Déficit acquis et isolé en facteur VII contemporain d'un traumatisme crânien grave : utilisation du substitut de facteur VII (facteur VII-LFB®)

Meaudre, Éric; Kenane, N.; Kaiser, É.; Gaillard, P; Saillol, Anne; Cantais, E.; Palmier, B.

doi:10.1016/j.annfar.2005.05.019

Cited by 6 publications

(2 citation statements)

References 23 publications

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“…In particular, it was reported during sepsis, as a potential consequence of proteolytic degradation induced by the activation of monocytes and endothelial cells [ 12 , 13 ]. Other cases associated with major trauma and bone marrow transplantation have been described; however, the mechanisms are not fully understood [ 14 , 15 ].…”

Section: Discussionmentioning

confidence: 99%

Factor VII Deficiency in Systemic Mastocytosis with an Associated Myeloid Neoplasm

Rosati,

Camerlo,

Fornari

et al. 2024

Hematology Reports

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Factor VII (FVII) deficiency is a rare bleeding disorder that can be classified as congenital or acquired, and the majority of acquired cases are due to vitamin K deficiency or liver disease. Isolated acquired FVII deficiency is a rare occurrence and has been associated with inhibitors or auto-antibodies. Here, we describe a patient with polycythemia vera who developed systemic mastocytosis and FVII deficiency simultaneously. FVII deficiency was not caused by inhibitors and improved with antineoplastic treatment. Acquired FVII deficiency has been reported in cases of sepsis, possibly due to proteolytic degradation induced by the activation of monocytes or endothelial cells. Malignancies have been shown to cause a depletion in circulating FVII through the direct binding of cancer cells. This case report suggests a potential association between SM associated with a hematological neoplasm (SM-AHN) and acquired FVII deficiency. Further evaluations are recommended in patients with systemic mastocytosis to gain a better understanding of the relationship between pathological mast cells and clotting factor concentrations.

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Section: Discussionmentioning

confidence: 99%

Factor VII Deficiency in Systemic Mastocytosis with an Associated Myeloid Neoplasm

Rosati,

Camerlo,

Fornari

et al. 2024

Hematology Reports

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“…Acquired FVII deficiency may also occur due to bone marrow transplantation and bacteremia. Clinical manifestations of acquired FVII deficiency are usually mild to moderate, which may become relevant in the case of surgery (56,(65)(66)(67).…”

Section: Asymptomatic Casesmentioning

confidence: 99%

Coagulation Factor VII: Genetic, Molecular, and Clinical Characteristics

Mashayekhi

Ghasemi

2022

Trends in Med Sci

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: Coagulation factor VII (FVII) is a vitamin K-dependent serine protease that plays a pivotal role in normal hemostasis. Mature FVII is a glycoprotein comprised γ-carboxyglutamic acid-rich (Gla) domain, two epidermal growth factor (EGF)-like domains, an activation domain, and a serine protease domain. FVII requires proteolytic activation followed by tissue factor (TF) binding for maximal activity. The F7 gene (14.8 kb) is located on 13q34, composed of nine exons and eight introns. The congenital FVII deficiency is a rare coagulopathy with an autosomal recessive pattern of inheritance that occurs due to mutation in the F7 gene. A considerable number of mutations of different types have been identified throughout this gene affecting the expression, structure, and post-translational alterations of the protein. FVII deficiency is the most frequently recessively inherited bleeding disorder. Subjects with FVII deficiency show a wide range of symptoms, including cutaneous hemorrhage, mucosal hemorrhage, gastrointestinal bleeding, joint bleeding, and central nervous system (CNS) hemorrhage. Unlike other coagulation factor deficiencies, serum levels of FVII do not demonstrate the severity of the disease, and there is no direct correlation between serum levels and clinical complications. Replacement therapy is the treatment of choice for FVII deficiency. Various therapeutic products such as prothrombin complex concentrate, plasma-derived FVII concentrate, fresh frozen plasma, and activated recombinant FVII are available to treat FVII deficient individuals. This review aims to provide information on molecular, biochemical, and clinical aspects of coagulation FVII, its role in hemostasis, and the consequences of its deficiency.

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Hémorragie sous-arachnoïdienne par rupture d'anévrisme et déficit en facteur VII, à propos d'un cas

Tafer

Julliac

Morel

et al. 2007

Annales Françaises d'Anesthésie et de Réanimation

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Déficit acquis et isolé en facteur VII contemporain d'un traumatisme crânien grave : utilisation du substitut de facteur VII (facteur VII-LFB®)

Cited by 6 publications

References 23 publications

Factor VII Deficiency in Systemic Mastocytosis with an Associated Myeloid Neoplasm

Factor VII Deficiency in Systemic Mastocytosis with an Associated Myeloid Neoplasm

Coagulation Factor VII: Genetic, Molecular, and Clinical Characteristics

Hémorragie sous-arachnoïdienne par rupture d'anévrisme et déficit en facteur VII, à propos d'un cas

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