Symptoms of factor V Leiden include:
What is the Treatment for Factor V Leiden ? Most people with Factor V Leiden do not form abnormal clots and require no treatment. If abnormal clots become an issue, "blood-thinning" medications, like Coumadin, can be used to impair the clotting system. This will halt growth of the clot and reduce the risk of future clots. Complications
Group 1CodeDescription81241F5 (COAGULATION FACTOR V) (EG, HEREDITARY HYPERCOAGULABILITY) GENE ANALYSIS, LEIDEN VARIANT81291MTHFR (5,10-METHYLENETETRAHYDROFOLATE REDUCTASE) (EG, HEREDITARY HYPERCOAGULABILITY) GENE ANALYSIS, COMMON VARIANTS (EG, 677T, 1298C)1 more row
2.
D68. 2 - Hereditary deficiency of other clotting factors. ICD-10-CM.
ICD-10 code D68. 9 for Coagulation defect, unspecified is a medical classification as listed by WHO under the range - Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism .
Factor V Leiden is an inherited disorder that makes blood more likely to clot. If you have this disorder you are at risk of developing blood clots, especially in your leg veins. Most people with this disorder have no problems.
Factor V deficiency is caused by a lack of factor V. When certain blood clotting factors are low or missing, your blood does not clot properly. Factor V deficiency is rare. It may be caused by: A defective factor V gene passed down through families (inherited)
Factor VII, also called proconvertin, is one such clotting factor produced by the liver. It requires vitamin K for its production. Along with other clotting factors and blood cells, it promotes blood clotting at the site of an injury. It forms normal blood clots and closes the wound to prevent blood loss.
Factor V(5) Leiden is the most common genetic condition that can lead to blood clots. Almost all people with factor V Leiden have one affected gene and one normal gene.
Abstract. Combined deficiency of vitamin K-dependent clotting factors is usually an acquired clinical problem, often resulting from liver disease, malabsorption or warfarin overdose. However, an inherited form of the disease is very rare.
Factor vii is a vitamin k dependent glycoprotein essential to the extrinsic pathway of coagulation.
A blood coagulation disorder characterized by the complete absence of fibrinogen in the blood, resulting in bleeding. A deficiency of blood coagulation factor v (known as proaccelerin or accelerator globulin or labile factor) leading to a rare hemorrhagic tendency known as owren's disease or parahemophilia.
The 2022 edition of ICD-10-CM D68.2 became effective on October 1, 2021.
A usually inherited blood coagulation disorder characterized by the partial or complete absence of fibrinogen in the blood, resulting in bleeding. A very rare autosomal recessive inherited blood coagulation disorder characterized by deficiency of factor v, resulting in bleeding.
Factor V leiden is also known as activated Protein C resistance, anticardiolipin syndrome, antiphospholipid syndrome, antiphospholipid syndrome complication in pregnancy, antiphospholipid syndrome in pregnancy, antiphospholipid syndrome postpartum, antithrombin 3 deficiency, antithrombin III deficiency, factor 5 Leiden mutation, factor 5 Leiden mutation heterozygous, factor 5 Leiden mutation homozygous, factor V Leiden mutation, factor V Leiden mutation heterozygous, factor V Leiden mutation homozygous, hereditary antithrombin III deficiency, hereditary heparin cofactor II deficiency, hereditary protein C deficiency, hereditary protein S deficiency, hereditary thrombophilia, heterozygous Factor V Leiden mutation, heterozygous protein C deficiency, heterozygous protein S deficiency, heterozygous prothrombin G20210A mutation, homozygous Factor V Leiden mutation, homozygous protein C deficiency, homozygous protein S deficiency, homozygous prothrombin G20210A mutation, hypercoagulability state, hypercoagulable state, hypercoagulable state (tendency to form clots), hypercoagulable state primary, lupus anticoagulant, lupus anticoagulant disorder, postpartum (after childbirth) antiphospholipid syndrome, postpartum antiphospholipid syndrome, protein C deficiency disease, protein C deficiency disorder, protein C resistance, protein S deficiency disease, protein S deficiency disorder, prothrombin G20210A mutation, prothrombin gene mutation, resistance to activated protein C due to Factor V Leiden, thrombophilia due to acquired antithrombin III deficiency, thrombophilia due to acquired protein C deficiency, thrombophilia due to acquired protein S deficiency, thrombophilia due to antiphospholipid antibody, and upper gastrointestinal hemorrhage associated with hypercoagulability state.
Factor V leiden is a mutation in the clotting factor V in the blood. This mutation greatly increases a persons chance of developing blood clots in veins. Men and women are equally affected by this mutation.
Factor V Leiden ( rs6025 or F5 p.R506Q) is a variant (mutated form) of human factor V (one of several substances that helps blood clot), which causes an increase in blood clotting ( hypercoagulability ). Due to this mutation, protein C, an anticoagulant protein which normally inhibits the pro-clotting activity of factor V, ...
Factor V Leiden is the most common hereditary hypercoagulability (prone to clotting) disorder amongst ethnic Europeans. It is named after the Dutch city of Leiden, where it was first identified in 1994 by Rogier Maria Bertina under the direction of (and in the laboratory of) Pieter Hendrick Reitsma.
When factor V remains active, it facilitates overproduction of thrombin leading to generation of excess fibrin and excess clotting. The excessive clotting that occurs in this disorder is almost always restricted to the veins, where the clotting may cause a deep vein thrombosis (DVT).
In the normal pathway, factor V functions as a cofactor to allow factor Xa to activate prothrombin, resulting in the enzyme thrombin . Thrombin in turn cleaves fibrinogen to form fibrin, which polymerizes to form the dense meshwork that makes up the majority of a clot. Activated protein C is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V.
The presence of acquired risk factors for venous thrombosis—including smoking, use of estrogen-containing (combined) forms of hormonal contraception, and recent surgery —further increase the chance that an individual with the factor V Leiden mutation will develop DVT.
Studies have found that about 5 percent of Caucasians in North America have factor V Leiden. Data have indicated that prevalence of factor V Leiden is greater among Caucasians than minority Americans.
As there is no cure yet, treatment is focused on prevention of thrombotic complications. Anticoagulants are not routinely recommended for people with factor V Leiden, unless there are additional risk factors present, but are given when such an event occurs. A single occurrence of deep vein thrombosis or pulmonary embolism in people with factor V Leiden warrants temporary anticoagulant treatment, but generally not lifelong treatment. In addition, temporary treatment with an anticoagulant such as Heparin may be required during periods of particularly high risk of thrombosis, such as major surgery.