Indication

Hereditary factor XIII a subunit deficiency

Hereditary factor XIII A-subunit deficiency is an extremely rare, life-threatening autosomal recessive bleeding disorder affecting the hematologic system, caused by mutations in the *F13A1* gene. Read more about Hereditary factor XIII a subunit deficiency

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TRETTEN (factor XIII A-subunit, recombinant)

FACTOR XIII·HEREDITARY FACTOR XIII A SUBUNIT DEFICIENCY

NOVO NORDISK

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About Hereditary factor XIII a subunit deficiency.

Hereditary factor XIII A-subunit deficiency is an extremely rare, life-threatening autosomal recessive bleeding disorder affecting the hematologic system, caused by mutations in the *F13A1* gene.

This genetic defect results in the absence or dysfunction of the catalytic A subunit of coagulation factor XIII, impairing the cross-linking and stabilization of fibrin polymers during clot formation.

Consequently, blood clots form normally but remain unstable and prone to premature breakdown, leading to severe hemorrhagic manifestations such as delayed umbilical cord bleeding in neonates, spontaneous intracranial hemorrhage, intramuscular hematomas, defective wound healing, and recurrent pregnancy loss.

bleeding.org
Hereditary factor XIII A-subunit deficiency is an extremely rare, life-threatening autosomal recessive bleeding disorder affecting the hematologic system, caused by mutations in the *F13A1* gene
scholasticahq.com
Hereditary factor XIII A-subunit deficiency is an extremely rare, life-threatening autosomal recessive bleeding disorder affecting the hematologic system, caused by mutations in the *F13A1* gene This genetic defect results in the absence or dysfunction of the catalytic A subunit of coagulation factor XIII, impairing the cross-linking and stabilization of fibrin polymers during clot formation
nih.gov
Hereditary factor XIII A-subunit deficiency is an extremely rare, life-threatening autosomal recessive bleeding disorder affecting the hematologic system, caused by mutations in the *F13A1* gene
nih.gov
This genetic defect results in the absence or dysfunction of the catalytic A subunit of coagulation factor XIII, impairing the cross-linking and stabilization of fibrin polymers during clot formation Consequently, blood clots form normally but remain unstable and prone to premature breakdown, leading to severe hemorrhagic manifestations such as delayed umbilical cord bleeding in neonates, spontaneous intracranial hemorrhage, intramuscular hematomas, defective wound healing, and recurrent pregnan...
nih.gov
This genetic defect results in the absence or dysfunction of the catalytic A subunit of coagulation factor XIII, impairing the cross-linking and stabilization of fibrin polymers during clot formation
rarediseases.org
Consequently, blood clots form normally but remain unstable and prone to premature breakdown, leading to severe hemorrhagic manifestations such as delayed umbilical cord bleeding in neonates, spontaneous intracranial hemorrhage, intramuscular hematomas, defective wound healing, and recurrent pregnancy loss
medicover-genetics.com
Consequently, blood clots form normally but remain unstable and prone to premature breakdown, leading to severe hemorrhagic manifestations such as delayed umbilical cord bleeding in neonates, spontaneous intracranial hemorrhage, intramuscular hematomas, defective wound healing, and recurrent pregnancy loss
nih.gov
Consequently, blood clots form normally but remain unstable and prone to premature breakdown, leading to severe hemorrhagic manifestations such as delayed umbilical cord bleeding in neonates, spontaneous intracranial hemorrhage, intramuscular hematomas, defective wound healing, and recurrent pregnancy loss

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