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Biomedical subjects

W Muntean

Publications and source records attributed to W Muntean.

At least 37 records · Page 2Linked to original sources
PubMed2000

Plasma concentrations after intravenous administration of phylloquinone (vitamin K(1)) in preterm and sick neonates.

Vitamin K prophylaxis usually is administered orally or intramuscularly, but in neonatal intensive care oral administration might not be feasible and intramuscular administration is not general practice in very small infants. No data are available about plasma levels after intravenous administration of vitamin K to neonates. Therefore, we investigated plasma levels in 18 infants: 14 preterms with a birthweight of 1785+/-648 g and 4 sick newborns with a birth-weight of 3167+/-510 g after administration of a single dose of 0.3+/-0.1 mg/kg phylloquinone (vitamin K(1)) (Konakion MM((R)), Roche) intravenously after birth. Blood was collected 22.9+/-18.4 hours after intravenous administration of vitamin K(1). In 10 neonates a second sample was obtained 111.8+/-49.1 hours after the first vitamin K(1) administration. Gas chromatography-mass spectrometry (GC-MS) was used as the method for determination of vitamin K(1). The measured plasma concentration after intravenous administration of vitamin K(1) was 191.3+/-102.6 ng vitamin K in the first sample /mL in the first sample and 98.7+/-75.2 ng vitamin K(1)/mL in the second samples. These results are similar to those described in newborns after oral administration of 3 mg vitamin K(1) and after intramuscular administration of 1.5 mg vitamin K(1). In conclusion, the recommendation of the producer to give 0.4 mg/kg of vitamin K intravenously to neonates, in whom oral or intramuscular administration is not feasible, seems to be rational.

Female↗
PubMed2000

Determinants of haemostatic risk factors for coronary heart disease in obese children and adolescents.

OBJECTIVE: To investigate the contribution of serum lipids, parameters of glucose metabolism, body composition and cardiovascular fitness to the variance of several haemostatic risk factors for coronary heart disease (CHD) in obese children and adolescents. SUBJECTS AND MEASUREMENTS: Forty-two healthy, obese children and adolescents (20 male, 22 female, age 12.6 +/- 3.2y; body mass index (BMI), 30.4 +/- 5.3 kg/m2), were screened for haemostatic and metabolic risk factors for CHD. Thirty-five of the participants (18 male, age 13.5 +/- 2.9y; BMI, 29.9 +/-4.5kg/m2; 17 female, age 12.8+/-2.1 y, BMI, 31.1 +/- 5.3 kg/m2) were assessed for cardiovascular fitness by means of incremental cycle ergometer exercise. RESULTS: After adjustment for age, fat mass correlated significantly with plasminogen activator inhibitor-1 antigen (PAI-1-Ag) in boys and girls and factor VIIc only in girls. Children with lower power output (< or = 2.77W/kg) showed significantly higher values for factor VIIc, fibrinogen and tissue-type plasminogen activator antigen (tPA-Ag). Neither body composition nor cardiovascular fitness contributed independently to the variance of the determined haemostatic risk factors, except PAI-1-Ag, which has been shown to be determined by fat mass. In multiple linear regression analysis, triglycerides and PAI-1-Ag explained significant independent proportions of the variance of tPA-Ag. Factor VIIc was explained by C-peptide, insulin and fibrinogen. Von Willebrand factor antigen (vWF-Ag) was significantly related to glucose and insulin. CONCLUSION: The results suggest that in obese children and adolescents the haemostatic risk factors factor VIIc, vWF-Ag and tPA-Ag are mainly determinated by plasma insulin and triglyceride concentrations, but are primarily independent of body composition and cardiovascular fitness.

Adolescent↗
PubMed2000

Treatment of children with haemophilia in Europe: a survey of 20 centres in 16 countries.

A survey was made of the current status of treatment of haemophilic boys at 20 centres in 16 European countries and includes approximately 1500 of the estimated 6500 haemophiliacs in the participating countries. Many mild haemophiliacs are not seen, or seen infrequently, at haemophilia centres and this requires study. Nine of 18 centres provide continuous prophylaxis to 80-100% of their patients, five centres provide it to 55-80% and the remaining four centres to 15-40% of the boys. The median dose given was 6240 U kg-1 year-1 (range 3120-7800). Four centres administered only recombinant concentrates to children with severe haemophilia A, while seven centres administered recombinant concentrates to 75-90% and the remaining centres to less than 50% of the boys (two centres < 10%). When asked for the choice of concentrate for a newly diagnosed boy with severe haemophilia A, all but one centre preferred recombinant concentrate. Most boys below 6 years received concentrates via a peripheral vein but three centres preferred a central venous line for 80-100% of the boys. Thirteen of 18 centres applied home treatment to 84-100% of the boys and the remaining five centres to 57-77% of the boys.

Adolescent↗
PubMed2000

Effect of heparin, platelets, activated platelets, platelet fragments, and hematocrit on activated clotting time.

Activated clotting time (ACT) is the most commonly used laboratory test to control the heparin effect during extracorporeal techniques. The study was undertaken in order to test in vitro the influence of heparin, platelet count, hematocrit, platelet fragmentation, and platelet activation on ACT. Blood was drawn from volunteer donors into syringes containing citrate. Platelet counts and hematocrit were modified. Platelets were fragmented by sonifier or activated by collagen and adenosine diphosphate (ADP). Different heparin final concentrations were created. Increasing concentrations of heparin had a significant effect on ACT. However, it was not predictable in every case in concentrations lower than 1.0 U/ml. Platelet count generally had no significant effect on ACT. The effect of hematocrit was detectable in a group but not in single cases. Fragmented platelets significantly shortened ACT only without addition of heparin, and the effect was only partly predictable. Activation of platelets by collagen and ADP induced no significant changes. Our results show that heparin is reflected by ACT but that effect is not predictable in every specific patient. Our results also show that other variables that may be altered during extracorporeal techniques such as platelet count, hematocrit, activation, and fragmentation of platelets do not severely influence the ACT.

Adenosine Diphosphate↗
PubMed2000

Relationship between plasminogen activator inhibitor-1 antigen, leptin, and fat mass in obese children and adolescents.

Hyperleptinemia may be associated with cardiovascular risk and is linked with parameters of fibrinolytic processes in adults. We studied whether body fatness, leptin, and insulin interact with plasminogen activator inhibitor-1 antigen (PAI-1-Ag) and tissue-type plasminogen activator antigen (tPA-Ag) in obese children and adolescents. Twenty-three boys (mean +/- SD: age, 10.7 +/- 3.3 years; body mass index [BMI], 28.7 +/- 5.4 Kg/m2) and 19 girls (age, 11.9 +/- 2.7 years; BMI, 29.4 +/- 4.8 Kg/m2) were investigated. Body fat mass (FM) in the children was calculated by bioelectrical impedance analysis, and blood samples were obtained for leptin, insulin, C-peptide, PAI-1-Ag, and tPA-Ag. The children were divided into 3 subgroups according to maturation. Maturity was associated with greater adiposity and higher levels of leptin and C-peptide, but insulin and PAI-1-Ag were not different between prepubertal, pubertal, and late/postpubertal children. PAI-1-Ag was associated with leptin and insulin, but not after adjustment for fatness. PAI-1-Ag was independently associated with tPA-Ag (r = .36, P < .02). Multiple regression analysis showed that tPA-Ag failed to reach the level of significance (P = .07), but FM contributed to the variation in PAI-1-Ag (adjusted R2 = .29). The BMI was the main determinant for the variation in leptin (adjusted R2 = .386) and in insulin (adjusted R2 = .60, all P < .001). Neither gender, maturation, chronological age, or leptin contributed significantly to the variation in either PAI-1-Ag or tPA-Ag. Our data suggest that adiposity and other variables contribute to higher levels of PAI-1-Ag. Leptin seems not to be independently linked with fibrinolytic parameters, but an unfavorable metabolic and fibrinolytic risk profile might emanate from the obese pubertal stage.

Adipose Tissue↗
PubMed2000

Effects of the glycoprotein IIb/IIIa receptor antagonist c7E3 Fab and anticoagulants on platelet aggregation and thrombin potential under high coagulant challenge in vitro.

The present study was performed to investigate the combined effects of the platelet glycoprotein IIb/IIIa receptor antagonist c7E3 Fab (abciximab) and the anticoagulants unfractionated heparin (UH), low molecular weight heparin (LMWH), and recombinant hirudin (rH) on platelet aggregation and thrombin generation under high coagulant challenge by extrinsic activation of platelet-rich plasma. Platelet aggregation and thrombin generation were assessed simultaneously in the presence of different concentrations of abciximab and anticoagulants. Increasing concentrations of abciximab resulted in a dose-dependent anti-aggregating effect with a maximum at 20 microg/ml. Doses of 5, 10, and 20 microg/ml abciximab prolonged the lag phase until the onset of platelet aggregation, but this effect was independent of the dosage used. Abciximab had no influence on the thrombin potential under our high coagulant challenge. UH, LMWH, and rH showed a dose-dependent prolongation of the lag phase until the onset of platelet aggregation and decreased the thrombin potential. Addition of anticoagulants did not contribute to further inhibition of platelet aggregation in the presence of abciximab, but the combination of abciximab and anticoagulants exhibited an additive effect on prolongation of the lag phase until the onset of platelet aggregation. Addition of abciximab to anticoagulants did not result in further decrease of the thrombin potential. Our study demonstrates the respective specific effects of abciximab and anticoagulants on platelet aggregation and thrombin potential under high coagulant challenge, and also an additive effect of abciximab and the anticoagulants UH, LMWH, and rH on the lag phase until the onset of platelet aggregation.

Abciximab↗
PubMed2000

Correlation between cholesterol, soluble P-selectin, and D-dimer in obese children and adolescents.

Thirty-eight obese children and adolescents were investigated for a possible relation between cholesterol and markers of platelet activation, endothelial cell dysfunction, and activation of the coagulation system. Soluble P-selectin, von Willebrand factor antigen (vWf-Ag), D-dimer, and prothrombin fragment 1 + 2 (F1 + 2) were determined by enzyme-linked immunosorbent assays, and factor VIII coagulant activity (VIIIc) was measured by means of one-stage clotting assay. Cholesterol correlated significantly with log P-selectin (r = 0.43, P = 0.003) and log D-dimer (r = 0.33, P = 0.02). Cholesterol did not correlate with vWf-Ag, factor VIIIc, and F1 + 2. Log P-selectin correlated significantly with log D-dimer (r = 0.42, P = 0.003), which remained significant after adjustment for cholesterol (P = 0.02). Log D-dimer correlated significantly with F1 + 2 (r = 0.38, P = 0.01). Our study demonstrates that, in obese children and adolescents, cholesterol is significantly associated with P-selectin and D-dimer, and suggests an unfavorable intercorrelation between metabolic and hemostatic risk factors for coronary heart disease in childhood obesity.

Adolescent↗
PubMed1999

Effects of antithrombin and protein C on thrombin generation in newborn and adult plasma.

It has been suggested that antithrombin (AT) and protein C (PC) might be less important in newborn plasma than in adult plasma for the inhibition of clotting activation. To assess the importance of AT and PC for the regulation of thrombin generation in newborn as compared with adult plasma, thrombin generation was determined in the presence of different concentrations of AT and PC. In both, newborn and adult plasmas, reduction of AT and PC resulted in an increase of thrombin generation after intrinsic activation. On the other hand, supplementation of AT and PC decreased thrombin generation in a dose-dependent manner. Clotting times were influenced by different PC concentrations, whereas clotting times were almost not affected by different amounts of AT. Our study suggests that the significance of AT and PC in the regulation of thrombin generation is the same in newborn and adult plasma. Our experimental results also support the notion that administration of AT or protein C concentrates may be beneficial in some clinical situations leading to an increased clotting activation in newborns.

Adult↗
PubMed1999

Coagulation and anticoagulation in extracorporeal membrane oxygenation.

The hemostatic system poses a major problem in extracorporeal membrane oxygenation (ECMO). The foreign surface in the extracorporeal circuit activates platelets and the clotting system. To avoid loss of platelets and activation of the clotting system, anticoagulation is necessary. In addition, in many patients on ECMO, preexisting clotting disorders are present. Therefore, bleeding and/or thrombosis are frequent complications in ECMO patients that require specific treatment and may even necessitate termination of ECMO. Most ECMO centers use heparin for anticoagulation and the activated clotting time (ACT) for monitoring. Reduction of problems with hemostasis may be obtained with less thrombogenic surfaces, new anticoagulants with a short half-life, platelet inhibitors, protease inhibitors, or selective anticoagulation in the extracorporeal circuit. While there will probably never be a complete nonthrombogenic surface available and all anticoagulants will have some risk of bleeding, improvement can be obtained by a combination of measures including better surfaces, more sophisticated anticoagulation regimens, and close laboratory monitoring.

Anticoagulants↗
PubMed1999

Recombinant factor VIIa does not induce hypercoagulability in vitro.

Recombinant factor VIIa (rVIIa) has been reported to be clinically effective and safe in haemophilic patients with inhibitor antibodies. Compared to activated prothrombin complex concentrates the risk of thrombotic complications seems to be very low after rVIIa administration. Determination of free thrombin generation has been shown to identify hypercoagulability. Therefore, free thrombin and prothrombinase activity (Xa generation) were assessed after extrinsic activation of rVIIa supplemented factor VIII and factor IX deficient plasma. Free thrombin generation was also determined after supplementation of (activated) prothrombin complex concentrates. Addition of 150 U rVIIa/ml shortened the clotting times markedly in control, factor VIII, and factor IX deficient plasma. In contrast, free thrombin and Xa generation were not different in the absence or presence of 150 U rVIIa/ml. Addition of (activated) prothrombin complex concentrates resulted in a marked increase of free thrombin generation in all investigated plasmas. Although in vitro studies cannot reflect specific clinical circumstances our results support the notion that rVIIa does not induce a hypercoagulable state as sporadically observed after administration of (activated) prothrombin complex concentrates.

Blood Coagulation↗
PubMed1998

Activation of the haemostatic system in children with juvenile rheumatoid arthritis correlates with disease activity.

Twenty-four children with juvenile rheumatoid arthritis (JRA) and 10 children with postinfectious arthropathies were investigated for markers of blood coagulation and fibrinolytic activity: Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), and D-Dimer were measured using solid phase enzyme linked immunosorbent assays (ELISA). Results were compared with clinical and conventional laboratory signs of disease activity. F1+2, TAT, D-Dimer, and fibrinogen were significantly elevated in children with JRA as compared with healthy children and children with postinfectious arthropathies. F1+2, TAT, and D-Dimer correlated significantly with disease activity, assessed by determination of the joint index score and C-reactive protein (CRP). The study demonstrates a subclinical activation of the haemostatic system in children with JRA correlating with disease activity, which might be caused by the action of several immunomediators on cells (monocytes, endothelial cells) playing a role in the regulation of blood coagulation activity.

Adolescent↗
PubMed1998

Factor V Leiden and prothrombin gene G 20210 A variant in children with ischemic stroke.

OBJECTIVE: To investigate if the factor V Leiden mutation (F-V-LM) and/or the prothrombin gene G 20210 A variant (P-G20210A-V) are risk factors for acute stroke in Austrian children. PATIENTS: 33 children with acute ischemic stroke documented by computer tomography and/or magnetic resonance imaging of the brain were enrolled in an open multicenter survey. RESULTS: 6/33 children had F-V-LM (5 heterozygous, 1 homozygous). This represents 18% (95% CI: 6.7-39.9%) of our pediatric stroke population and thus exceeds the expected prevalence in the Austrian population of 4,6% (Fischer's exact test, p = 0.01). F-V-LM was not found in 11 children with neonatal stroke but in 6/22 children with stroke after the neonatal period. 5/6 children with F-V-LM had an underlying disorder that is a risk factor for stroke in children. The P-G20210A-V was detected in 1/26 (3.85%; 95% CI: 0.1-21.4%) patients. Comparison of the prevalence of P-G20210A-V in our study with that in the general population of Austria of 1% revealed no statistical significance (Fischer's exact test, p = 0.38). CONCLUSION: Our data suggest that the F-V-LM is a risk factor for acute stroke in Austrian children beyond the neonatal period. The P-G20210A-V apparently does not represent a risk factor for stroke in Austrian children.

Activated Protein C Resistance↗
PubMed1997

Longer aPTT values in healthy children than in adults: no single cause.

We have shown that activated partial thromboplastin time values in children are considerably longer than in adults, but the causes for this observation remained unclear. Therefore, we investigated the correlation between activated partial thromboplastin time values and concentrations of clotting factors, quotients and titers of the tissue thromboplastin inhibition test, and antiphospholipid antibodies in healthy children, children with recurrent infections, and adults. Concentrations of factors VIII, IX, and HMWK were significantly lower in children than in adults. Simple linear regression analysis failed to show a correlation between the concentration of a single clotting factor and the activated partial thromboplastin time values. No significant correlation was found between activated partial thromboplastin time and elevation of the tissue thromboplastin inhibition test quotients or titers, or antiphospholipid antibodies values. The determined activated partial thromboplastin time was best described by a function including all measured coagulation factors. Our study suggests, that no single clotting factor or lupus anticoagulants are responsible for the longer activated partial thromboplastin time in healthy children, but that activated partial thromboplastin prolongation is caused by the combination of several slightly lower clotting factors.

Adolescent↗
PubMed1997

Hyporeactivity of neonatal platelets is not caused by preactivation during birth.

UNLABELLED: Little information exists concerning platelet function in neonates due to the small blood volume. Most studies using conventional aggregation methods have shown a diminished response to various agonists. This is in contrast to the lack of a bleeding tendency and to a short bleeding time in healthy neonates. In previous work we have shown that in healthy term neonates even after an uncomplicated delivery signs of thrombin generation can be demonstrated. This activation of the clotting system may also lead to platelet activation in the neonate. We investigated by means of flow cytometry the expression of activation markers GMP 140 and GP 53 on the surface of neonatal platelets and GP 53 intracellularly by means of a newly developed assay. The expression of GMP 140 and of GP 53 after thrombin stimulation was significantly higher on adult rather than neonatal platelets, while there was no difference between neonatal and adult platelets using GP 53 as intracellular marker. In none of the healthy term neonates after an uncomplicated delivery were activated platelets demonstrated. CONCLUSION: Our data show that the decreased reactivity of neonatal platelets is not caused by preactivation during birth but rather represents a developmental phenomenon. Possibly the observed hyporeactivity of neonatal platelets to thrombin helps to prevent harmful effects of birth stress on the clotting system of neonates.

Antigens, CD↗