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Biomedical subjects

G Patrassi

Publications and source records attributed to G Patrassi.

At least 19 recordsLinked to original sources
PubMed1992

Impaired release of tissue plasminogen activator (t-PA) following DDAVP infusion in von Willebrand's disease with low platelet von Willebrand factor content.

Tissue plasminogen activator (t-PA) and von Willebrand factor (vWF) are both released by vascular endothelial cells after the infusion of DDAVP. Such release has not been observed in patients with severe von Willebrand's disease (vWD). In the present work we demonstrate that the degree of simultaneous DDAVP-induced release of t-PA and vWF, in patients with vWD, is strictly related to the platelet vWF content. Twelve patients with type I, and three patients with type III vWD were studied. The type I vWD group included three patients with reduced platelet vWF content (platelet-low) and nine patients with normal levels (platelet-normal). In all patients studied the plasma t-PA levels were within the normal range. No significant change in either t-PA or vWF was observed after DDAVP in the patients with undetectable levels of platelet vWF (type III vWD). A mild increase was found in those patients with type I platelet-low, while in type I platelet-normal vWD the response was similar to that observed in normal subjects. The release of the two molecules appeared, therefore, to be linked to platelet vWF content and the rates of increase in both t-PA and vWF were similar in each group of patients studied. Since platelets are regarded as a tissue compartment of vWF our findings seem to suggest that the presence of vWF and its release from endothelial cells is required for a normal concomitant release of t-PA. In contrast, post-DDAVP release of vWF seems to be independent from that of t-PA since it was normal in a patient with congenital deficiency of t-PA release.

Adolescent↗
PubMed1988

Cardiovascular and hormonal responses to DDAVP before and after beta-blockade in patients with mild essential hypertension.

The aim of this study was to assess the cardiovascular and hormonal responses to 1-desamino-8,D-arginine vasopressin (DDAVP) in hypertensive patients before and after non-selective beta-blockade. We infused DDAVP at 400 ng/kg body weight for 10 min in nine subjects with mild essential hypertension before and 14 days after administration of nadolol at 80 mg/day. Blood pressure and heart rate were recorded, and blood was drawn at 0, 30 and 60 min for measurement of plasma renin activity, aldosterone, cortisol, noradrenaline, adrenaline and dopamine. Before the administration of nadolol, DDAVP induced a significant decrease in blood pressure, and significant increases in the heart rate, plasma renin activity, cortisol and noradrenaline; there were no changes in adrenaline or dopamine. After the administration of nadolol, baseline noradrenaline was significantly increased, while cortisol, adrenaline and dopamine remained unchanged. A second infusion of DDAVP did not significantly alter blood pressure, [corrected] heart rate, noradrenaline, adrenaline or dopamine, but plasma renin activity, aldosterone and cortisol still showed a significant increase. The blunted hypotensive effect of DDAVP after the administration of nadolol may be aspecific, due to lower basal blood pressure levels, or may indicate a mechanism of action common to both drugs. A similar post-DDAVP increase before and after beta-blockade suggests that the drug has a direct effect on the renin-secretory apparatus. An indirect effect, mediated by changes in intrarenal haemodynamics or by other factors with renin-stimulating activity, e.g. tissue plasminogen activator, can also be hypothesized.

Adult↗
PubMed1978

No change of whole blood of plasma viscosity in cardiac patients after subcutaneous calcium heparin.

Whole blood viscosity, plasma viscosity and haematocrit were studied in a group of cardiac patients before and during subcutaneous heparin treatment. No significant change was noted in any of the parameters investigated. Relative viscosity (whole blood viscosity/plasma viscosity ratio) was also unaffected. These data indicate that heparin has no effect on the rheology of blood in vitro.

Adult↗
PubMed1977

Glass activation-induced decrease or disappearance of normotest-thrombotest discrepancy in congenital coagulation disorders of the prothrombin complex.

Exposure of plasma to glass for 60 minutes will cause a sharp, progressive shortening of Thrombotest clotting times in all congenital disorders of the prothrombin complex. On the other hand Normotest clotting times will change only slightly or moderately after the same glass activation. Consequently the Normotest-Thrombotest percentile discrepancy, quite marked at zero time, became progressively smaller. This behaviour is similar to that observed in a group of coumarin treated patients. These studies indicate that the Normotest/Thrombotest discrepancy does not allow any differentiation to be made between congenital coagulation disorders and coumarin induced defect. This is consistent with the non-specificity of the phenomenon.

Blood Coagulation Disorders↗
PubMed1976

An immunological investigation of factor VIII associated antigen in combined factor V and factor VIII deficiency.

The behavior of factor VIII associated antigen of three patients with combined factor V and factor VIII deficiency has been evaluated in several immunological systems. Factor VIII associated antigen resulted to be normal or higher than normal in all three patients in the radial immunodiffusion and in the electroimmunoassay systems. In the bidimensional electrophoresis system only one factor VIII precipitate was evident and such factor VIII precipitate showed the same electrophoretic mobility as normal factor VIII antigen. These findings firmly establish the fact that the factor VIII defect in congenital combined factor V and factor VIII deficiency is of the hemophilia type.

Antigens↗
PubMed1976

Decrease of normotest/thrombotest discrepancy in non-contacted coumarin plasma after glass or ellagic acid activation.

Activation of coumarin plasmas in glass tubes for 60 min resulted in a clear shortening of Thrombotest clotting times. Normotest clotting times were shortened too but to a much lesser extent. As a consequence the Normotest (NT)/Thrombotest (TT) discrepancy which was quite large at 0 time, became progressively smaller. This phenomenon was observed both in undiluted and 6:10 diluted plasma. After ellagic acid activation a similar phenomenon was noted even though a less pronounced shortening of Thrombotest was noted. These data suggest that Thrombotest is very sensitive to contact phase and to factor VII activation and not to any coumarin-induced inhibitors.

Blood Coagulation Tests↗
PubMed1976

Combined deficiency of factor V and factor VIII. A report of another case.

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.

Blood Coagulation Tests↗
PubMed1976

Increased whole blood viscosity on cooling in a patient with cold hemoagglutinin disease.

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.

Aged↗
PubMed1976

Factor X Friuli coagulation disorder. Report of a newly recognized patient and some considerations on the frequency of the disease in the Friuli area.

A newly recognized patient with the factor X Friuli coagulation disorder is presented. The propositus is a 10-year-old boy who presented excessive bleeding after a tooth extraction. This is the 11th patient with this peculiar coagulation disorder discovered in Friuli and the 12th so far described. His parents are consanguineous and heterozygotes together with other family members. The main laboratory features, typical of the disease were prolonged prothrombin time, a prolonged partial thromboplastin time, and a normal Stypven-cephalin clotting time. The incidence of the homozygotes in the Friuli area appear to be 0.000005 (11 cases in a population of 2,000,000). The probable frequency of the abnormal f gene is 0.0033, whereas that of the normal gene F is 0.9967. The theoretical frequency of the heterozygote, Ff condition is 0.007, namely 7 heterozygotes every 1,000 persons. However, only about 70 ascertained heterozygotes have been discovered so far.

Adolescent↗
PubMed1976

Combined congenital deficiency of factor V and factor VIII. Report of a further case with some considerations on the hetereditary transmission of this disorder.

A patient with combined factor V and factor VIII deficiency is presented. The bleeding manifestations were mild. 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 or plasma of another patient with combined factor V and factor VIII deficiency. TGT was also clearly abnormal and was corrected by the addition of adsorbed normal plasma but not by the addition of normal serum. Prothrombin consumption was mildly defective. The prothrombin time was slightly prolonged. Facotr VIII was 12% and factor V 55% of normal. Factor-VIII-associated antigen was normal. The father and a sister of the propositus revealed mild factor V deficiency but normal factor VIII activity and antigen. The parents were not consanguineous. A tentative classification of combined deficiency of factors V and VIII in two groups is proposed. The hereditary transmission of the two types of deficiencies is discussed.

Adult↗
PubMed1976

The "echis carinatus venom" prothrombin assay in coumarin treated patients. A comparison with one-stage and immunological assays.

Prothrombin (factor II) was assayed in a group of coumarin treated patients using the Echis carinatus venom as thromboplastin. The levels obtained were comparable to those observed using the classical one-stage method. A good correlation was in fact observed between the two methods. The levels observed by the Echis carinatus method were definitely lower than those obtained using two immunological methods indicating that Echis carinatus venom activated, in our system, only normal prothrombin. However, even the levels obtained immunologically were slightly decreased, regardless of the method used, as compared to pooled normal plasma. In congenital prothrombin deficiency (homozygotes and heterozygotes) the level obtained by the Echis carinatus method was comparable to that observed by the one-stage method. On the contrary, in a congenital dysprothrombinemia (prothrombin Padua) a normal level was observed whereas the one-stage and two-stage methods yielded constantly levels of about 50% of normal.

Animals↗
PubMed1975

The K-test (trypsin clotting time) in coumarin treated patients and in congenital deficiencies and abnormalities of the prothrombin complex.

The behavior of K-test (Trypsin clotting time) has been studied in 38 patients on long-term coumarin therapy and in 19 patients with congenital coagulation disorders of the prothrombin complex. All coumarin treated patients showed a clear prolongation of the test. The results obtained were compared with the standard prothrombin time, the Hepato-Quick-test (P-P test) and the Factor II + X test values, observed in the same patients. A good correlation was observed in each instance. The highest correlation was observed between K-test and the Factor II + X test (r=+0,78;t=7,80;p less than 0.001). All congenital coagulation disorders of the prothrombin complex yielded a prolonged K-test value but for Factor VII deficiency. In three patients with this latter condition a perfectly normal value was obtained. The K-test together with the prothrombin time may be useful in the differential diagnosis of factor VII deficiency from factor X deficiency and from the factor X Friuli abnormality.

Blood Coagulation Disorders↗