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Results for “Factor X Deficiency”

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At least 217 records · Page 12Linked to original sources
PubMed1976

Acquired coagulation factor X activity deficiency connected with Hymenoxys odorata DC (Compositae), bitterweed poisoning in sheep.

An acquired coagulation factor X activity deficiency was demonstrated in sheep fed Hymenoxys odorata, bitterweed plant. All coagulation tests were normal before the sheep were given the plant material. All tests involving the function of factor X, including a specific factor assay, became abnormal after the sheep were given bitterweed. Other specific factors remained within normal limits. The presence of an inhibitory activity could not be shown.

Animals↗
PubMed1990

Autologous bone marrow transplantation and factor XII, factor VII, and protein C deficiencies. Report of a new association and its possible relationship to endothelial cell injury.

Four patients who underwent treatment with high-dose chemotherapy (HDC) and autologous bone marrow transplantation (ABMT) and in whom posttreatment deficiencies of Factor XII and protein C subsequently developed are reported. Factor VII or Factor X deficiencies also developed in several of these patients. Three of these patients experienced chemotherapy-related cardiac, hepatic, or pulmonary toxicity. It is believed by many that endothelial cell injury may be the underlying lesion responsible for these various organ system toxicities seen in the setting of ABMT, although direct evidence of this is lacking. It is proposed that the factor deficiencies described in this report may be an additional consequence of endothelial cell injury or dysfunction. These coagulation factor deficiencies may therefore serve as both a marker to follow these organ system toxicities with and as a useful tool to better study and understand the mechanisms underlying these events. Additionally, deficiencies of either Factor VII or Factor X developed in several patients that were of a sufficient magnitude such that factor replacement therapy would be indicated before any invasive procedures or in the event of significant hemorrhage.

Adolescent↗
PubMed1979

Inactivation of factor VIII by a mechanism independent of the generation of thrombin.

Thrombin first activates and then inactivates factor VIII and for this reason thrombin has been considered responsible for the inactivation of factor VIII which occurs during clotting. Experiments described in this paper indicated that the activity of factor VIII is not reduced in factor IX or factor X deficient sera, while on the other hand this factor becomes inactivated in blood anticoagulated with high concentrations of hirudin which inhibit thrombin activity completely. This suggests that some other factor, besides thrombin, which is generated only in trace amounts in factor IX or factor X deficient plasmas, is also able to inactivate factor VIII. Purified factor X activated with insolubilized trypsin was added to purified preparations of factor VIII, which were free of both fibrinogen and prothrombin. Factor X a was allowed to act for 5-60 minutes and then inactivated with phenylmethanesulfonyl fluoride. Depending on the duration of the action of factor X a partial or complete inactivation of factor VIII was observed. This inactivation was also observed in the presence of hirudin, thus excluding the possibility that the effect was due to contamination with trace amounts of thrombin.

Anticoagulants↗
PubMed1994

A NlaIII polymorphism within the human factor VII gene.

The polymorphism is located within exon 5 of the human coagulation factor VII gene and is silent at the amino acid level. The distribution pattern is similar in Caucasians and African Americans. This polymorphism may be useful for restriction fragment length polymorphism (RFLP) diagnosis of factor X deficiency as well as factor VII deficiency, since the factor X gene is closely linked to the factor VII locus.

Base Sequence↗
PubMed1998

Molecular abnormality observed in a patient with coagulation factor X (FX) deficiency: a novel three-base-pair (CTT) deletion within the polypyrimidine tract of the FX intron D.

We investigated the molecular defect underlying congenital factor X (FX) deficiency in a Japanese patient. A novel three-base-pair deletion was identified within intron D of the FX gene. An allele-specific restriction analysis showed the propositus was homozygous and her two daughters were heterozygous for the deletion. It was not detected in 53 unrelated Japanese (106 alleles), indicating a probable cause of the FX deficiency. The deletion resides within a polypyrimidine tract of the acceptor splicing site where U2 snRNP binds to form spliceosomes. The defect could alter the formation of spliceosomes, resulting in incorrect splicing and decreased FX production.

Animals↗
PubMed1980

Factor X assays using chromogenic substrate S-2222.

Factor X was assayed using chromogenic substrate S-2222 for four patients with severe factor X deficiency and for nine patients with homozygous or heterozygous factor X Friuli disorder. Factor X Friuli disorder is characterized by the presence of an abnormal factor X that is normally activated by Russell's viper venom, but is not activated by tissue thromboplastins. The levels of factor X found in factor X deficiency varied between 2 and 10% of normal and therefore were higher than those found in the same plasmas using "clotting" methods (1% or less than 1% of normal). The levels of factor X found in homozygous factor X Friuli patients varied between 4 and 11% of normal, and therefore were practically identical to those found by means of clotting methods that employed tissue thromboplastins (7-9% of normal). These values were definitely lower than those obtained using a Russell's viper venom and cephalin mixture as thromboplastin (82-92%). A similar pattern was observed for patients heterozygous for the abnormality. These findings indicate that "amidolytic" methods are not necessarily identical to clotting methods. Furthermore, they indicate that substrate S-2222 is not specific for factor X.

Blood Coagulation Tests↗
PubMed1995

[Applicability of activated partial thromboplastin time (APTT) as a screening test of milk to medium deficiencies of coagulation factors in cats].

The present investigation examined if the aPTT shows sufficient sensitivity for single factor activities also in cats when measured with the test optimized for humans using a commercial reagent. Comparative measurements were done with different modifications of the aPTT (sample predilution, addition of fibrinogen). Measurements of the aPTT using different methods and the activity of the coagulation factors II, V, X, VIII, IX, XI, and XII were performed in 42 healthy cats in order to determine the reference ranges. The same measurements were done on 21 cat plasmas where at least one of the coagulation factors was diminished in relation to the corresponding reference range. The conventional aPTT reflected the decrease in coagulation factor activity in each of the 21 plasmas by prolongation above the reference range (14.6-24.4 s). The test thus possesses high sensitivity and is a suitable screening test also for the cat. In contrast, in tests with sample predilution the sensitivity was lower (3-4 false negative results). This was probably caused by the distinct increase of the range of the reference values.

Animals↗
PubMed1998

Frequency of inherited bleeding disorders in women with menorrhagia.

BACKGROUND: Although menorrhagia is a common gynaecological symptom, a specific cause is identified in less than 50% of affected women. We investigated the frequency of inherited bleeding disorders in women with menorrhagia. METHODS: Women referred for investigation of menorrhagia whose pelvis was normal on clinical examination and who had an estimated menstrual blood loss of more than 80 mL were studied. A detailed menstrual history and history about other bleeding symptoms was taken. The activated partial thromboplastin time, factor VIII activity, von-Willebrand-factor antigen and activity, and factor XI (FXI) were measured in all patients; further tests were done when results were at or outside the limits of the assays. FINDINGS: 150 women were screened. An inherited bleeding disorder was diagnosed in 26 (17%) patients: the disorders were von Willebrand's disease of mild (15) or moderate severity (three), mild FXI deficiency (four), mild von Willebrand's disease and FXI deficiency (one), combined von Willebrand's disease, FXI deficiency, and factor X deficiency (one), carriage of haemophilia-A gene (one), and platelet dysfunction (one). The frequency of von Willebrand's disease and FXI deficiency were 13% (95% CI 7.9-18.8%) and 4% (1.5-8.5%), respectively. Menorrhagia since menarche was noted in 11 (8.9%) of 123 women without a bleeding disorder compared with 13 (65%) of 20 women with von Willebrand's disease (p=0.001) and four (66.7%) of six women with FXI deficiency (p<0.001). INTERPRETATION: Inherited bleeding disorders are found in a substantial proportion of women with menorrhagia and a normal pelvis examination. We suggest that such patients should be investigated for these disorders-especially von Willebrand's disease-before invasive procedures are done.

Adult↗
PubMed1983

Cyclic AMP independent inhibition of platelet aggregation by prostaglandin E1 is mediated through factor Xa.

Normal plasma exposed to an insolubilized omega-NH2-hexyl-agarose derivative of PGE1 inhibits ADP-induced platelet aggregation. To define the plasma macromolecule responsible, we tested plasma congenitally deficient in coagulation factors for this property. Only plasma deficient in factor X failed to inhibit platelet aggregation under these conditions. The inhibition could be restored by reconstituting the defective plasma with bovine or human factor X. Purified factor X or Xa exposed to insolubilized PGE1 also inhibited ADP-induced platelet aggregation. Factor Xa could reverse suggesting that factor Xa was the responsible component. This conclusion was further supported by the ability of heparin to reverse the inhibitory effect of altered factor Xa when the anticoagulant was added simultaneously to platelets. The results were not due to the release of PGE1 from the insoluble derivative. Factor Xa may have a heretofore unrecognized effect on modulating platelet functions.

Alprostadil↗
PubMed1988

Inherited coagulation disorders.

Inherited coagulation disorders have been diagnosed in many breeds of dogs as well as in mongrels and cats. This article presents the different coagulation factor deficiencies that are known to exist in small animals. A description is given of each coagulation factor along with the relevant clinical signs, inheritance, and the breeds affected. Suggestions are also given for the diagnosis and therapy of these deficiencies.

Afibrinogenemia↗
PubMed1977

Surgery in patients with congenital disorders of blood coagulation.

Surgical procedures on patients with congenital disorders of blood coagulation can be performed with a high degree of confidence and an acceptable incidence of complications. During the period 1960-1975, 42 patients with congenital disorders of blood coagulation underwent 94 operative procedures at the New York Hopital-Cornell Medical Center. The coagulation defect was diagnosed preoperatively, in nearly all patients. Careful hematologic management, including specific factor replacement, is essential. The importance of meticulous hemostasis at surgery and careful monitoring of blood coagulation in the postoperative period is strongly emphasized.

Adolescent↗
PubMed1983

Thrombosis or myocardial infarction in congenital clotting factor abnormalities and chronic thrombocytopenias: a report of 21 patients and a review of 50 previously reported cases.

Nine patients are described with hereditary clotting factor abnormalities and thrombosis and 35 others previously reported in the literature. An additional 11 patients with myocardial infarction observed by the authors and 12 more reported by others are also included. A patient with non-immune thrombocytopenia and myocardial infarction is presented, as well as three additional patients recorded in the literature. This study underscores the little-recognized phenomenon of uncontrolled thrombosis in these patients with "experiments of nature," in whom clotting studies reflect an impairment of coagulation comparable in degree to that achieved by oral anticoagulant therapy.

Adult↗
PubMed1988

Inherited bleeding disorders in the Eastern Province of Saudi Arabia.

Thirty-four cases of inherited bleeding disorders are reported. All are Saudi patients from the Eastern Province of Saudi Arabia. There were 15 haemophiliacs, 1 factor VII deficiency, 1 factor X deficiency, 12 Glanzmann's thrombasthenia, and 5 unidentified platelet function disorders. Consanguinity was common among the families of these patients. Different age groups were affected and the severity of bleeding varied in the different conditions reported.

Adenosine Diphosphate↗