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Biomedical subjects

M Moia

Publications and source records attributed to M Moia.

At least 55 records · Page 3Linked to original sources
PubMed1994

A pilot study of pro-urokinase in the treatment of deep vein thrombosis.

Safety and efficacy of the thrombolytic agent pro-urokinase (pro-UK) in the treatment of deep vein thrombosis of the lower limbs (DVT) have been investigated in an open, uncontrolled, pilot study. Fifteen patients were infused with 800.000 IU (5 mg)/h of pro-UK over 24 h (120 mg), together with unfractionated heparin adjusted to maintain the activated partial thromboplastin time between 1.5 and 2.5 times the basal value. Efficacy was assessed comparing venographic changes in the 11 evaluable limbs before and after pro-UK infusion. The Marder score decreased from a median pre-thrombolysis value of 28 (range 4-40) to 16 (3-38) (p < 0.05). One major hemorrhagic event (retroperitoneal bleeding 4 days after the end of the pro-UK infusion) occurred. Fibrinogen, alpha 2-antiplasmin and plasminogen significantly decreased from baseline values after 12 and 24 h, fibrin(ogen) degradation products significantly increased. Changes in hemostasis parameters were unrelated to thrombolytic efficacy. The results of this pilot study indicate that pro-UK is thrombolytic in DVT and that it can be administered simultaneously with conventional heparin treatment.

Adult↗
PubMed1993

Effects of hirudin on activated partial thromboplastin time determined with ten different reagents.

Hirudin prolongs the APTT when added to normal plasma and the extent of prolongation depends on the type of reagent used. The aim of this study was to compare the dose-response curves of 10 widely used APTT reagents for linearity and parallelism. On each of 10 working days a normal pooled plasma was mixed with increasing amounts of recombinant hirudin (HBW023) ranging from 0 to 5 micrograms/ml and tested for APTT by photo optical coagulometer. Within each working day, clotting times were measured in duplicate and the order of testing with each reagent was changed every day. Results were expressed as ratios of clotting times with hirudin to clotting times without hirudin, and the values plotted against the hirudin concentration on a log-log scale. The dose-response curves for all reagents were linear over 0.3-1.2 micrograms/ml. The reagent-related slopes ranged from 0.225 +/- 0.003 to 0.303 +/- 0.003 (mean +/- SE) and were significantly different. Precision studies indicated that the least sensitive reagent was also the least precise. These findings indicate that the clotting time values obtained for patients treated with hirudin will vary depending on the APTT reagent used.

Blood Coagulation↗
PubMed1993

Ischemic stroke in congenital (type II C) defective antithrombin III.

Type II C is a subtype of defective antithrombin III deficiency in which there is a molecular defect in the heparin binding site. Usually, heterozygous patients with this defect have little or no thrombotic symptoms. Ischemic stroke has never been described. We report the case of a young woman who had an episode of right-sided hemiparesis. The computed tomographic scan showed an ischemic lesion in the left hemisphere. There were no previous thrombotic episodes in the patient's history and the sole risk factor for thrombosis was taking of an oral contraceptive. Her family history was midly positive for thrombosis (superficial thrombophlebitis in two relatives). Laboratory tests showed normal antithrombin III antigen, low heparin cofactor activity and an increased slow-moving peak in crossed-immunoelectrophoresis with heparin. The same pattern was found in 7 of 20 relatives. Thus, a diagnosis of congenital type II C defective antithrombin III was made. This report suggests that young patients with ischemic stroke should be screened for defective antithrombin III.

Adult↗
PubMed1993

Type I von Willebrand disease, subtype 'platelet low': decreased platelet adhesion can be explained by low synthesis of von Willebrand factor in endothelial cells.

Endothelial cells (EC) were isolated from the umbilical vein of a newborn girl with type I 'platelet low' von Willebrand disease (I vWD) and endothelial localization and release and the ability of subendothelial von Willebrand factor (vWF) to support platelet adhesion were compared with those of normal EC. vWF was detectable by immunofluorescence in Weibel-Palade bodies, but the number of Weibel-Palade bodies positive for vWF was lower than in control EC. Patient EC released into the medium significantly smaller amount of vWF, both constitutively and after their stimulation. The vWF content of the extracellular matrix of patient EC was 38% that of control EC matrix. Platelet adhesion studies were performed under flow conditions with umbilical arteries and EC matrices of cultured EC. Using normal citrated whole blood as perfusate, platelet adhesion was lower in the umbilical artery of the patient (9 +/- 1% v 35 +/- 4% for the control) and in her EC matrix (7 +/- 1% v 21 +/- 2% of control). When patient EC matrix was perfused with vWF-deficient reconstituted blood, adhesion was 17 +/- 3% v 32 +/- 3% for control EC matrix; preincubation of patient EC matrix with 1 U/ml vWF increased the adhesion to 30 +/- 6%. These data establish that low contents of vWF in EC and subendothelium are important characteristics of type I vWD 'platelet low', and that such characteristics correlate with low platelet adhesion to the subendothelium.

Cells, Cultured↗
PubMed1992

Prognostic value of hemostatic parameters after liver transplantation.

The prognostic value of hemostatic parameters after orthotopic liver transplantation was evaluated in 37 consecutive patients. Six simple hemostatic parameters (prothrombin time, activated partial thromboplastin time, thrombin time, thrombin coagulase time, plasma fibrinogen and platelet count) were obtained for each patient pre-transplantation and daily post-transplantation for at least 8 days. Using the results of these tests, the degree of hemostatic impairment was arbitrarily scored from 0 to 6. Starting from the first day post-transplantation, hemostatic parameters improved progressively, reaching plateau values on day 7 post-transplantation. On day 8 there were significant differences in the activated partial thromboplastin time, prothrombin time, and in the overall hemostatic scores between patients who survived at least 6 months and those who died. Comparing these hemostasis parameters with such liver function tests as AST, ALT and serum bilirubin, univariate analysis showed that activated partial thromboplastin time, coagulation score and AST were significant predictors of 6-month survival, but by multivariate analysis (Cox proportional hazard rate model) only the activated partial thromboplastin time was an independent predictor. Hence, a simple coagulation test is useful for predicting the survival of patients undergoing liver transplantation.

Adolescent↗
PubMed1991

Effects of subcutaneously administered dermatan sulfate (MF 701) on the coagulation and fibrinolytic parameters of healthy volunteers.

Eight healthy volunteers were given single subcutaneous doses of dermatan sulfate (DS, 100, 200 and 400 mg), heparin (5,000 IU) and placebo in random order. Wash-out between treatments was greater than or equal to 10 days. Serial blood samples were taken before and up to 24 hours after treatment to measure coagulation and fibrinolytic parameters. Thrombin generation was significantly inhibited by DS and heparin as compared to placebo. The effect of DS was dose-dependent. Peak inhibition after 200 mg DS was comparable to that of 5,000 IU heparin, but lasted longer. A small, bordeline significant prolongation of APTT was observed after 400 mg DS and heparin. The changes in PAI and fibrinolytic activities were those of the circadian variation. No changes were seen in the other parameters tested. In conclusion, single s.c. doses of DS (200, or 400 mg) inhibit ex vivo thrombin generation equally or more than 5,000 IU heparin and for a longer time. The effect of both treatments on fibrinolysis is negligible.

Adult↗
PubMed1991

[Medical aspects of thrombosis of the limbs].

Deep vein thrombosis (DVT) of the limbs is a common event that may cause disability or even death. Of the triad of Virchow, which indicates the pathogenic factors involved in DVT, hypercoagulability is very important. The clinical diagnosis of DVT is not reliable and needs objective confirmation before a therapeutic decision can be made. Phlebography is still considered the treatment of choice for DVT diagnosis. Non invasive, less expensive diagnostic procedures have become available: among these, real time B-mode ultrasonography is the most promising. Laboratory tests are essentially non-specific and of little help in DVT diagnosis: they are essential to monitor anticoagulant therapy however, and to screen for congenital disorders that predispose to thrombosis. Therapy of DVT is based on the correct use of heparin and oral anticoagulants: only a few patients should be treated with thrombolytic drugs. Low-dose heparin is considered the most effective treatment for post-surgical DVT prevention and should be more widely used. New low molecular weight heparins have proven to be more efficacious and safe in DVT prophylaxis after orthopedic surgery.

Anticoagulants↗
PubMed1989

DDAVP shortens the prolonged bleeding times of patients with severe von Willebrand disease treated with cryoprecipitate. Evidence for a mechanism of action independent of released von Willebrand factor.

After infusion of cryoprecipitate, the very prolonged bleeding time of patients with severe von Willebrand disease (vWD) is shortened but not always normalized in spite of normalization of plasma von Willebrand factor (vWF) levels. Therefore treatments that further improve primary hemostasis in severe vWD patients are needed. Since DDAVP shortens the bleeding time in a variety of bleeding disorders, we investigated in a double-blind, placebo-controlled crossover study the effects of the intravenous (IV) infusion of DDAVP (0.3 microgram/kg) on the bleeding times of 10 patients with severe vWD treated with cryoprecipitate. Their very prolonged bleeding times (greater than 30 minutes), partially corrected by the infusion of cryoprecipitate (14 +/- 2 minutes, mean +/- SEM), were further shortened by the administration of DDAVP (9 +/- 2 minutes, P less than .01) but not of saline (15 +/- 3 minutes, ns). Plasma vWF levels, raised from unmeasurable to normal values by cryoprecipitate, were not changed after DDAVP or saline. The defective deposition of platelets from eight patients onto human umbilical artery subendothelium was increased but not normalized by cryoprecipitate and was not significantly affected by DDAVP or saline. Therefore the infusion of DDAVP after cryoprecipitate may be of clinical benefit for management of bleeding episodes in severe vWD patients. Since severe vWD patients do not have releasable tissue stores of vWF, DDAVP must shorten their prolonged bleeding times independently of released vWF.

Bleeding Time↗
PubMed1989

Role for platelet von Willebrand factor in supporting platelet-vessel wall interactions in von Willebrand disease.

Twelve infusions of plasma concentrates of von Willebrand factor (vWF) were given to four patients with severe (type III) von Willebrand disease (vWD). Their prolonged bleeding times were either completely or partially corrected after five infusions and had not changed after the remaining seven. In contrast, the low platelet coverage of the subendothelial surface of rabbit aorta perfused with normal washed platelets and red cells resuspended in preinfusion patient plasma was completely or partially corrected in ten instances by replacing preinfusion plasma with postinfusion plasma and remained unchanged in two. Postinfusion improvement in surface coverage was greater than that in bleeding time, suggesting that vWF from normal platelets is needed to support optimal platelet-vessel wall interactions in vWD. This possibility was further explored through other perfusion experiments. The subendothelial surface covered by platelets from an untreated patient with type III vWD (containing no measurable vWF) or from a type IIA vWD patient (containing dysfunctional vWF) resuspended in normal plasma was much smaller than that covered by normal platelets resuspended in normal plasma. These results establish that platelet vWF is important in supporting platelet-vessel wall interactions in vWD and also provide experimental support in favour of the therapeutic transfusion of normal platelets in addition to vWF concentrates to correct the bleeding time in vWD patients.

Blood Platelets↗
PubMed1987

Improvement in the haemostatic defect of uraemia after treatment with recombinant human erythropoietin.

Patients with uraemia have a defect of primary haemostasis expressed as long skin bleeding times and reduced platelet adhesion to the arterial subendothelium. Transfusion of red cells shortens the bleeding time and stops bleeding symptoms in uraemia. This study investigated whether the efficacy of recombinant human erythropoietin in correcting anaemia and the improvement in haemostasis are correlated. Recombinant human erythropoietin was given to seven consecutive patients with chronic uraemia, a history of bleeding, severe anaemia (haematocrit below 23%), and long bleeding times (above 19 min). The progressive rise in haematocrit induced by increasing doses of recombinant human erythropoietin was paralleled by a pronounced shortening of the bleeding time. Platelet adhesion to the subendothelium of human umbilical arteries, very low before the study, increased greatly in all patients and became normal in six. None of the patients bled during the study period.

Adult↗
PubMed1987

Correction of the bleeding time in treated patients with severe von Willebrand disease is not solely dependent on the normal multimeric structure of plasma von Willebrand factor.

Even though it is generally held that cryoprecipitate and fraction I-O correct the prolonged bleeding time (BT) in patients with von Willebrand disease (VWD), perusal of reported data indicates that the correction is usually short-lasting and often partial. We decided to do a controlled study of the relationship between the multimeric structure of von Willebrand factor (VWF) and the BT in five patients with severe (type III) VWD after infusion of three plasma concentrates ("wet" cryoprecipitate, lyophilized cryoprecipitate, and fraction I-O) given in random order. The dosage of concentrates was tailored from in vitro measurements to achieve post-infusion levels of ristocetin cofactor above the lower normal limit (50 U/dL) for at least 3 hours. The postinfusion BT became transiently normal in only two of five patients treated with wet cryoprecipitate, whereas it remained prolonged in all five patients treated with lyophilized cryoprecipitate or fraction I-O. For all the concentrates, the proportion of large VWF multimers calculated by scanning the electrophoretic gels were the same as those for normal standard plasmas. An intact multimeric structure was recovered in postinfusion plasmas of patients treated with wet cryoprecipitate, whereas there was a postinfusion loss of large multimers after lyophilized cryoprecipitate and fraction I-O. These findings indicate that the attainment of a normal BT is the exception rather than the rule after the infusion of three plasma fractions used in the treatment of severe VWD, and that an intact multimeric structure in concentrates and postinfusion plasmas is necessary but not sufficient to sustain a normal BT.

Bleeding Time↗
PubMed1985

[The role of erythrocyte deformability in the prolonged bleeding time in liver disease patients].

Hematocrit (Ht), red cell deformability (RCD) determined using a filtration method and bleeding time (BT) have been studied in 28 patients with severe chronic liver disease. Our results show a decrease of Ht (p less than 0.001), RCD (p less than 0.05) and a prolongation of BT (p less than 0.001) not related to the platelet count. Moreover, inverse relationships between Ht and BT (r = -0.52; p less than 0.01) and between RCD and BT (r = -0.54; p less than 0.01) have been found. We conclude that hemorheological alterations, such as decreased Ht and RCD, play an important role in primary hemostasis of patients with chronic liver disease.

Adult↗
PubMed1984

Hemodialysis without anticoagulants: efficiency and hemostatic aspects.

In 29 patients with high risk of bleeding, 111 hemodialyses have been performed without heparin (WHD) or other anticoagulants. The same patients were switched to low dose heparin dialysis (LDHD) as soon as the bleeding risk had ceased. The dialyzer had to be changed in 11 and the drip chamber in 20 WHDs because of partial clotting. This phenomenon did not occur during LDHD. The comparative efficiencies of the two techniques were evaluated by measuring the urea and creatinine clearances of the dialyzers. No significant difference between LDHD and WHD clearances was observed. In 7 of 29 patients, hemostasis variables were studied before, during and after both modes of treatment. Fibrinogen, platelet count, antithrombin III and prothrombin time did not differ with the different dialysis procedures. During dialysis, platelet factor 4 (PF4) levels were significantly higher than baseline values (P less than 0.01), with no difference between WHD and LDHD. Plasma fibrinopeptide A (FPA) levels remained normal during LDHD, but significantly increased during WHD (P less than 0.001). Our data indicate that WHD is feasible, with a low risk of extravascular coagulation. The bleeding risk is not increased during or after dialysis, and the danger of intravascular coagulation is low as confirmed by the isolated elevation of FPA plasma levels, unaccompanied by changes in other variables.

Acute Kidney Injury↗