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Results for “AFIBRINOGENEMIA”

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At least 667 records · Page 37Linked to original sources
PubMed1999

Low fibrinogen level: A predisposing factor for venous thromboembolic events with hormone replacement therapy.

Several studies have reported an association between hormone replacement therapy (HRT) in postmenopausal women and increased risk of idiopathic venous thromboembolic events (VTEs). Given the widespread use of HRT, it is important to identify factors that may predispose women on HRT to VTEs. To address this concern, we examined potential risk factors for VTEs in women assigned to HRT in the Postmenopausal Estrogen/Progestin Interventions (PEPI) study, a three-year, double-blinded, placebo-controlled trial of 875 postmenopausal women designed to assess the effects of HRT on heart disease risk factors (HDL cholesterol, fibrinogen, blood pressure, and insulin). Women with a history of estrogen-associated VTEs were excluded from the trial. Ten women, all assigned to HRT, had a VTE during PEPI. Only baseline fibrinogen varied significantly between those who did (mean = 249.0 mg/dl) and did not (mean = 280.8 mg/dl) have a VTE while assigned to HRT (P < 0.03). Adjusting for covariates including age, smoking, body mass index, lipid levels, blood pressure, alcohol, exercise, and prior HRT or oral contraceptive use did not affect this finding. The significantly lower fibrinogen levels seen among women subsequently reporting VTEs may be a marker for a specific, but as yet undefined, coagulopathy that is magnified in the presence of exogenous hormones. However, larger studies are needed to confirm this finding.

Afibrinogenemia↗
PubMed1975

Hypofibrinogenemia associated with vincristine and prednisone therapy in lymphoblastic leukemia.

Three patients with acute lymphoblastic leukemia and one with lymphosarcoma cell leukemia developed transient hypofibrinogenemia during a course of treatment with vincristine and prednisone. There was no evidence of overt, disseminated intravascular coagulation or significant liver impairment. Fibrinogen survival using homologous-125-I-labelled fibrinogen was measured in two patients; it was moderately shortened in both, perhaps indicating subclinical intravascular coagulation. Rapid lysis of leukemic cells might have been responsible for activating coagulation and fibrinolysis in vivo. These four patients, however, were not different in any clinical or laboratory parameter from nine others with lymphoblastic leukemia similarly treated and investigated without observing any defect in their fibrinogen. There were no bleeding complications and the fibrinogen level became normal within 13 to 30 days.

Adult↗
PubMed1977

The effect of L-asparaginase of plasma coagulation factors in acute lymphoblastic leukemia.

Serial coagulation studies were performed in 26 pediatric patients with acute lymphoblastic leukemia during initial induction therapy with vincristine, prednisone, and L-asparaginase. Prolongation of screening coagulation tests was frequent: prothrombin time (in 16 of 26 patients), partial thromboplastin time (23/26) and thrombin time (21/26). In all 26 patients fibrinogen levels fell below .20 g/100 ml and 16 had levels below .10 g/100 ml. Sixteen patients had plasma coagulation factor assays performed. In these 16 patients, Factor XI was less than 40% in 14 and Factor XI was less than 70% in 9, with only a few scattered low levels of other factors. There were no clinical bleeding episodes. Coagulation abnormalities returned to normal at the completion of L-asparaginase therapy while the patients remained on vincristine and prednisone.

Afibrinogenemia↗
PubMed1977

Hemostatic factors in primary hepatocellular cancer.

Detailed coagulation studies were performed in a group of 19 patients with primary hepatocellular cancer (PHC) and the results were compared statistically with the findings in 19 control subjects. Various funcitonal and immunochemical methods were employed in determining the possible presence of functional or structural coagulant protein abnormalities. The patient group was characterized by prolonged prothrombin times, partial thromboplastin times, and Reptilase times, increased levels of fibrinogen, factor VIII, and factor VIII-related antigen, moderately devreased levels of factor V, factor IX, factor X, antithrombin III, and plasminogen, and reduced levels of factor II and factor VII. Functional, immunochemical, and biochemical analysis failed to detect the presence of acquired protein abnormalities. These findings indicate that hemostatic changes in primary hepatocellular cancer are nonspecific in character. Severe alterations in the plasma levels of one or more of these hemostatic factors may occur.

Adolescent↗
PubMed1980

Fibrinogen Chapel Hill: hypodysfibrinogenemia with a tertiary polymerization defect.

A patient with a functionally defective fibrinogen (fibrinogen Chapel Hill) has been investigated. Fibrinogen Chapel Hill is characterized by hypofibrinogenemia, with a plasma concentration about one third of normal, as measured both functionally and immunochemically. Fibrinogen survival is normal; so also is fibrinopeptide release. A polymerization defect in this fibrinogen results in the delay of fibrin fibrils in solution to form a normal three-dimensional gel. This defect is not associated with end-to-end aggregation or with lateral associations in solution. Delayed gelation results from an abnormality in a tertiary contact site involved in network branching, which is associated with the hydrophilic, carboxy-terminal segment of the alpha chain. Fibrinogen Chapel Hill exhibits two additional abnormal responses, which are also associated with the same region. The early plasmin cleavages of fibrinogen and fragment X are delayed, and there is a concomitant delay in the appearance of fragments Y, D, and E. This fibrinogen also has an unusual sensitivity to Ancrod proteolysis, whereby Ancrod cleaves a large carboxy-terminal segment of the alpha chain more rapidly than in normal fibrinogen. The abnormalities in fibrinogen Chapel Hill can be explained by a structural abnormality which is functionally related to an alpha chain associated polymerization domain.

Adult↗
PubMed1980

Platelet interaction with bacteria. VI. contrasting the role of fibrinogen and fibronectin.

The roles of fibrinogen and fibronectin were contasted in the responses of human platelets to Staphylococcus aureus and collagen. Congenital afibrinogenemic (CA) platelets and washed normal platelets had delayed aggregation due to a prolonged latent phase in response to contact with the bacteria when fibrinogen was absent from the suspending media. When a physiologic level of human fibrinogen was added to the CA platelets in autologous plasma or to the washed platelets in balanced saline, the times to aggregation were significantly shortened (P < 0.05) and restored to rates comparable to those of normal platelets in whole plasma. In contrast, the presence or absence of fibrinogen in the media had no significant effect on the initial adherence and shape-change response of CA or washed platelets to collagen. Platelets with a demonstrated aberration of fibronectin responded normally to all ratios of S aureus, but they responded only to doses of collagen that were several times the threshold levels for normal platelets. These results demonstrate an important role for fibrinogen as a cofactor in platelet interactions with S aureus and indicate that fibronectin is not a major factor in the responses of human platelets to this microorganism.

Afibrinogenemia↗
PubMed1986

Congenital thrombotic disorders.

The investigation of kindreds with recurrent thrombotic disease has advanced the understanding of the mechanisms of coagulation and fibrinolysis. In those cases where an etiology has been established, congenital thrombotic disorders are associated either with deficiencies or qualitative abnormalities in inhibitors of activated coagulation factors, qualitative abnormalities of fibrinogen, fibrinolytic defects that impair clot lysis, or an inborn error of metabolism, homocystinuria. The etiologies of congenital thrombotic disorders, their clinical features, and an approach to their laboratory diagnosis are summarized in this review.

Afibrinogenemia↗
PubMed1987

Fibrinogen giessen I: a congenital homozygously expressed dysfibrinogenemia with A alpha 16 Arg----His substitution.

Clinical reports are published for only two patients with homozygously expressed congenital dysfibrinogenemia. The patients, both of whom have a bleeding diathesis, have amino acid substitutions in the fibrinogen molecule at A alpha 16 Arg----Cys and A alpha 19 Arg----Ser, respectively. We report that a third patient with dysfibrinogenemia (fibrinogen Giessen I) is homozygous for A alpha 16 Arg----His. Although this patient has had excessive postpartum bleeding, she has had normal hemostasis throughout several minor surgical procedures and hysterectomy. Elucidation of the amino acid alterations in patients with dysfibrinogenemia may expand our understanding of structural determinants of fibrinogen that are critical to its function in vivo.

Adult↗
PubMed1989

Treatment of von Willebrand's disease and hypofibrinogenemia with single donor cryoprecipitate from plasma exchange donation.

Conventional replacement therapy for hypofibrinogenemia and von Willebrand's disease requires multiple donor exposures and a correspondingly high risk of blood-borne infection. We describe the collection and successful use of cryoprecipitate derived from a single donor by plasma exchange donation to support such patients through major hemostatic stresses. The father of an epileptic patient with von Willebrand's disease produced cryoprecipitate containing 23,546 units of von Willebrand factor (vWF) in nine desmopressin-stimulated donations; this provided total factor replacement for neurosurgery to remove a seizure focus. The average yield was 2,616 units per donation and the average VWF concentration in cryoprecipitate was 17.7 units/ml. The husband of a hypofibrinogenemic patient with a history of postpartum hemorrhage provided cryoprecipitate containing 13.4 g of fibrinogen in five donations; this supported his wife through parturition without recourse to other blood products. The average yield was 2.7 g per donation, and the average fibrinogen concentration was 15.3 g/liter. Plasma exchange donation is a practical alternative source for cryoprecipitate. It can provide vWF and fibrinogen that carry a reduced risk of infectious disease transmission.

Adult↗