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At least 19 recordsLinked to original sources
PubMed1976

Platelet aggregation and adhesiveness in classical factor X deficiency and in the abnormal factor X (factor X Friuli) coagulation disorder.

Platelet aggregation to common inductors and to Ristocetin, Thrombofax and Ionophore is normal in congenital factor X deficiency and in factor X Friuli coagulation disorders. Washed normal platelets resuspended in the patient's plasma and in adsorbed normal plasma showed a normal aggregation. On the contrary, normal platelets resuspended in normal serum failed to aggregate. These studies indicate that factor X plays no role in normal platelet aggregation.

Adenosine Diphosphate↗
PubMed1977

Acquired factor X deficiency and amyloidosis.

A selective acquired Factor X deficiency is an unusual occurrence. Six cases of an acquired Factor X deficiency in association with amyloidosis have been reported. This paper describes two additional cases, suggesting that this relationship may be more than coincidental. The mechanism by which amyloid may affect Factor X levels remains unknown, but suggestions include consumption, inactivation or decreased synthesis of Factor X. Factor II, VII, IX, and X concentrate transiently increased the Factor X level to normal in one of the patients. In an adult patient who has an isolated Factor X deficiency, amyloidosis should be actively sought.

Amyloidosis↗
PubMed1977

Syndrome of acquired factor X deficiency and systemic amyloidosis; in vivo studies of the metabolic fate of factor X.

To determine the metabolic fate of factor X in primary amyloidosis associated with factor X deficiency, we examined the pathways of its catabolism in a man with this syndrome. Intravenous infusion of human or bovine 131I-labeled factor X established a triphasic plasma clearance pattern for factor X. About 85 per cent of the factor X disappeared, with a disappearance half-time of less than 30 seconds. A second and third phase showed a T1/2 of 90 minutes and nine hours respectively. 131I-labeles factor X in plasma did not appear to be rapidly modified or degraded. Relatively minor quantities of 131I were cleared into the urine. We observed a diffuse distribution of radioactivity over the body surface, with a concentration in the hepatic and splenic regions. These studies demonstrate than factor X deficiency associated with systemic amyloidosis is due to binding of factor X to body tissue, probably within the circulatory system.

Amyloidosis↗
PubMed1975

Classical factor X deficiency. Report of a further case.

A case of classical factor X deficiency is reported. The propositus is a 28-year-old male who presented easy bruising, epistaxis, hematomas, hematuria and occasional hemartrosis since early childhood. The severely prolonged prothrombin time was corrected by normal serum but not by adsorbed normal plasma. The abnormality was not corrected by the plasma of a patient with factor X deficiency, but by the plasma of patients with factor II or VII deficiencies. Partial thromboplastin time, prothrombin consumption and the thromboplastin generation test were abnormal. The thromboelastogram showed a prolonged 'K' and 'r' together with a normal 'ma'. Factor X was very low (smaller than 1%). Platelet tests were normal. No factor X band or precipitates were seen on electroimmunoassay and on the cross-over electrophoresis. The non-consanguineous parents and several other members of the family were found to be heterozygotes.

Adult↗
PubMed1976

Treatment of amyloidosis associated factor X deficiency.

This is the tenth patient in thirteen years to be reported with the findings of an isolated factor X deficiency associated with primary amyloidosis. A favorable response to factor IX concentrate was manifested by temporary clinical and laboratory correction of her diathesis. This mode of treatment, therefore, provides an approach to therapy for bleeding complications in this group of patients who have previously failed to response to fresh frozen plasma.

Amyloidosis↗
PubMed1979

Acquired, transient factor X (Stuart factor) deficiency in patient with mycoplasma pneumonial infection.

A case of severe haemorrhagic diathesis due to acquired deficiency of factor X (both immunologically and in procoagulant activity) is presented. The clinical and serological features of this case indicated mycoplasma pneumonial infection. Factor X in the peripheral blood did not appear to be influenced by administration of vitamin K, prothrombin-complex concentrate, fresh plasma or fresh whole blood. Circulating inhibitors of blood coagulation were absent and systemic amyloidosis could not be demonstrated. After 20 d, factor X spontaneously returned to normal. In view of the absence of other known causes of factor X deficiency, a possible relationship with mycoplasma pneumonial infection is suggested.

Blood Transfusion↗
PubMed1978

Chronic peritoneal dialysis in a patient with primary amyloidosis, renal failure, and factor X deficiency.

Chronic peritoneal dialysis was used in a patient with renal failure due to primary amyloidosis. Paraprotein was demonstrated in serum and urine, and was removed in peritoneal dialysate. The patient objectively improved as long as he was receiving peritoneal dialysis. When dietary indiscretion necessitated hemodialysis for fluid removal, he died shortly thereafter of subdural hematomas, possibly aggravated by factor X deficiency. Reasons for selecting chronic peritoneal dialysis as the treatment of choice in patients with renal failure associated with overproduction of paraprotein are discussed.

Amyloidosis↗
PubMed1975

Factor X Friuli: An immunological study in plasma and in serum using several methods.

An immunological study of factor X Friuli was carried out using an anti-human-factor X antiserum. The results obtained with different methods were compared. Only an ill-defined factor X band or precipitate was evident on standard immuno-electrophoresis and on immunodiffusion. Using a non-absorbed antiserum a precipitate was evident on eletroimmunoassay, in normal, factor X Friuli and in factor X deficient plasma. On the contary, using an antiserum which had been previously absorbed with factor X deficient plasma, a precipitate was evident only with factor X Friuli plasma or normal plasma. Excellent results were obtained with the cross-over electrophoresis. Using this method a major or factor X band was evident in normal plasma, factor II,P FACTOR VII, factor IX deficient plasmas and in the factor X FRIULI PLASMA. No factor X band was evident in factor X deficient plasmas and in absorbed normal plasma. Lighter, more cathodic bands were seen in all plasmas. These were due to secondary activities of the antiserum and could be disregarded. Friuli serum factor X and normal serum factor X showed a slightly more anodic migration as compared to their plasma counterparts. In coumarin plasma two factor X bands were evident; one normal in position and one slightly more catholidic. In the bidimensional immunoelectrophoresis two precipitates are visible in normal plasma and in factor X Friuli plasma. In factor X deficient plasma only one precipitate is evident. This latter precipitate is due to the secondary activity of the antiserum used. On the basis of these data it is concluded that factor X Friuli behaves, immunologically, as normal factor X.

Blood Coagulation Disorders↗
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↗
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↗