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PubMed1998

Elevated activation markers of coagulation in patients undergoing orthognathic surgery.

Surgery is associated with a variable but increased incidence of postoperative venous thromboembolism (VTE). The risk of VTE after orthognathic surgery is unknown. Recently developed assays for activation markers of blood coagulation allow the detection of a prethrombotic state and may thus help to identify surgical procedures with a risk of postoperative VTE. The pre- and postoperative levels of thrombin-antithrombin complex (TAT) and prothrombin fragment 1+2 (F1+2) were studied in ten patients undergoing orthognathic surgery. Mean levels of TAT and F1+2 were within the normal range preoperatively (TAT:2.6+1.0 microg/L, F1+2:0.8+0.2 nmol/L). A significant increase in both parameters occurred postoperatively (TAT:21.8+21.4 microg/L, P<0.005; F1+2:1.3+0.4, P<0.02). No increase was observed in a control group (n=13) consisting of patients undergoing minor surgical procedures in general anesthesia. Our study shows that a marked activation of the coagulation cascade occurs during orthognathic surgery which warrants further studies on the true incidence of postoperative VTE in patients undergoing orthognathic surgery.

Adolescent↗
PubMed2005

Markers of coagulation activation, endothelial stimulation and inflammation in patients with peripheral arterial disease.

OBJECTIVES: Patients with peripheral arterial disease have a significantly increased risk of cardiovascular and cerebrovascular mortality. Studies have shown that some haemostatic and inflammatory markers are elevated in these patients but the effect of the severity of the disease has not been fully documented. The aim of this study was to assess the level of coagulation activation, endothelial stimulation and inflammation in patients with claudication and critical limb ischaemia (CLI) compared to healthy controls. DESIGN AND METHODS: A prospective observational study was conducted amongst 202 subjects: 132 claudicants, 30 patients with critical ischaemia, and 40 controls. D-dimer (DD) and thrombin-antithrombin III (TAT) levels measured using ELISA as markers of coagulation activation. von Willebrand factor (vWF) and high-sensitivity C-reactive protein (CRP) levels were measured as markers of endothelial and inflammatory stimulation. RESULTS: vWF and CRP levels were significantly higher in patients with intermittent claudication (1.9 U/ml, range 0.78-4.05; p < 0.001; 3.4 mg/l, range 0.15-24; p > 0.001, respectively) and critical ischaemia (2.36 U/ml; range 1.03-5.69; p < 0.001; 7.17 mg/ml, range 0.15-174; p < 0.001, respectively) compared to controls (1.28 U/ml, range 0.62-3.13; 1.04, range 0.15-7.59 mg/l). DD was also significantly higher in claudicants (48.6 microg/ml; range 2-1741; p < 0.001) and in patients with CLI (61.1 microg/ml, range 3.65-1963; p < 0.001) compared to controls (26.1 microg/ml, range 9.65-203.1). TAT levels were significantly higher in CLI (3.14 mg/l, range 2.09-58.11), compared to controls (2.36 mg/l, range 1.49-7.38; p = 0.004). Patients with CLI had significantly higher levels of CRP, vWF, and TAT than claudicants. CONCLUSIONS: Coagulation activation and endothelial stimulation are significantly increased in patients with peripheral arterial disease compared to healthy controls. Coagulation and endothelial activation increases with the severity of the arterial disease.

Aged↗
PubMed1998

Markers of coagulation and fibrinolysis as measures of disease activity in inflammatory bowel disease.

BACKGROUND: Activation of coagulation and fibrinolysis occurs in patients with inflammatory bowel disease. Our aim was to study the course of a marker for activation of the coagulation cascade, prothrombin fragment 1 + 2 (F1+2), and fibrinolysis, fibrin degradation products (FbDP), in patients with ulcerative colitis and Crohn's disease before and during therapy with glucocorticoids. METHODS: Twenty-seven patients with active ulcerative colitis and 42 with active Crohn's disease treated with glucocorticoids were studied. Plasma samples were drawn before, during, and at end of therapy or at time of treatment failure. F1+2 and FbDP were measured with commercially available enzyme immunoassays. RESULTS: Mean base-line concentrations of F1+2 were significantly increased in patients with ulcerative colitis (4.77 +/- 0.50 nmol/l; P < 0.0001) and in Crohn's disease (4.66 +/- 0.59 nmol/l; P < 0.0001) compared with healthy controls (1.57 +/- 0.09 nmol/l). Mean base-line concentrations of FbDP were significantly increased in patients with ulcerative colitis (1264 +/- 161 microg FE/l; P < 0.0001) and in Crohn's disease (491 +/- 51 microg FE/l; P < 0.0001) compared with healthy controls (194 +/- 21 microg FE/l). During treatment with glucocorticoids the plasma concentrations of FbDP decreased in patients with Crohn's disease achieving remission and in patients with ulcerative colitis avoiding surgery but remained unchanged in patients not responding to therapy. In contrast, F1+2 remained increased in patients with Crohn's disease and ulcerative colitis irrespective of outcome. CONCLUSION: The present data support the concept that coagulation cascade and fibrinolysis is activated in patients with active inflammatory bowel disease. F1+2 and FbDP correlate poorly with the clinical disease activity and acute-phase reactants. The clinical response to treatment with glucocorticoids is accompanied by a decrease in plasma concentrations of FbDP but not in F1+2. FbDP may emerge as a new marker in the assessment of disease activity in patients with inflammatory bowel disease.

Adult↗
PubMedDate not supplied

Hypercoagulable state in patients with hypercholesterolemia: effects of pravastatin.

Molecular markers of the coagulation system and the effects of pravastatin on lipid levels and the coagulation markers were studied in 48 patients (mean age, 55 years) with hypercholesterolemia (plasma total cholesterol levels > 280 mg/dl). Each patient received 10 mg of pravastatin daily for 3 months. Plasma total cholesterol and low-density lipoprotein cholesterol levels decreased significantly during treatment and high-density lipoprotein cholesterol levels increased significantly. Above-normal plasma levels of thrombin-antithrombin III complex, fibrinopeptide A, FDP-D-dimer, plasminogen activator inhibitor-I, and thrombomodulin were found in the patients before treatment; each of these was reduced significantly during treatment. The findings suggest the presence of a hypercoagulable state in hypercholesterolemia and that pravastatin might prevent the hypercoagulable state by reducing hypercholesterolemia.

Adult↗
PubMed2005

Coagulation and inflammatory markers in Alzheimer's and vascular dementia.

Alzheimer's disease is classified as a degenerative dementia while vascular dementia is known to be associated with atherothrombosis and classical vascular risk factors. However, over the last decade, there is increasing evidence of the role of haemostatic factors and inflammatory mechanisms in the pathogenesis of Alzheimer's disease. Serum markers of hypercoagulability and markers of inflammation could lead to thrombosis, accelerated atherogenesis and resulting dementia of both Alzheimer's and vascular dementia. In this case control study, we studied these serum markers of coagulation and inflammation in patients suffering from dementia.

Alzheimer Disease↗
PubMed1999

Neutrophil activation and hemostatic changes in healthy donors receiving granulocyte colony-stimulating factor.

Granulocyte colony-stimulating factor (G-CSF) enhances neutrophil functions in vitro and in vivo. It is known that neutrophil-derived products can alter the hemostatic balance. To understand whether polymorphonuclear leukocyte (PMN) activation, measured as PMN degranulation and phenotypical change, may be associated to hemostatic alterations in vivo, we have studied the effect of recombinant human G-CSF (rHuG-CSF) administration on leukocyte parameters and hemostatic variables in healthy donors of hematopoietic progenitor cells (HPCs). Twenty-six consecutive healthy donors receiving 10 micrograms/kg/d rHuG-CSF subcutaneously for 5 to 7 days to mobilize HPCs for allogeneic transplants were included in the study. All of them responded to rHuG-CSF with a significant white blood cell count increase. Blood samples were drawn before therapy on days 2 and 5 and 1 week after stopping rHuG-CSF treatment. The following parameters were evaluated: (1) PMN activation parameters, ie, surface CD11b/CD18 antigen expression, plasma elastase antigen levels and cellular elastase activity; (2) plasma markers of endothelium activation, ie, thrombomodulin (TM) and von Willebrand factor (vWF) antigens; (3) plasma markers of blood coagulation activation, ie, F1+2, TAT complex, D-dimer; and (4) mononuclear cell (MNC) procoagulant activity (PCA) expression. The results show that, after starting rHuG-CSF, an in vivo PMN activation occurred, as demonstrated by the significant increment of surface CD11b/CD18 and plasma elastase antigen levels. Moreover, PMN cellular elastase activity, which was significantly increased at 1 day of treatment, returned to baseline at day 5 to 6, in correspondence with the elastase antigen peak in the circulation. This change was accompanied by a parallel significant increase in plasma levels of the two endothelial and the three coagulation markers. The PCA generated in vitro by unstimulated MNC isolated from rHuG-CSF-treated subjects was not different from that of control cells from untreated subjects. However, endotoxin-stimulated MNC isolated from on-treatment individuals produced significantly more PCA compared with both baseline and control samples. All of the parameters were decreased or normal 1 week after stopping treatment. These data show that rHuG-CSF induces PMN activation and transiently affects some hemostatic variables in healthy HPC donor subjects. The clinical significance of these findings remains to be established.

Adolescent↗
PubMed1993

Normalization of markers of coagulation activation with a purified protein C concentrate in adults with homozygous protein C deficiency.

Homozygous or double heterozygous protein-C deficiency can present at birth with purpura fulminans or later in life with venous thrombosis. Two homozygous patients who had previously sustained thrombotic episodes were investigated at a time when they were asymptomatic and not receiving antithrombotic therapy. The plasma levels of protein-C antigen and activity in both individuals were approximately 20% of normal. We administered a highly purified plasma-derived protein C concentrate to these individuals and monitored levels of several markers of in vivo coagulation activation. Assays for protein-C activation (activated protein C and protein C activation peptide) showed a sustained increase from reduced baseline levels, whereas thrombin generation (as measured by prothrombin fragment F1 + 2) gradually decreased over about 24 hours into the normal range. These investigations provide direct evidence that protein C is converted to activated protein C in vivo, and that the protein-C anticoagulant pathway is a tonically active mechanism in the regulation of hemostatic system activation in humans.

Adult↗
PubMed1994

Age and functional correlations of markers of coagulation and inflammation in the elderly: functional implications of elevated crosslinked fibrin degradation products (D-dimers).

OBJECTIVE: To measure markers of inflammation in a cohort of young and old subjects and relate these findings to the functional level of the individuals. DESIGN: For the pilot study, blood samples were obtained from 18 young (age 20-35 years) and 18 old (age 68-83 years) subjects. The main study population included community-dwelling subjects between the ages of 70 and 79. The group consisted of 282 subjects with minimal physical limitations, 17 subjects from the middle third, and 16 from the lower third of physical function rankings. METHODS: Plasma markers were measured by ELISA techniques, and certain biochemical values were obtained through routine clinical tests performed by a commercial laboratory. RESULTS: D-Dimers were higher for physically impaired subjects in all groups, but most prominently among black females, who also had significantly higher D-Dimer levels in every functional group. To inquire whether higher D-Dimers were associated with markers of inflammation, we also examined the macrophage metabolite, neopterin, the neutrophil product, elastase complexed to antitrypsin (E/a), and the albumin globulin ratio (A/G ratio). No differences were found in neopterin or E/a levels on the basis of gender, race, or functional status. The A/G ratio was significantly lower in functionally impaired subjects. CONCLUSION: These preliminary findings demonstrate racial/ethnic and gender differences in D-Dimers in a population of community-dwelling elderly, and suggest that factors influencing hemostasis may be particularly relevant to physical functional status in black women. A sample containing more subjects with lower physical function will be needed to establish the relationship between inflammation, altered hemostasis, and physical function decline.

Adult↗
PubMed1999

Clinical trials of low-molecular-weight heparins in cardiology.

Our understanding of the pathophysiology of acute coronary syndromes is evolving as the role of prognostic coagulation markers and the different effects unfractionated heparin and low-molecular-weight heparins have on these coagulation markers are investigated. The results of recent clinical trials of low-molecular-weight heparins in acute coronary syndromes are summarized, and an economic evaluation of enoxaparin for these indications is reviewed.

Acute Disease↗
PubMed2003

Markers of coagulation and angiogenesis in cancer-associated venous thromboembolism.

PURPOSE: We sought to determine whether venous thromboembolism in cancer patients is associated with aberrant plasma levels of hemostatic and angiogenic factors. PATIENTS AND METHODS: Peripheral blood was collected before anticoagulant therapy from cancer patients with acute deep venous thrombosis (DVT; DVT + cancer group, n = 32), those without DVT (cancer control group, n = 36), and patients with acute DVT but no cancer (DVT control group, n = 58). Plasma assays of activation and inhibition of coagulation and fibrinolysis, as well as angiogenesis activation, were then performed. RESULTS: Median levels of thrombin-antithrombin complex, prothrombin fragments 1 + 2, and von Willebrand factor antigen were significantly greater in the DVT + cancer group than in the cancer control and DVT control groups (17.8 ng/mL v 4.6 ng/mL and 9.8 ng/mL, P =.0001 and P =.003, respectively; 3.65 nmol/L v 1.60 nmol/L and 2.71 nmol/L, P <.0001 and P =.011, respectively; and 4.04 U/mL v 2.26 U/mL and 2.06 U/mL, P <.0001, respectively). Median levels of tissue-type plasminogen activator were also significantly higher, while protein C activity was lower in the DVT + cancer group than in the DVT control group (14.6 ng/mL v 9.50 ng/mL, respectively, P =.0005; 0.89 U/mL v 1.11 U/mL, respectively, P =.0008). CONCLUSION: These data not only support prior observations of coagulation activation in patients with malignancy, but also provide new evidence for enhanced coagulation activation in the setting of acute venous thromboembolism in cancer. Future prospective studies are warranted to determine whether these and other potential markers of hypercoagulability may help to identify cancer patients at highest risk for venous thromboembolism.

Biomarkers↗
PubMed1997

Biochemical markers of coagulation activation in mitral stenosis, atrial fibrillation, and cardiomyopathy.

Advances in the understanding of the biochemistry of the mechanism of hemostasis have led to the development of sensitive methods for determining levels of markers which reflect thrombin activity (thrombin-antithrombin III complex, fibrinopeptide A, F1 + 2 fragment), active fibrinolysis (D-dimer, plasmin-alpha 2-plasmin inhibitor complex), and platelet activity (platelet factor 4, beta-thromboglobulin) in vivo. Measurement of these markers may be useful in identifying patients with various cardiovascular disorders at high risk of thromboembolism.

Atrial Fibrillation↗
PubMed1999

Variations in coagulation factors in women: effects of age, ethnicity, menstrual cycle and combined oral contraceptive.

To assess variations of coagulation factors in women, 123 women were included in a cross-sectional study of the effect of age, ethnic origin, blood group and menstrual cycle on surface induced coagulation time (activated partial thromboplastin time) and plasma levels of Factor VIII clotting assay, von Willebrand factor antigen, von Willebrand factor activity and factor XI. The effect of menstrual cycle was further assessed in a longitudinal study including 39 Caucasian women, 20 of whom were using combined oral contraceptives. Activated partial thromboplastin time was longer in women with blood groups B or O, and plasma levels of factor VIII clotting assay, von Willebrand factor antigen and von Willebrand factor activity were significantly higher in black women. Fibrinogen, von Willebrand factor antigen and von Willebrand factor activity concentrations showed strong cyclic variations with peak values in the luteal phase. This pattern was dampened for von Willebrand factor antigen and von Willebrand factor activity but completely disappeared for fibrinogen with the use of combined oral contraceptives. There was a cyclical pattern for factor VIII clotting assay in pill users, evidence of which was not evident in non-pill users. There were strong associations between the levels of von Willebrand factor antigen and von Willebrand factor activity and age, with levels rising by an average of 0.17 and 0.15 U/ml, respectively, for each 10 year increase in age. In conclusion, there are great inter- and intraindividual variations in coagulation markers in women due to different physiological conditions such as age, ethnicity, blood group and phases of the menstrual cycle. However, there were no significant associations between coagulation markers and weight, alcohol consumption or smoking status.

Adolescent↗
PubMed1999

Activation markers of coagulation and fibrinolysis: alterations and predictive value in acute coronary syndromes.

Several alterations of the coagulation, of the fibrinolysis and of inflammation are known in patients with acute coronary syndromes. To extent current knowledge of the pathophysiology and to optimize therapeutical strategies, the new molecular markers can be used in clinical studies. Furthermore, several studies were undertaken to assess the prognostic value of activation markers of these systems for patients with unstable angina pectoris and acute myocardial infarction with or without thrombolytic therapy. The majority of studies focussed on markers of thrombin activation, fibrinogen, fibrin degradation products and t-PA and its main inhibitor PAI-1. While there are stimulating results from larger studies, the value for prognosis for the individual patient still is limited by the overlap of patients with good versus a poor outcome.

Acute Disease↗
PubMed1998

Progressive expansion of hypertensive intracerebral hemorrhage by coagulopathy.

To test the hypothesis that an impaired coagulation system facilitates rapid expansion of hypertensive intracerebral hemorrhage (HICH), coagulation markers were assayed in plasma and their relations to both the hemorrhage size and its progressive expansion were analyzed. Ninety patients with HICH were studied. On admission, plasma samples were taken for the coagulation assay. Hematoma volume was calculated from a computed tomography (CT) scan and its enlargement was estimated by comparison to the volume of the hematoma calculated from a second CT scan taken later within 24 hr. Nine out of 90 patients showed enlargement in their hematoma size (enlarged hematoma group). Four of the enlarged hematoma group fell into acute fatal deterioration and died. Plasma levels of both fibrino peptide A (17.2+/-7.8 vs. 4.0+/-0.6 ng/ml, P < 0.05) and thrombin-antithrombin complex (21.9+/-3.1 vs. 7.4+/-2.8 ng/ml, not significant) were higher in the unchanged group than those in the enlarged hematoma group. In the hematoma-enlarged group fibrino-peptide A level did not exceed 10 ng/ml. In the hematoma unchanged group thrombin-AT-III complex values were positively correlated to hematoma volume. Thus, the coagulation system seemed to be highly activated depending on the hemorrhage volume within three hr after ictus in hypertensive intracerebral hemorrhage patients. When thrombin generation was not sufficient after bleeding, the hematoma seemed to be progressively enlarged. In conclusion, plasma levels of the coagulation markers on admission could be useful predictors of the possible enlargement of hematoma which leads to a poor outcome.

Aged↗
PubMed1992

Gemfibrozil reduces plasma prothrombin fragment F1 + 2 concentration, a marker of coagulability, in patients with coronary heart disease.

The effects of gemfibrozil on several indices of haemostatic activity were explored in male patients with coronary heart disease (CHD). Sixty-three of 71 patients completed a crossover study in which gemfibrozil 1,200 mg/day and matching placebo were each taken in randomised order for 2 months in a double-blind manner, separated by a 2-month washout period. Serum cholesterol decreased by an average (95% confidence interval) of 12 (9 to 15)% and non-fasting triglyceride concentration by 43 (34 to 51)% during active treatment. Plasma prothrombin fragment F1 + 2 concentration, a marker of the in vivo rate of generation of thrombin, was 25 (12 to 37)% lower on average while on gemfibrozil than during the placebo phase. Factor VII coagulant activity (VIIc) and antigen concentration, and fibrinopeptide A concentration were not influenced by gemfibrozil in the group overall. However, the VIIc response appeared to be dependent upon the untreated cholesterol level. Hypercholesterolaemic men (cholesterol greater than 6.5 mmol/l) experienced a significant reduction in VIIc averaging 6% of standard during active therapy. Other effects of gemfibrozil were a 5 (2 to 9)% increase in plasma fibrinogen by a gravimetric method, an 11 (8 to 13)% increase in platelet count, and a 6 (2 to 10)% reduction in white cell count. The reduced incidence of CHD following gemfibrozil therapy in hyperlipidaemic patients may arise in part through a reduction in procoagulant activity and thus the risk of an occlusive coronary thrombosis.

Biomarkers↗
PubMed1994

[Markers of intravascular activation of coagulation].

New markers of intravascular activation of coagulation have been developed, based on advance in our understanding of the biochemistry of the haemostatic mechanism. These are sensitive methods for measuring of peptides liberated with the generation of thrombin (factor IX activation peptide, factor X activation peptide, peptide F1 + 2), for measuring concentration of enzyme-inhibitor complexes (eg. thrombin-antithrombin III-TAT complexes), as well as for investigating the effect of thrombin on fibrinogen (fibrinopeptide A-FPA) or on protein C (protein C activation peptide). Studies employing these markers indicate that a state of hypercoagulability can be detected in the blood of humans prior to the appearance of thrombotic phenomena. However, further studies will be required to determine whether these methods can identify individuals who are entering a clinically relevant hypercoagulable state as well as to monitor an antithrombotic treatment.

Animals↗
PubMed2004

Impact of lifestyle habits on the prevalence of the metabolic syndrome among Greek adults from the ATTICA study.

BACKGROUND: Individuals with the metabolic syndrome (MS) are at high risk for coronary heart disease and may benefit from aggressive lifestyle modification. In this study, we evaluated the effect of leisure time physical activity (PA) and the Mediterranean diet (MD) on the prevalence of the MS. METHODS: The ATTICA study is a health and nutritional survey. On the basis of a multistage, random sampling, 1128 men and 1154 women (>18 years old) without any evidence of cardiovascular disease or diabetes mellitus were enrolled from the greater Athens area during 2001 to 2002. The MS was defined according to the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III criteria. PA was determined from a detailed questionnaire and graded according to the kcal/min expanded. MD was assessed through a validated nutrient questionnaire. RESULTS: The overall prevalence of the MS was 453 of 2282 subjects (19.8%). Of these subjects, 284 (25.2%) were men and 169 (14.6%) were women (P <.001). The prevalence of the MS increased accordingly to age (P for trend <.001). With multiple logistic regression analysis, the odds ratio of having the MS when the participant consumed the MD was 0.81 (95% CI, 0.68-0.976), and when even a little to moderate PA (<7 kcal/min)was reported, the odds ratio was 0.75 (95% CI, 0.65-0.86). The higher levels of inflammation and coagulation markers among participants with MS did not explain much of the aforementioned effect of lifestyle modification. CONCLUSION: MS is common in Greece and is becoming even more common in the middle-aged population. The suggested therapeutic lifestyle approach may contribute to the reduction of the prevalence of the MS, beyond the levels of several lipid, inflammation, and coagulation markers.

Adult↗