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At least 73 records · Page 4Linked to original sources

PubMed2002

Influence of HMG-CoA reductase inhibitors on markers of coagulation, systemic inflammation and soluble cell adhesion.

BACKGROUND: Beneath its lipid-lowering properties additional non-lipid effects of statin therapy are discussed. We therefore examined the impact of statins on laboratory markers of coagulation, inflammation and soluble cell adhesion to further explore these effects in 950 hospitalised patients with angiographically proven CAD. METHODS AND RESULTS: Although no significant differences were found in total cholesterol, LDL and HDL and triglyceride levels a statistically lower value in 277 statin-treated patients was found for von Willebrand factor [162(130/224) vs. 208(154/283)%, P=0.0001], leukocyte count [6.9(5.8/8.4) vs. 7.3(6.1/9.4)/nl, P=0.0005], high sensitive CRP [4.3(1.8/10.8) vs. 7.6(2.8/20.0) mg/dl, P=0.0001], interleukin-6 [9.5(5.1/18.7) vs. 14.4(7.2/28.1) mg/dl, P=0.0001] and soluble p-selectin [112.6(82.0/146.0) vs. 127.8(93.8/162.4) mg/dl, P=0.001] compared to 673 patients without statin therapy. This result was confirmed in a subgroup of 510 patients matched for age, gender and percentage of acute coronary syndromes. CONCLUSIONS: In statin treated patients significantly lower levels of coagulation, systemic inflammation and soluble cell adhesion markers were found. Therefore the effect of statin therapy may also be mediated by additional non-lipid-lowering effects.

Aged↗

PubMed1994

Markers of coagulation and fibrinolysis in portal blood from patients with and without gastric malignancy.

BACKGROUND: The origin of coagulation and fibrinolysis abnormalities in cancer patients is unknown. The aim of this study was to measure markers of coagulation and fibrinolysis in portal and peripheral blood from patients with and without gastric malignancy. METHODS: Blood samples were drawn from the portal vein and a peripheral vein in 39 patients undergoing elective gastric surgery, 18 for gastric malignancy and 21 for benign disorders, and analyzed for prothrombin fragment 1 + 2 (F1 + 2), thrombin-anti-thrombin III complex (TAT), fibrinogen and fibrin degradation products (FgDP, FbDP), and fibrinopeptide A (FpA). RESULTS AND CONCLUSIONS: In portal blood, levels of F1 + 2, TAT, FpA, FgDP, and FbDP did not differ in the two groups. In peripheral blood, levels of FpA and FbDP were higher in cancer patients, but in a multiple regression model malignancy did not contribute significantly to variation in peripheral FpA or FbDP levels. In both groups FpA levels were higher in portal blood than in peripheral blood.

Antithrombin III↗

PubMed2001

Fibrin D-dimer, markers of coagulation activation and the risk of major ischaemic heart disease in the caerphilly study.

We have previously reported that plasma fibrin D-dimer (a marker of turnover of cross-linked fibrin) showed a strong and independent association with incident ischaemic heart disease (IHD) in the Caerphilly Study cohort of 1,998 men aged 49-65. To establish the specificity of this finding, we assayed plasma samples from this cohort with a more specific assay for fibrin D-dimer: this showed an association with incident IHD which was at least as strong and independent as that for the original assay (odds ratio, OR for top fifth compared to bottom fifth 3.79; 95% CI 1.77-8.10; p < 0.0001). To establish potential causes of the increased fibrin turnover, we also assayed several potential markers of coagulation activation or thrombotic tendency (prothrombin fragment F1+2, thrombin-antithrombin complexes, factor VIIc, activated partial thromboplastin time [APTT] and activated protein C resistance): none of these variables were associated with incident IHD in this cohort. We suggest that further studies are required to establish the causes of increased cross-linked fibrin turnover, which is associated with incident IHD in the general population when measured by a specific assay.

Activated Protein C Resistance↗

PubMed2004

Homocysteine and markers of coagulation and endothelial cell activation.

OBJECTIVES: In vitro studies suggest an influence of hyperhomocysteinemia on the coagulation system, but the influence of mild hyperhomocysteinemia in vivo is unclear. METHODS AND RESULTS: We studied the relation between homocysteine and markers of coagulation activation and endothelial cell activation in 279 patients with established atherosclerotic disease. In addition, we performed an investigator-blinded placebo-controlled cross-over study to investigate the influence of acute hyperhomocysteinemia by oral methionine load on these markers in 20 healthy volunteers. In the atherosclerotic patients prothrombin fragment F1+2 and soluble thrombomodulin (sTM) were associated with homocysteine in univariate analyses (P = 0.003 and P = 0.001, respectively), but not in multivariate analyses. Age, creatinine and MTHFR C677T polymorphism were major determinants of homocysteine concentration. MTHFR C677T polymorphism status was not associated with F1+2 and sTM. Median homocysteine concentrations increased in the healthy volunteers after methione load. However, after methionine load or after placebo, we did not observe different plasma concentrations of F1+2 (0.9 nmol L-1 vs. 0.9 nmol L-1, P = 0.39), d-dimer (153 micro g L-1 vs. 151 micro g L-1, P = 0.63) and von Willebrand factor (103% vs. 107%, P = 1.00). CONCLUSIONS: These results provide evidence against a major effect of mild hyperhomocysteinemia on activation of the coagulation system and endothelial cell activation in vivo.

Arteriosclerosis↗

PubMed2002

Fluctuations in levels of antiphospholipid antibodies and increased coagulation activation markers in normal and heparin-treated antiphospholipid syndrome pregnancies.

Antiphospholipid antibodies (aPL) are associated with an increased risk of thrombosis and recurrent miscarriage. We assessed levels of coagulation activation markers and aPL during normal pregnancy and in women with the antiphospholipid syndrome (aPS). Fluctuations in aPL levels were observed in all patients with aPS. No particular pattern of antibody positivity, or fluctuation in aPL level, was associated with poor pregnancy outcome. A significant increase was observed in levels of factor Xlla (FXIIa; P < 0.001), factor VIIa (FVIIa, P < 0.001), thrombin antithrombin complexes (TAT; P < 0.001), prothrombin fragment F1.2 (F1.2; P < 0.001) and D-dimer (DD; P < 0.05) during normal pregnancy. Factor VIIa, TAT, F1.2 and DD increased significantly before 20 weeks gestation, while a statistically significant increase in FXIIa levels was first detected between weeks 20 and 30 of gestation. In pregnant women with aPS, increases in FXIIa were similar to those in normal pregnancy, but increased FVIIa levels were not observed until after 30 weeks gestation. Similar to normal pregnancy, increased levels of TAT and F1.2 were detected in aPS pregnancies before 20 weeks gestation, but increased DD were not observed until after week 20. Surprisingly, women with aPS receiving low molecular weight heparin prophylaxis had significantly higher (P = 0.02) levels of TAT (median 8.6; interquartile range (IQR) 6.5-20.8) between weeks 20 and 30 of gestation compared to the normal pregnant population (median 5.9; IQR 4.7-7.9), thus indicating increased thrombin generation in women with aPS in mid-pregnancy.

Antibodies, Antiphospholipid↗

PubMed2005

Analysis of combination anti-angiogenesis therapy on markers of coagulation, platelet activation and angiogenesis in patients with advanced cancer.

The effects of combination anti-angiogenesis therapy (marimastat, captopril and fragmin) on plasma levels of coagulation initiator tissue factor (TF), platelet marker soluble P-selectin and angiogenic vascular endothelial growth factor (VEGF) were tested in 25 patients with advanced cancer. They had higher soluble P-selectin (P<0.001) and TF (P<0.001), but not VEGF (P=0.066) than 25 age and sex-matched controls. VEGF and TF correlated significantly (r=0.8, P<0.001) in cancer patients. Soluble P-selectin, TF and VEGF did not change at 4- and 8-weeks whilst on treatment. We provide further evidence linking coagulation and angiogenesis but combination anti-angiogenesis therapy does not influence plasma soluble P-selectin, TF or VEGF.

Adult↗

PubMed2005

The effects of 12 weeks of HMR 3339, a novel selective estrogen receptor modulator, on markers of coagulation and fibrinolysis: a randomized, placebo-controlled, double-blind, dose-ranging study in healthy postmenopausal women.

OBJECTIVE: To investigate the short-term effects of HMR 3339, a novel selective estrogen receptor modulator, on markers of coagulation and fibrinolysis. STUDY DESIGN: In a multicenter, 14-week, randomized, placebo-controlled, double-blind, dose-ranging study, healthy postmenopausal women received daily placebo (n = 22), HMR 3339 2.5 mg (n = 25), HMR 3339 10 mg (n = 24), HMR 3339 50 mg (n = 24), or raloxifene 60 mg (n = 23). Statistical analysis was performed using standard parametric tests. RESULTS: After 12 weeks, compared with placebo, HMR 3339 50 mg induced the largest mean percentage changes in antithrombin (-14.6%, P < .001), protein C (-12.9%, P = .029), and fibrinogen (-26.3%, P = .001). Decreases were observed in the HMR 3339 2.5 mg group, compared with placebo, in tissue-type plasminogen activator (-55.0%, P = .026 after 4 weeks), plasmin-alpha2-antiplasmin complex (-85%, P = .031 and -63.3%, P = .008, respectively, after 4 and 12 weeks), and D-dimer (-91.4%, P = .018 after 12 weeks). Compared with placebo, raloxifene 60 mg decreased total protein S (-8.2%, P = .009) after 4 weeks and antithrombin (-6.0%, P = .034) and fibrinogen (-18.1%, P = .007) after 12 weeks. CONCLUSION: HMR 3339 and raloxifene decreased fibrinogen levels. In the low dosage, HMR 3339 showed potentially beneficial effects on some markers of fibrinolysis. Both drugs impaired the anticoagulatory potential.

Biomarkers↗

PubMed2004

More fibrosis and thrombotic complications but similar expression patterns of markers for coagulation and inflammation in symptomatic plaques from DM2 patients.

OBJECTIVE: One of the possible pathological mechanisms behind the increased vascular injury in diabetes mellitus type 2 (DM2) is the formation of advanced glycation end products (AGEs). The aim of this study was to investigate whether the presence of AGEs and specific markers for coagulation and inflammation in symptomatic atherosclerotic plaques from DM2 patients differs from plaques from nondiabetics. METHODS AND RESULTS: Carotid atherectomies were obtained from DM2 patients (n=11) and controls without DM2 matched for age and other cardiovascular risk factors (n=12) who were treated for symptomatic carotid artery stenosis. Plaques were graded according to the American Heart Association classification of lesions. More fibrosis and more thrombotic complications (p=0.007) were observed in carotid atherectomies from DM2 patients. Percentages of immunostained smooth muscle cells and macrophages in the lesions, quantified planimetrically, did not differ between the two groups. No differences were found in the immunostaining for T cells, tissue factor (TF), endothelial protein C receptor (EPCR), nuclear factor kappaB, and the AGE carboxymethyllysine. CONCLUSIONS: These findings demonstrate that DM2 is associated with increased plaque complications; however, a local changed presence of AGEs, TF, and EPCR seems not to be involved in this end stage of atherosclerosis.

Aged↗

PubMed2001

Effects of oral and transdermal estrogen replacement therapy on markers of coagulation, fibrinolysis, inflammation and serum lipids and lipoproteins in postmenopausal women.

We compared the effects of oral estradiol (2 mg), transdermal estradiol (50 microg), and placebo on measures of coagulation, fibrinolysis, inflammation and serum lipids and lipoproteins in 27 postmenopausal women at baseline and after 2 and 12 weeks of treatment. Oral and transdermal estradiol induced similar increases in serum free estradiol concentrations. Oral therapy increased the plasma concentrations of factor VII antigen (FVIIag) and activated factor VII (FVIIa), and the plasma concentration of the prothrombin activation marker prothrombin fragment 1+2 (F1+2). Oral but not transdermal estradiol therapy significantly lowered plasma plasminogen activator inhibitor-1 (PAI-1) antigen and tissue-type plasminogen activator (tPA) antigen concentrations and PAI-1 activity, and increased D-dimer concentrations, suggesting increased fibrinolysis. The concentration of soluble E-selectin decreased and serum C-reactive protein (CRP) increased significantly in the oral but not in the transdermal or placebo groups. In the oral but not in the transdermal or placebo estradiol groups low-density-lipoprotein (LDL) cholesterol, apolipoprotein B and lipoprotein (a) concentrations decreased while high-density-lipoprotein (HDL) cholesterol, apolipoprotein AI and apolipoprotein All concentrations increased significantly. LDL particle size remained unchanged. In summary, oral estradiol increased markers of fibrinolytic activity, decreased serum soluble E-selectin levels and induced potentially antiatherogenic changes in lipids and lipoproteins. In contrast to these beneficial effects, oral estradiol changed markers of coagulation towards hypercoagulability, and increased serum CRP concentrations. Transdermal estradiol or placebo had no effects on any of these parameters. These data demonstrate that oral estradiol does not have uniformly beneficial effects on cardiovascular risk markers and that the oral route of estradiol administration rather than the circulating free estradiol concentration is critical for any changes to be observed.

Administration, Cutaneous↗

PubMed2004

Evaluation of venous thromboembolism and coagulation-fibrinolysis markers in Japanese patients with inflammatory bowel disease.

BACKGROUND: Arterial or venous thromboembolism is rarely encountered clinically as an extradigestive tract complication in inflammatory bowel disease (IBD). However, it is one of the important prognostic factors for IBD patients. The present study was designed to evaluate the relationship between pulmonary embolism (PE) and deep vein thrombosis (DVT) with coagulation-fibrinolysis markers in patients with active IBD. METHODS: In 47 consecutive cases hospitalized due to active IBD [26 with Crohn's disease (CD) and 21 with ulcerative colitis (UC)], we evaluated the disease severity, blood tests, pulmonary ventilation-perfusion scan (V/Q scan), and magnetic resonance venography (MRV) or conventional venography. RESULTS: PE was diagnosed by V/Q scan in 5 (2 with CD and 3 with UC; 10.6%). DVT was diagnosed in 5 (2 with CD and 3 with UC; 10.6%). Of the 47 patients, 8 (17.0%) had venous thromboembolism (either PE or DVT), and 2 of them (4.3%) had both conditions. In UC patients, the thrombosis group was in more severe stages based on endoscopic grading than the nonthrombosis group. In all patients, the thrombosis group were older (50.3 +/- 14.3 years) than the nonthrombosis group (29.2 +/- 11.7 years). Furthermore, the thrombosis group had higher thrombin-antithrombin III complex (13.1 +/- 17.7 ng/ml) and d-dimer (964 +/- 1402 ng/ml) values than the nonthrombosis group (5.3 +/- 5.5 ng/ml, P=0.0245, and 207 +/- 192 ng/ml, P=0.0016, respectively). There were no significant differences in leukocyte and platelet counts, C-reactive protein, and fibrinogen between the two groups. CONCLUSIONS: A high incidence of venous thromboembolism was suggested in Japanese patients with active IBD. We should be careful with thrombosis in treatment of IBD patients, especially those who are of older age and in more severe stages.

Adult↗

PubMed1997

Coagulation activation markers in the prediction of venous thrombosis after elective hip surgery.

BACKGROUND: Despite prophylaxis, deep vein thrombosis (DVT) after hip surgery continues to occur frequently. Thus it would be helpful if before surgery patients at higher risk of DVT could be identified and more adequate prophylaxis given. As part of an international study on the prevention of DVT after total hip replacement, we investigated whether preoperative levels of three coagulation activation markers, prothrombin fragment F1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT) and D-dimer, correlate with results of postoperative venography. METHODS: 159 patients undergoing total hip replacement were randomized to receive 10, 15 or 20 mg desirudin bid or 5000 IU unfractionated heparin tid immediately before surgery and then for 11 days, until bilateral venography was performed. Preoperative F1 + 2, TAT and D-dimer plasma levels were measured using ELISA procedures. As no difference among anticoagulant treatments or in the interaction between treatments and DVT was detected for any of the three variables, results are reported as pooled data. FINDINGS: The frequency of DVT was 18.8% in the low (0.75-1.33 nM) vs 65.7% in the high third of distribution (1.77-3.47 nM) of F1 + 2 (p < .001), 27.3% in the low (2.00-2.50 micrograms/l) vs 57% in the high third (5.10-61.00 micrograms/l) of TAT (p = .042), and 29.4% in the low (39-59 micrograms/l) vs 57.1% in the high third (129-651 micrograms/l) of D-dimer (p = .051). INTERPRETATION: Preoperative F1 + 2, TAT and D-dimer levels are associated with the risk of development of DVT after total hip replacement.

Adult↗

PubMed1992

Determination of markers of coagulation activation and reactive fibrinolysis in patients with mechanical heart valve prosthesis at different intensities of oral anticoagulation.

In a group of 60 patients with mechanical heart valve prosthesis prothrombin fragment 1 + 2, thrombin-antithrombin III complexes and D-dimer have been determined in order to assess the residual coagulation activation and the extent of the reactive fibrinolysis. The patients were divided into three subgroups of 20 patients each with different intensities of oral anticoagulation as indicated by International Normalized Ratio (INR) values in the ranges 4.8-3.6, 3.5-2.5 and 2.4-2.1. From the two markers of coagulation activation studied (prothrombin fragment 1 + 2 and thrombin-antithrombin III (TAT)) the prothrombin fragment 1 + 2 was dependent on the INR level in all groups, although the median values were still significantly beneath the lower limit of the reference range. The D-dimer concentrations were unexpectedly high with respect to the low coagulation activation levels, as indicated by the D-dimer/TAT and D-dimer/F 1 + 2 ratios. This demonstrates the enhanced presence of fibrin degradation products as a scarcely described side-effect of oral anticoagulation. The anticoagulant properties of fibrin degradation products might contribute partly to the in vivo haemorrhagic risk in high-intensity oral anticoagulation. These results show, inasmuch as the prothrombin fragment 1 + 2 is concerned, that from the laboratory point of view the residual thrombin activity is low enough to be adequate under the therapeutical regimen followed in this study. However, the question of the efficacy of anticoagulation intensities can only be finally answered by clinical trials.

Administration, Oral↗

PubMed1999

Activation markers of coagulation.

Advances in our understanding of the biochemistry of the haemostatic mechanism have led to the development of sensitive methods for measuring peptides, enzyme-inhibitor complexes, and enzymes that are liberated with the activation of the coagulation system in vivo. Studies employing these markers have provided important mechanistic information regarding haemostatic mechanism function both under normal conditions and in response to pathogenic stimuli. While assays for particular components can denote the presence of a 'biochemical' hypercoagulable state prior to the appearance of overt thrombotic phenomena, most of these markers thus far have not been shown to be useful in managing individual patients. Properly designed prospective studies will be required to determine whether these assay techniques will aid in the identification of patients predisposed to thrombotic events or the monitoring of antithrombotic therapy.

Animals↗

PubMed1993

Laboratory markers of coagulation activation.

Advances in our understanding of the biochemistry of the hemostatic mechanism have led to the development of sensitive methods for measuring peptides, enzyme-inhibitor complexes, or enzymes that are liberated with the activation of the coagulation system in vivo. Studies employing these markers indicate that a biochemical imbalance between procoagulant and anticoagulant mechanisms can be detected in the blood of humans prior to the appearance of thrombotic phenomena. Properly designed prospective studies will be required to determine whether these assay techniques will enable us to identify individuals who are entering a clinically relevant hypercoagulable state and intervene with appropriate therapy prior to the onset of overt thrombotic disease.

Aged↗

PubMed1994

Activation markers of coagulation.

Advances in our understanding of the biochemistry of the haemostatic mechanism have led to the development of sensitive methods for measuring peptides, enzyme-inhibitor complexes or enzymes that are liberated with the activation of the coagulation system in vivo. Studies employing these markers indicate that a biochemical imbalance between procoagulant and anticoagulant mechanisms can be detected in the blood of humans prior to the appearance of thrombotic phenomena. Properly designed prospective studies will be required to determine whether these assay techniques will enable us to identify individuals who are entering a clinically relevant hypercoagulable state, and intervene with appropriate therapy prior to the onset of overt thrombotic disease.

Animals↗

PubMed1992

Markers of coagulation and fibrinolysis after fractures of the lower extremities.

The study was performed to detect activation of coagulation and fibrinolysis in terms of prothrombin fragment 1 and 2 (F1 + 2), thrombin-antithrombin III complex (TAT), fibrin degradation products (FbDP), fibrinogen degradation products (FgDP), and soluble fibrin monomers (FM) in plasma from 39 patients with fractures of the lower extremities. We found substantially elevated levels of the molecular markers at admission and on the day after admission (Day 1) compared with control levels. Admission levels of F1 + 2, TAT, FbDP and FgDP were significantly higher compared with levels on day 1, whereas levels of FM were not significantly different between the two days. Generally there were good correlations between all markers of coagulation and fibrinolysis at admission whereas correlations were weaker or absent on day 1. In conclusion we found substantial haemostatic activation as a immediate response to trauma. Increased levels of F1 + 2, TAT, FM, FbDP and FgDP appear to be a normal physiological reaction after fractures of the lower extremities.

Adult↗

PubMed2003

Changes in coagulation and markers of fibrinolysis in horses undergoing colic surgery.

Activation of coagulation can be frequently found in horses with colic. However, it has also been demonstrated as a sequela of surgical trauma alone in humans. The purpose of the present study was to determine changes in coagulation and fibrinolysis in horses that underwent colic surgery and to evaluate whether these changes were secondary to the colic or the surgery and wound healing. Thirty horses that underwent colic surgery with uncomplicated recovery were included. Ten horses with a Forssell's procedure served as control group with a standardized surgical trauma. Besides daily physical examinations during the observation period of 10 days, activated partial thromboplastin time (aPTT), prothrombin time and thrombin time as well as fibrin monomer (FM), D-Dimer (DD) and antithrombin (AT) III were determined. Compared with the control group the aPTT was the only standard coagulation test that was significantly prolonged before and after the event of colic surgery. After surgery, hyperfibrinogenaemia occurred in all groups. In colic groups FM and DD concentrations were within reference range at admission,and were significantly greater than in control horses after surgery. AT III activity decreased after colic surgery, but did not change in the control group. It was concluded that an activated coagulation state after colic surgery has to be expected, resulting not only from the colic disease, but also from the event of surgery.

Animals↗

PubMed1995

Markers of coagulation activation for evaluation of the antithrombotic efficacy of heparin: a prospective study in acute deep venous thrombosis.

The potential value of measurements of prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin complexes (TAT) and D-dimer for the assessment of antithrombotic efficacy of heparin in acute deep venous thrombosis (DVT) was prospectively investigated. These variables were determined at presentation and subsequently once daily during a course of seven days heparin therapy. Heparin doses were adjusted according to the activated partial thromboplastin time (APTT). Compression ultrasonography was performed at presentation and on day 7 to determine the extent of thrombosis according to a predefined score. Out of a total of 50 patients accrued to the study 44 patients had reduced or unchanged extent of thrombosis, whereas in six patients an extension was documented. Although thrombin generation was significantly inhibited after initiation of heparin therapy as reflected by a decrease in F1 + 2 and TAT levels, these markers were not useful for the detection of patients with DVT extension. In contrast, anti-factor-Xa activities but not APTT measurements were significantly lower in the group of patients with propagation of DVT (median: 0.22 U/ml versus 0.38 U/ml, interquartile range: 0.1-0.33 U/ml versus 0.19-0.55 U/ml; P = 0.001). D-dimer decreased within the first days of heparin therapy but failed to indicate DVT progression. These data suggest that plasma anti-factor-Xa activity correlates better with the antithrombotic efficacy of heparin than APTT measurements and markers of coagulation or fibrinolysis activation.

Adult↗