Effect of low-dose subcutaneous heparin on whole-blood viscosity.
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Biomedical subjects
Publications and source records attributed to G Cella.
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A patient with combined factor V and factor VIII deficiency is presented. The bleeding manifestations were: easy bruising, post-traumatic bleeding, bleeding after tooth extractions. The main laboratory feature was a prolonged partial thromboplastin time which was corrected by the addition of adsorbed normal plasma but not by the addition of normal serum, hemophilia A plasma of another patient with combined factor V and factor VIII deficiency. The thromboplastin generation test was clearly abnormal and was corrected by the addition of adsorbed normal plasma but not by addition of normal serum. Prothrombin consumption was also defective. Prothrombin time was slightly prolonged too, Thrombin time, platelet and vascular tests were within normal limits and there was no hyperfibrinolysis. Factor VIII was 8% of normal, whereas factor V was 14% of normal. Factor VIII associated antigen was normal. All other clotting factors were within normal limits. The parents of the propositus were consanguineous (first cousins) but had normal factor V and factor VIII activity and normal factor VIII antigen. The same was true for other family members. The hereditary transmission of the condition appears autosomal recessive.
The whole blood and plasma viscosities have been evaluated in a patient with cold hemoagglutinin disease at different temperatures and at different shear rates. At 37 and 42 degrees C, whole blood viscosity values, regardless of the shear rate applied, resulted to be correspondent to the hematocrit value (31%). The values observed were similar to those noted in a patient with chronic bleeding anemia and an approximately equivalent hematocrit (33%). The same was true for plasma viscosity. At 32 degrees C, whole blood viscosity, regardless of the shear rate, resulted to be higher than expected. The values observed were similar to those noted in a normal subject with a clearly higher hematocrit value (44%) and definitely higher than those noted in the chronic anemia patient. On the contrary, plasma viscosity remained unchanged. These studies indicate that in cold hemoagglutinin disease, red cell aggregation and piling are capable of increasing blood viscosity.
A patient with a combined hereditary deficiency of factors VII and VIII is presented together with a family study. The main bleeding manifestations were easy bruising and bleeding after tooth extractions. No hemarthrosis was ever observed. The main laboratory features consisted in a mild prolongation of prothrombin time and of partial thromboplastin time. TG test was abnormal and was corrected by the addition of adsorbed normal plasma. Specific assays revealed a moderate defect of factors VII and VIII. All other clotting factors were within normal limits. The factor VII antigen in the propositus was normal or nearly normal. The factor-VIII-associated antigen was also normal. Five additional family members presented the same coagulation pattern and were variably symptomatic. The hereditary transmission pattern seems to be autosomal dominant. The defect appears to be due to a structural abnormality of a gene controlling factors VII and VIII activation.
Tranexamic acid in a dose of 50 mg/kg b.w. was unable to alter the ellagic acid induced hypercoagulable state. No change in the hypercoagulability pattern was observed regardless of the time of administration of the compound (before or after the ellagic infusion). The silicone clotting times after the infusion of ellagic acid were markedly shortened and remained so for about 60 minutes. The results observed in two control groups treated with saline were similar. The euglobulin lysis times were clearly prolonged after the administration of tranexamic acid, whereas no changes were observed after the administration of saline. These results indicate that tranexamic acid has no anti-factor XII activity.
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Beta-thromboglobulin and platelet factor 4 are the two best characterized platelet-specific proteins. They are stored in the platelet alpha-granules and released during platelet activation. Their physiological function is unknown. PF4 has high anti-heparin activity, whilst beta-TG does not. Certain factors can affect the plasma level of one or both of these two proteins and these must be borne in mind whenever the evaluation of beta-TG and PF4 are thought to represent true in vivo platelet activation: their artificial release due to sample collection and processing, the in vivo release of PF4 induced by heparin, and the elevation of beta-TG due to renal failure. What really represents an abnormal level of beta-TG and PF4 is unknown, since we do not know their pathophysiology. At present, however, the platelet-specific proteins, even if they are considered as 'markers' of platelet activation, do not necessarily reflect the severity of the cardiovascular disorders nor do they signal thrombus formation, as thrombosis is a consequence of several interacting factors.
Levels of beta-thromboglobulin and platelet factor 4 in 46 patients with transient ischemic attacks and the influence of treatment with dipyridamole or aspirin plus dipyridamole were evaluated. Patients not receiving therapy showed levels of beta-thromboglobulin significantly higher than controls. However, patients taking only dipyridamole showed values of beta-thromboglobulin significantly lower than untreated patients or those taking aspirin plus dipyridamole. No significant difference was observed with regard to platelet factor 4 between the patients.