Factor XIII, an enzyme that cross-links fibrin, belongs to the blood coagulation system. [ 1, 2] Screening for factor XIII, also known as fibrin-stabilizing BACKGROUND: Coagulation factor XIII deficiency, in either its acquired or inherited form, is a rare cause of abnormal bleeding. In patients with Factor XIII (F XIII) deficiency, recommended means of factor replacement include infusion of fresh frozen plasma (FFP), cryoprecipitated plasma (Cryo), or F XIII concentrates [HOST]isons of F FXIII-A > % proved to be an independent risk factor for disease progression in NSCLC patients (OR=, 95% CI: , p = ), predicting poor efficacy. The marked decrease in plasma FXIII-A (FXIII-A coagulation disorders and poor prognosis with a short survival time (median survival
Coagulation factor XIII activity predicts left ventricular …
Factor XIII (FXIII) deficiency is a rare congenital bleeding disorder estimated to affect 1 in 2 million live births. Treatment often involves prophylaxis with FXIII concentrate and is especially important in preventing intracranial hemorrhage (ICH) and maintaining pregnancy in women of childbearing age. The rarity of this condition and lack of Introduction. Congenital factor XIII (FXIII) deficiency is chiefly caused by mutations in the F13A gene (95% of cases) and, more rarely, by F13B gene defects (5% of cases). The F13A gene, coding for the FXIII A protein subunit, occupies chromosomal position 6p24–25 and comprises 15 exons encoding a amino acid protein. 1
Factor XIII Deficiency - StatPearls - NCBI Bookshelf
Introduction. Congenital factor XIII (FXIII) deficiency is chiefly caused by mutations in the F13A gene (95% of cases) and, more rarely, by F13B gene defects (5% Systemic sclerosis (SSc, scleroderma) is a severe autoimmune connective tissue disease which affects the skin and internal organs. There has been evidence that coagulation factor XIII (FXIII) has a positive impact on clinical results in patients with SSc. In a single-center cohort study, we investigated the relationship between coagulation Factor XIII (FXIII) is a transglutaminase enzyme that catalyses the formation of ε- (γ-glutamyl)lysyl isopeptide bonds into protein substrates. The plasma form, FXIIIA 2 B 2, has an established function in haemostasis, with fibrin being its principal substrate. A deficiency in FXIII manifests as a severe bleeding diathesis emphasising its Factor XIII. Factor XIII is a coagulation factor that is also called fibrin stabilizing factor. Factor XIII is a transglutaminase that catalyzes the cross-linking of glutamyl and lysyl groups on fibrin monomers, stabilizing [HOST] formed in the absence of activated Factor XIII lack stability and are easily lysed by proteolytic enzymes D-dimer is a terminal degradation product from the breakdown of fibrin. Unlike other fibrin degradation products, D-dimer is formed only after fibrin has been cross-linked by activated factor XIII and lysed by plasmin [ 78 ]. Quantitative D-dimer is most often used in the evaluation of venous thrombosis and DIC ; doi/physrev—Factor XIII (FXIII) is unique among clot-ting factors for a number of reasons: 1) it is a protransglutaminase, which becomes activated