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Des-gamma carboxyprothrombin (DCP), also known as protein induced by vitamin K absence/antagonist-II (PIVKA-II), is an abnormal form of the coagulation protein, prothrombin. Normally, the prothrombin precursor undergoes post-translational carboxylation (addition of a carboxylic acid group) by gamma-glutamyl carboxylase in the liver prior to ...
Vitamin K should be taken orally unless the patient has cirrhosis or biliary obstruction, in which case it should be administered subcutaneously. The full effect of vitamin K is not obtained for 12–24 hours, unlike fresh frozen plasma which immediately reverses clotting abnormalities. The intravenous formulation of vitamin K reverses ...
The treatment of chronic liver disease depends on the cause. Specific conditions may be treated with medications including corticosteroids, interferon, antivirals, bile acids or other drugs. Supportive therapy for complications of cirrhosis include diuretics, albumin, vitamin K, blood products, antibiotics and nutritional
Vitamin K2 (menaquinone): Vitamin K2 supports bone and heart health. Fermented foods are excellent sources of it. Fermented foods are excellent sources of it. When we don't get enough vitamin K ...
Vitamin K is a family of structurally similar, fat-soluble vitamers found in foods and marketed as dietary supplements. [1] The human body requires vitamin K for post-synthesis modification of certain proteins that are required for blood coagulation ("K" from Danish koagulation, for "coagulation") or for controlling binding of calcium in bones and other tissues. [2]
Research has shown the pivotal role of the stellate cell, that normally stores vitamin A, in the development of cirrhosis. Damage to the liver tissue from inflammation leads to the activation of stellate cells, which increases fibrosis through the production of myofibroblasts, and obstructs hepatic blood flow. [59]
The prothrombin time can be prolonged as a result of deficiencies in vitamin K, warfarin therapy, malabsorption, or lack of intestinal colonization by bacteria (such as in newborns). In addition, poor factor VII synthesis (due to liver disease ) or increased consumption (in disseminated intravascular coagulation ) may prolong the PT.
Vitamin K is changed to its active form in the liver by the enzyme Vitamin K epoxide reductase. Activated vitamin K is then used to gamma carboxylate (and thus activate) certain enzymes involved in coagulation: Factors II, VII, IX, X, and protein C and protein S. The inability to activate the clotting cascade via these factors leads to the ...
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