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Results for “AFIBRINOGENEMIA”

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At least 811 records · Page 45Linked to original sources
PubMed1980

Intracranial hemorrhage and focal seizures secondary to use of L-asparaginase during induction therapy of acute lymphocytic leukemia.

L-Asparaginase is commonly used for induction therapy of acute lymphocytic leukemia of childhood. Severe clinical bleeding secondary to clotting dysfunction has not been previously reported. We observed intracranial hemorrhagic infarcts with focal seizures and hemiparesis associated with clotting abnormalities, including severe hypofibrinogenemia, probably the result of L-asparaginase administered during induction therapy of acute lymphocytic leukemia.

Afibrinogenemia↗
PubMed1984

Restoration of complement function in vivo by plasma infusion in factor I (C3b inactivator) deficiency.

The serum complement activities of a 1-year-old infant with recurrent life-threatening bacterial infections and persistent C3-Coombs-positive red blood cells were investigated. The patient's serum had a depressed serum level of CH50, C3, factor B, and factor H as well as undetectable antigenic or functional factor I. The complement profile of the parents was normal, with the exception of factor I, which was approximately 50% of normal in each parent. The Coombs positivity of the patient's red blood cells could be reversed in vitro by incubation with normal serum containing factor I. Infusion of normal plasma into the patient resulted in increased levels of CH50, with concomitant increases in serum C3, factor B, and factor H levels. The patient's red blood cells became transiently Coombs negative. At no time after plasma infusion was factor I detectable in the patient's serum. All complement functions and the C3 Coombs reactivity of the patient's red blood cells returned to preinfusion levels within 14 days. These findings are consistent with an inherited deficiency of factor I and emphasize the critical role this protein plays in the regulation of the alternative complement pathway. Plasma therapy may be an adjunct to the management of acute infection in patients with factor I deficiency.

Afibrinogenemia↗
PubMed2003

Hypodysfibrinogenemia during pregnancy, labor, and delivery.

BACKGROUND: Hypodysfibrinogenemia is an autosomally dominant disorder that can result in excessive bleeding as well as specific pregnancy complications. Increased risks of spontaneous abortion, postpartum hemorrhage, poor wound healing, and placental abruption have been reported. CASE: A woman with hypodysfibrinogenemia presented for care in the first trimester. Her antepartum course was uncomplicated, and she was administered intermediate-purity factor VIII during labor and did not have excessive bleeding postpartum. The infant's cord fibrinogen was low, at 43 mg/dL (normal 215 +/- 30), showing it was similarly affected. CONCLUSION: Pregnancy in patients with hypodysfibrinogenemia can be associated with various complications; however, coordination of care and anticipation of specific problems can result in a successful outcome for both mother and infant.

Adult↗
PubMed1996

Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency.

Plasmin(ogen) is an extracellular serine protease implicated in the activation of latent growth factors and procollagenase, degradation of extracellular matrix components, and fibrin clearance. Plasminogen (Plg) deficiency in mice results in high mortality, wasting, spontaneous gastrointestinal ulceration, rectal prolapse, and severe thrombosis. Furthermore, Plg-deficient mice display delayed wound healing following skin injury, a defect partly related to impaired keratinocyte migration. We generated mice deficient in Plg and fibrinogen (Fib) and show that removal of fibrin(ogen) from the extracellular environment alleviates the diverse spontaneous pathologies previously associated with Plg deficiency and corrects healing times. Mice deficient in Plg and Fib are phenotypically indistinguishable from Fib-deficient mice. These data suggest that the fundamental and possibly only essential physiological role of Plg is fibrinolysis.

Afibrinogenemia↗