the body’s factor VIII protein and almost all its factor IX. But proteins don’t normally stay in the liver. They’re released into other tissues—the blood.
When blood vessels are damaged, molecules leak into the blood, where they wouldn’t normally be there. First, some nearby platelets (a type of blood cell) activate and adhere to the injury.
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