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K Zawilska

Publications and source records attributed to K Zawilska.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of fibrinolytic and metabolic system parameters in obese patients with polycystic ovary syndrome and women with simple obesity.

The present study aimed to assess the fibrinolytic and metabolic system parameters in obese patients with polycystic ovary syndrome (PCOS) and to compare them in obese PCOS patients and women with simple obesity. We studied 19 obese women with PCOS (age: 25.1 +/- 4.6 years, body mass index (BMI): 34.7 +/- 3.9 kg/m2; mean +/- standard deviation) and 20 age- and BMI-matched ovulatory controls. We measured blood levels of 17beta-estradiol, testosterone, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), dehydroepiandrosterone sulfate (DHEAS), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), glucose and insulin. The following fibrinolytic tests were also performed: euglobulin clot lysis time, plasminogen level, alpha2-antiplasmin activity, plasminogen activator inhibitor-1 activity, fibrinogen concentration and estimated fibrinolytic activity. Testosterone and LH levels were significantly higher in obese women with PCOS (p < 0.01 and p < 0.001, respectively). The groups did not differ with regard to 17beta-estradiol, prolactin, FSH, DHEAS, TC, TG, HDL-C, LDL-C, glucose and insulin. All of the fibrinolysis parameters with the exception of plasminogen were comparable between the two groups. Serum plasminogen level was lower in obese PCOS patients than in women with simple obesity (p < 0.05). Euglobulin clot lysis time was positively correlated with insulin (r = 0.88, p < 0.05) in both groups. Our results show that fibrinolysis is not suppressed in women with PCOS and that there is no difference in fibrinolytic activity between obese patients with PCOS and women with simple obesity.

Adult↗
PubMed2004

Addition of cladribine to daunorubicin and cytarabine increases complete remission rate after a single course of induction treatment in acute myeloid leukemia. Multicenter, phase III study.

To assess the efficacy of an original DAC-7 regimen: daunorubicine (DNR) 60 mg/m2/day, days 1-3; cytarabine (AraC) 200 mg/m2/day, days 1-7; cladribine (2-CdA) 5 mg/m2/day, days 1-5, 400 untreated adult acute myeloid leukemia patients (including 63 with preceding myelodysplastic syndrome), aged 45 (16-60) years were randomized to either DAC-7 (n=200) or DA-7 (without 2-CdA, n=200). The overall CR rate equaled 72% for DAC-7 and 69% for DA-7 arm (P=NS). After a single course of DAC-7 induction, the CR rate equaled 64% and was significantly higher compared to 47% in the DA-7 arm (P=0.0009). Median hospitalization time during the induction was 7 days shorter for DAC-7 compared to the DA-7 group (33 vs 40 days, P=0.002). Toxicity was comparable in both groups. The probability of 3-year leukemia-free survival (LFS) for DAC-7 and DA-7 group equaled 43 and 34%, respectively (P=NS). There was a trend toward higher LFS rate for patients aged >40 years receiving DAC-7 compared with DA-7 regimen (44 vs 28%, P=0.05). This study proves that addition of 2-CdA increases antileukemic potency of DNR+AraC regimen, thus resulting in a higher CR rate after one induction cycle when compared to DA-7, without additional toxicity. It shortens hospitalization time and may improve long-term survival in patients aged >40 years.

Adolescent↗
PubMed2002

The treatment of acute myeloid leukemia with mitoxantrone, etoposide and low-dose cytarabine in elderly patients - a report of Polish Acute Leukemia Group (PALG) phase II study.

The common dilemma in the treatment of elderly patients with acute myeloid leukemia (AML) is whether to use intensive myelosuppresive therapy with higher risk of treatment related mortality (TRM), but a chance for complete remission (CR), or to treat less intensively in order to prolong survival time with a better quality of life. The aim of this prospective, phase II study was to assess the efficacy and toxicity of low dose combination induction treatment consisted of cytarabine at a dose of 10 mg/m2 every 12 h s.c. for 7 days, VP-16 at a dose of 100 mg/day p.o. for 7 days and mitoxantrone at a dose of 6 mg/m2 i.v daily on days 1-3. Two induction courses were planned. In the group of 44 patients 12 (27%) achieved CR, 4 (9%) patients were in PR and there were 9 (20%) early deaths (ED). Age, performance status, preceding myelodysplastic syndrome, karyotype, WBC and % of blasts in bone marrow were not significant prognostic factors for CR probability. The following initial factors appeared to be related to a shorter duration of survival time from the start of treatment: age >70 (p<0.03), poor performance status (p<0.03), and % of BM blasts 50 (p<0.05). We conclude that, despite promising results in the pilot study the efficacy of this induction treatment is not better than the efficacy of other regimens. The hematological toxicity of this treatment seems to be comparable with "3+7" regimen.

Acute Disease↗
PubMed2001

Subcutaneous enoxaparin once or twice daily compared with intravenous unfractionated heparin for treatment of venous thromboembolic disease.

BACKGROUND: Low-molecular-weight heparins administered subcutaneously once or twice daily have been reported to be as safe and efficacious as intravenous unfractionated heparin in the treatment of acute venous thromboembolic disease. OBJECTIVE: To determine whether subcutaneous enoxaparin administered once or twice daily is as effective as continuously infused unfractionated heparin in acute symptomatic venous thromboembolic disease. DESIGN: Randomized, controlled, partially blinded equivalence trial. SETTING: 74 hospitals in 16 countries. PATIENTS: 900 patients with symptomatic lower-extremity deep venous thrombosis, including 287 (32%) with confirmed pulmonary embolism. INTERVENTIONS: Initial therapy with dose-adjusted intravenous unfractionated heparin compared with subcutaneous enoxaparin at fixed dosages of 1.0 mg/kg of body weight twice daily or 1.5 mg/kg once daily. Long-term oral anticoagulation was started in all patients within 72 hours of randomization. MEASUREMENTS: Clinical end points assessed during a 3-month follow-up period. RESULTS: Equivalent efficacy was seen in the heparin group and both enoxaparin groups. Symptomatic venous thromboembolism recurred in 12 of 290 patients receiving unfractionated heparin (4.1%), 13 of 298 patients receiving once-daily enoxaparin (4.4%), and 9 of 312 patients receiving twice-daily enoxaparin (2.9%). Compared with unfractionated heparin, the treatment difference was 0.2% (95% CI, -3.04% to 3.49%) for once-daily enoxaparin and -1.2% (CI, -4.2% to 1.7%) for twice-daily enoxaparin. Incidence of major hemorrhage did not differ among the three treatment groups. Major hemorrhage occurred in 6 of 290 patients (2.1%) in the unfractionated heparin group, 5 of 298 patients (1.7%) in the once-daily enoxaparin group, and 4 of 312 patients (1.3%) in the twice-daily enoxaparin group. CONCLUSIONS: Subcutaneous enoxaparin once or twice daily is as effective and safe as dose-adjusted, continuously infused unfractionated heparin in the prevention of recurrent symptomatic venous thromboembolic disease.

Administration, Cutaneous↗
PubMed1999

Elevation of plasma fibrinogen in silent myocardial ischaemia.

High plasma levels of fibrinogen and plasminogen activator inhibitor (PAI-1) are reported to be correlated with coronary heart disease. Therefore the level of fibrinogen concentration in plasma was examined and verified for the possible correlation with the previously explored PAI-1 antigen and PAI-1 activity in the pathogenesis of premature atherosclerosis (Grzywacz et al., 1998, Blood Coagul Fibrinol. 9, 245-249). Examination included only men, aged 33-46 years, who were in a stable condition for at least six months after the acute event. They were divided into two subgroups: group A (n = 14) with and group B (n = 15) without ischaemic changes in 24 h Holter electrocardiogram. The number of involved vessels visible on the coronarography picture was similar in both groups. In the patients of group A the mean level of fibrinogen (3.92 vs 3.23 g/l, P < 0.05) was higher than in the controls (n = 15). No statistically differences were found between group B and control healthy subjects in any of the parameters measured. There were no correlation between fibrinogen concentration and PAI-1 antigen and activity levels, which were elevated in both groups of patients according to our previous study. Our results indicate that elevated levels of plasma fibrinogen and PAI-1 appeared in the group of patients with more severe disease, as revealed by silent myocardial ischaemia.

Adult↗
PubMed1999

Low molecular weight heparin versus acenocoumarol in the secondary prophylaxis of deep vein thrombosis.

The aim of this study was to determine the efficacy and safety of subcutaneous weight-adjusted dose low molecular weight heparin (LMWH) compared with oral anticoagulant (OA) in the prevention of recurrent venous thromboembolism. In a prospective multicenter trial, 202 patients with symptomatic proximal deep vein thrombosis (DVT) were included. As soon as the diagnosis of DVT was confirmed by phlebography, 101 were randomly assigned to receive LMWH (nadroparin) for secondary prophylaxis and 101 to receive OA (acenocoumarol). Patients in both groups were initially treated with nadroparin in a dose of 85 anti-Xa IU/kg s.c. every 12 h. Secondary prophylaxis with either nadroparin, 85 anti-Xa IU/kg s. c. once daily, or acenocoumarol was continued for at least 3 months. Three patients in the LMWH group and 6 in the OA group were excluded from analysis for various reasons. During the one-year combined secondary prophylaxis and surveillance period, 7 of of the 98 evaluable patients (7.1%) in the LMWH group and 9 of the 95 evaluable patients (9.5%) in the OA group had a documented recurrence of venous thromboembolism (Fisher's exact test, p = 0.61). Of these, 2 patients who received LMWH and 7 patients on acenocoumarol had recurrences in the 3-month period of secondary prophylaxis. Four patients (4.1%) in the LMWH group developed bleeding complications during this study period, as compared with 7 (7.4%) in the OA group (Fisher's exact test, p = 0.37). There were two major bleedings, one in the LMWH group and one in the OA group. Eleven patients died, 5 (5.1%) in the LMWH group and 6 (6.3%) in the OA group. It is concluded that nadroparin in a dose of 85 anti-Xa IU/kg s.c. once daily provides an effective and safe alternative to oral anticoagulants in the secondary prophylaxis of DVT.

Acenocoumarol↗
PubMed1998

Impairment of plasma fibrinolysis in young survivors of myocardial infarction with silent ischaemia.

The aim of this study was to compare fibrinolytic parameters in two subgroups of young survivors of myocardial infarction: group A (n = 14) with silent myocardial ischaemia and group B (n = 15) without silent myocardial ischaemia, as assessed by 24 h Holter electrocardiogram monitoring. Only men aged 33-46 years who were in a stable condition at least 6 months after the acute event were included in the survey. All patients were normolipaemic or had only mild hyperlipidaemia, non-diabetic, normotensive, non-current smokers and with a normal body mass index. The control group consisted of 15 age-matched healthy men. Blood samples were taken at 7.30 a.m. In the group A patients, we found higher mean levels of tissue plasminogen activator (t-PA) total antigen (11.1 versus 6.9 ng/ml, P < 0.01), its inhibitor plasminogen activator inhibitor-1 (PAI-1) antigen (58.1 versus 34.8 ng/ml, P < 0.01), PAI-1 activity (4.9 versus 3.4 U/ml, P < 0.05) and tPA-PAI-1 complexes (5.1 versus 3.5 ng/ml, P < 0.05) as well as a lower level of t-PA activity (0.5 versus 0.8 IU/ml, P < 0.01) and free t-PA antigen (0.8 versus 1.3 ng/ml, P < 0.01) compared with the controls. However, group A patients exhibited higher PAI-1 antigen levels (58.1 versus 41.6 ng/ml, P < 0.05) than those without silent ischaemia. There were no differences between group B and controls in any of the parameters measured. Our results indicate that patients with more severe disease, as revealed by silent myocardial ischaemia, had lower levels of free t-PA as a result of the excess of PAI-1.

Adult↗
PubMed1998

[Combined hemostatic defects in family members of symptomatic carriers of Leiden mutations of factor V].

The aim of the study was to determine the frequency of additional prothrombotic defect in family members of 14 symptomatic, heterozygous carriers of factor V Leiden mutation (FV Leiden). The FV Leiden was found in fifty-five from among 127 persons (43%). Thirty-two from 53 (68%) family carriers of FV Leiden had venous thromboembolic disease at the time of examination. Combined defects were found in 6 out of 14 families (in 4 families coexistence of FV Leiden mutation with protein S deficiency, in 1 with G20210 A mutation of prothrombin gene and in 1 with antithrombin III deficiency). Until now 63% (7/11) of combined defect carriers (mean age 48.5 years) and 59% (24/42) of heterozygous FV Leiden carriers (mean age 52.2 years) have been symptomatic. The thrombosis-free survival (Kaplan-Maier analysis) was comparable in combined and in single defect carriers groups.

Antithrombin III Deficiency↗
PubMed1997

An alternative method for identifying the factor V gene Leiden mutation.

The recently described point mutation of nucleotide 1691 of the factor V gene is responsible for the factor V resistance to a cleavage with an activated protein C (APC-resistance). Despite the high sensitivity and specificity of the APC-resistance test as a screening method for the detection of the factor V APC-resistance, there is still a necessity to develop a simple, cheap and accurate DNA-based assay. Herein, two different ASO-PCR methods were used for the detection of the Leiden mutation. The first involved a direct ASO-PCR with a consensus FV N1 primer and a sequence specific primer for the 1691 bp "G" normal allele (FV G1) or a specific primer for the 1691 bp "A" mutant allele (FV A1). The second method consisted of direct ASO-PCR by using the consensus FV N1 primer and one of two primers with an additional T-->G mismatch at the penultimate position from the 3'-end. One primer was specific for the 1691 bp "G" normal allele (FV G2) and the other was specific for the 1691 bp "A" mutant allele (FV A2). These permit clear and easy distinctions between homozygous normal and heterozygous and homozygous mutant probands. We also tested a T-->A mismatched primer to compare our method with that recently reported by Bellisimo et al. We found that within a large range of PCR conditions, T-->G mismatched oligonucleotides discriminated better than T-->A mismatched between three factor V 1691 position genotypes. We therefore recommend our method for the screening of a single 1691G-->A nucleotide mutation in the factor V gene.

Alleles↗
PubMed1996

Low molecular weight heparin and the heparin mobilisable pool of platelet factor 4 are reduced in young survivors of myocardial infarction.

The platelet factor 4 (PF4) mobilisation properties of low molecular weight heparin (Fraxiparine, Sanofi Winthrop, France) in young survivors of myocardial infarction (YSMI) and healthy volunteers have been investigated. The study group consisted of 42 YSMI less than 44 years old, all of them with angiographically proven occlusive coronary artery disease, studied 6 to 24 months after the acute event. The control group was composed of 30 healthy men of similar age. Subjects from the study and control groups were allocated to the following subgroups: those receiving 60 or 120 IU/kg b.w. of standard heparin (Polfa Kutno, Poland) and those receiving 60, 120 or 180 IC anti-Xa U/kg b.w. of low molecular weight heparin (Fraxiparine, Sanofi Winthrop, France) as a single intravenous injection. Additionally, in five YSMI patients the influence of prolonged aspirin administration (0.3g daily for more than 30 days) on the Fraxiparine mobilsable pool of PF4 and beta-thromboglobulin (beta-TG) concentration in the plasma was determined after injection of 180 IC anti-Xa U/kg b.w. of the drug. The PF 4 and beta-TG concentration in the plasma was evaluated using enzyme immunoassay methods before heparin or Fraxiparine intravenous injection and 2, 5, 10, 20, 30 and 60 min after. In both, the control and YSMI groups baseline PF4 levels were found to be normal. Moreover, similar marked dose-dependent increases of PF4 concentration in the plasma measured after 60 and 120 IU/kg b.w. of heparin as well as after 60 and 120 IC anti-Xa U/kg b.w. of Fraxiparine was found. The administration of 120 IU/kg b.w. of heparin resulted in a reduced rise in plasma PF 4 in YSMI as compared to healthy controls. The same phenomenon was observed when 180 IC anti-Xa U/kg b. w. of Fraxiparine was injected intravenously. In YSMI treatment with aspirin had no influence on the Fraxiparine mobilisable pool of PF 4 or the beta-TG concentration in the plasma. These results suggest that mobilisable pool of platelet factor 4 in young survivors of myocardial infarction derives from the "nonplatelet pool" and that reduction of heparin- or Fraxiparine-releasable pool of PF4 may reflect an impaired endothelium function, probably due to atherosclerosis.

Adult↗
PubMed1996

[Low molecular weight heparin (Fraxiparine) as adjunctive therapy with thrombolysis for acute myocardial infarction: a pilot study with a one year follow up].

In 53 patients with recent (< 6 hrs) acute myocardial infarction a study was undertaken to evaluate the safety of conjunctive therapy with streptokinase (1.5 mln U), aspirin (150 mg) and low molecular weight heparin (Fraxiparine). Patients were treated with Fraxiparine 250 U anti-Xa IC/kg/24 hrs iv for 2 days (with bolus 12.5 U anti-Xa IC/kg), and 125 U anti-Xa IC/kg twice a day sc for 5 subsequent days. Clinical course in one-year observation was compared regarding the time the therapy was initiated. In the group undergoing therapy 3-6 hrs after the infarct had occurred 4 (7.5%) patients died (2 during hospitalization, 2 after discharge). In 31 patients treated within 3 hrs of the myocardial infarction there were fewer cases of recurrent myocardial infarction, unstable angina or congestive heart failure necessitating rehospitalization their (9.1%) than in 22 patients included in the treatment regimen between 3 rd and 6th h of the infarction (27.3%). Earlier thrombolysis was also connected with higher left ventricular ejection fraction (55 +/- 8% vs 49 +/- 10%) and more frequent peak CK-MB values 12 hrs after thrombolysis (81% and 68% of patients respectively). Neither symptomatic deep vein thrombosis nor pulmonary embolism was detected. The left ventricular thrombosis was diagnosed by echocardiography in 4 of 20 patients (20%) with the first anterior myocardial infarction. There was neither bleeding requiring blood transfusion nor cerebrovascular stroke. The treatment with Fraxiparine did not induce the prolongation of APTT values. Conjunctive thrombolytic therapy with low molecular weight heparin was safe and followed by a favorable outcome of the acute myocardial infarction, especially if instituted within the first 3 hrs after the onset of infarction.

Adult↗
PubMed1996

[Point mutation G-->A nucleotide 1691 factor V gene as a cause of developing thrombotic complications in a family with plasma resistance to activated protein C].

The presence of point mutation G-->A of nucleotide 1691 of Factor V gene (Leiden mutation) is responsible for the resistance of factor Va to activated protein C (APC-resistance) and is associated with an increased risk for thrombosis. Herein, we reported on a case of 20 year male with a two years history of recurrent, extensive deep vein thrombosis. His family history showed grand-mother from mother side, who died from thromboembolic disease many years ago. His laboratory investigation reveals abnormal results of APC-resistance test (R = 1.80) and normalized APC-resistance test sensitivity ratio (0.57). Moreover, on the basis of a sequence specific primer polymerase chain reaction (SSP-PCR) a heterozygous from (G/A at 1691 position) of Leiden mutation was found. Family study showed two between 8 others asymptomatic persons with abnormal results of APC-resistance test and heterozygous genotype.

Adult↗
PubMed1996

[Similar risk of thrombosis complications in heterozygous carriers of Leiden mutation and in patients with idiopathic thromboembolic disease].

The aim of the study was to evaluate the thrombosis free survival in unrelated 24 heterozygous carriers for Leiden mutation and in unrelated 26 patients with "idiopathic" thromboembolic disease. The subjects with coexisting antithrombin III, protein C, S deficiency, obesity, antiphospholipid antibodies, cancer or taking oral contraceptives were excluded from analysis. The clinical manifestations of thrombosis were comparable in both investigated group, similarly the mean age of the first episode occurrence (37.2 vs 41.5 years). The probability for development of thrombosis in Kaplan-Meier analysis was not different between two groups. Moreover, during six months of observation period thrombosis reoccurrence rate was similar (1/24 vs 1/26).

Adult↗
PubMed1995

On the action of a heparan-like glycosaminoglycan (Hemovasal) on the mechanism of haemostasis and fibrinolysis.

Hemovasal produced by Manetti-Roberts, Florence, Italy, is a glycosaminoglycan obtained from porcine intestinal mucosa which belongs to the family of heparan sulfates. The substance was examined On 36 male survivors of myocardial infarction with an interval of at least 6 months after the acute event. No anticoagulants were given and ASA was withdrawn at least 2 weeks before the trial. Hemovasal was administered in 3 different i.m. doses as single injections. A further group received a daily oral dose of 300 mg for one week. A comparable placebo group of patients as well as a group of healthy volunteers was run in parallel. The coagulation profile showed only a slight prolongation of the aPTT, a trace of diminution of Antithrombin III and no activation of Heparin cofactor II. The fibrinolytic system showed an enhancement of the diurnal increase of t-PA without an alteration of the total increase of this activity. There was a considerable and highly significant diminution of the PAI-1 activity. This was dose dependent and could be found after i.m. as well as after oral administration. It was assumed that the thrombolytic effect which was repeatedly described was a consequence of the diminution of PAI-1.

Administration, Oral↗
PubMed1995

[Progress in the detection of intravascular activation of fibrinolysis].

Methods for measuring antigen and activity of plasminogen activators (t-PA, u-PA), plasminogen activator inhibitors (PAI-1, PAI-2) and their complex have been improved in the past few years, but few comparative data are available and they should be standardized. In particular the commercial kits for determination of PAI-1 activity seem to be not accurate for the measurement of PAI-1 in plasma. The amount of generated plasmin can be measured as plasmin-alpha-2-antiplasmin complex (PAP). There are also some new tests which could differentiate between fibrinogenolysis (FgDP) and fibrinolysis (FnDP, D-dimer) as between primary and secondary activation of fibrinolysis (B beta 15-42 peptide). Normal D-dimer plasma concentration allows for the ruling out of venous thromboembolism with high probability, but the specificity of this tests is poor.

Enzyme-Linked Immunosorbent Assay↗
PubMed1995

[Thrombophilia in a family with resistance to activated protein C and protein S deficiency].

Although patients with thromboembolic disease frequently have family histories of thrombosis, well-defined defects such as inherited deficiencies of anticoagulant proteins are found only in minority of cases. Herein, we present a family study of 42 years old woman with recurrent deep vein thrombosis which occurred first time four years ago during pregnancy, in subclavian vein, in relation to cardiac stimulator implantation because of atrio-ventricular III(0) block. Her laboratory investigation demonstrated normal APTT time, prothrombin time, platelet number, antithrombin III and protein C activity. Plasma antiphospholipid antibodies contents was within the normal range. The result of activated protein C(APC) resistance test was abnormal (R=1.64). Family study revealed similar degree of APC-resistance defect in her DVT symptomatic mother and two healthy young daughters (R=1.73 and 1.54 respectively). Additionally, a slightly reduced total protein S plasma concentration was found in the patient and her two children. The influence of a slightly reduced protein S level on the results of APC-resistance was excluded by evaluation of normalized activated protein C sensitivity ratio (nAPC-SR) as described de Ronde and Bertina.

Adult↗