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D-dimer Levels (d-dimer + level)
Kinds of D-dimer Levels Selected AbstractsCorrelation of a high D-dimer level with poor outcome in traumatic intracranial hemorrhageEUROPEAN JOURNAL OF NEUROLOGY, Issue 10 2007J.-R. Kuo The correlations between D-dimer and Glasgow Coma Scale (GCS), pupillary light reflex, distance of midline shift on brain computed tomography (CT), and Glasgow Outcome Score (GOS) in patients with trauma/non-trauma intracranial hemorrhage (ICH) are not consistent in studies. Ninety-eight traumatic and 59 non-traumatic ICH patients were studied. Pre-existing venous thrombosis, recent surgery, drug use (aspirin or coumadin), or malignancy, were excluded. D-dimer level was estimated within hours after acute insult, and statistical analyses were used for comparisons between groups. Traumatic ICH patients had higher D-dimer levels than controls (2984 vs. 256 ,g/l; P = 0.001). The GCS, midline shift on brain CT, pupillary reflex, and GOS at 3 months were significantly correlated with high D-dimer value in traumatic patients (individual P < 0.001), but not in the non-traumatic group. Using receiver-operating characteristic curve (ROC), the cutoff point was 1496 ,g/l, with sensitivity and specificity of 100% and 83%, respectively. D-dimer ,1496 ,g/l predicted a poor outcome [adjusted odds ratio (OR) 14.44, 95% CI 1.16,179.27; P = 0.038]. A high D-dimer level is associated with a poor outcome in patients with traumatic ICH. It can be used in addition to neurological assessment to predict the outcome. [source] Hemostatic Defect in Baboons Autotransfused Treated Plasma to Simulate Shed BloodJOURNAL OF CARDIAC SURGERY, Issue 6 2006C. Robert Valeri M.D. This study was done to determine how autotransfusion of nontreated plasma and plasma treated with urokinase with and without aprotinin affected hemostasis in healthy baboons. Methods: A 500-mL volume of blood was collected from the baboon, a 250-mL volume of plasma was isolated, and the RBCs were reinfused. Three baboons were autotransfused untreated plasma. Four baboons received plasma that had been treated with 3000 IU/mL urokinase at +37°C for 30 minutes. Eight baboons received plasma that had been treated first with urokinase 3000 IU/mL at +37°C for 30 minutes and then with aprotinin (1000 KIU/mL). Bleeding time, fibrinogen degradation products (FDP), D-dimer, and alpha-2 antiplasmin levels were measured. Results: During the 4-hour period following autotransfusion of the urokinase-aprotinin-treated plasma, the levels of D-dimer and FDP were significantly higher and fibrinogen and alpha-2 antiplasmin levels were significantly lower than those levels seen after the autotransfusion of nontreated plasma. FDP and D-dimer levels showed significant positive correlations with prothrombin time (PT) and activated partial thromboplastin time (aPTT). A significant negative correlation was observed between thrombin time (TT) and fibrinogen level. A significant positive correlation was observed between bleeding time and D-dimer level and a significant negative correlation between the bleeding time and the fibrinogen level. Conclusions: The infusion of a volume of urokinase or urokinase-aprotinin treated autologous plasma equivalent to 15% of the blood volume was not associated with a bleeding diathesis in healthy baboons. [source] High D-dimer levels increase the likelihood of pulmonary embolismJOURNAL OF INTERNAL MEDICINE, Issue 2 2008L. W. Tick Abstract. Objective., To determine the utility of high quantitative D-dimer levels in the diagnosis of pulmonary embolism. Methods., D-dimer testing was performed in consecutive patients with suspected pulmonary embolism. We included patients with suspected pulmonary embolism with a high risk for venous thromboembolism, i.e. hospitalized patients, patients older than 80 years, with malignancy or previous surgery. Presence of pulmonary embolism was based on a diagnostic management strategy using a clinical decision rule (CDR), D-dimer testing and computed tomography. Results., A total of 1515 patients were included with an overall pulmonary embolism prevalence of 21%. The pulmonary embolism prevalence was strongly associated with the height of the D-dimer level, and increased fourfold with D-dimer levels greater than 4000 ng mL,1 compared to levels between 500 and 1000 ng mL,1. Patients with D-dimer levels higher than 2000 ng mL,1 and an unlikely CDR had a pulmonary embolism prevalence of 36%. This prevalence is comparable to the pulmonary embolism likely CDR group. When D-dimer levels were above 4000 ng mL,1, the observed pulmonary embolism prevalence was very high, independent of CDR score. Conclusion., Strongly elevated D-dimer levels substantially increase the likelihood of pulmonary embolism. Whether this should translate into more intensive diagnostic and therapeutic measures in patients with high D-dimer levels irrespective of CDR remains to be studied. [source] Favorable response of pediatric stem cell recipients to human protein C concentrate substitution for veno-occlusive diseasePEDIATRIC TRANSPLANTATION, Issue 1 2007S. W. Eber Abstract:, Plasminogen activator inhibitor 1 is known to be elevated in patients with hepatic VOD after intensive chemotherapy. To re-establish endogenous fibrinolysis and to inhibit thrombin formation, we used non-APC (zymogen) to normalize PAI-1 levels. As a consequence of thrombin formation inhibition and the consecutive inhibition of the coagulation cascade, this treatment is expected to reduce the elevated D-dimer level. Six pediatric stem cell recipients with moderate or severe VOD after busulfan or total body irradiation conditioning regimen are reported here who were therapy-refractory to defibrotide or rt-PA therapy. All patients had low levels of PC activity (16,39%). The administration of PC (60,240 IU/kg) led to a rapid and sustained rise in PC activity (target level >80%) with near normalization of prothrombin and partial thromboplastin time in all patients. Elevated PAI-1 levels declined. Five of the six patients showed a good clinical response with prompt resolution of clinical, sonographic, and laboratory signs of hepatic blood flow obstruction, while one patient with severe VOD, as well as concomitant liver GVHD and CMV disease, had a slow but detectable response to PC therapy. All patients survived. [source] Preliminary study of D-dimer as a possible marker of acute bowel ischaemiaBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2001Dr S. Acosta Background: Occlusion of the superior mesenteric artery (SMA) demands prompt recognition and diagnosis. No accurate diagnostic method is available. The aim of this study was to determine whether the fibrinolytic marker D-dimer is a useful early marker of acute bowel ischaemia. Methods: Fourteen patients suspected of having acute bowel ischaemia were analysed for an increase in plasma D-dimer level. Results: Six patients had embolic or thrombotic occlusion of the SMA and all had significantly higher D-dimer levels than those without thromboembolic occlusion (P < 0·05). Four patients with strangulation of the small bowel due to adhesions and one with a ruptured aortic aneurysm also had raised D-dimer values. Conclusion: In patients with suspected thromboembolic occlusive disease of the SMA, a raised level of D-dimer indicated the presence of acute bowel ischaemia, whatever the cause. A more extensive prospective study is needed to evaluate a potential survival benefit using the test as a marker of the need for urgent laparotomy. © 2001 British Journal of Surgery Society Ltd [source] Correlation of a high D-dimer level with poor outcome in traumatic intracranial hemorrhageEUROPEAN JOURNAL OF NEUROLOGY, Issue 10 2007J.-R. Kuo The correlations between D-dimer and Glasgow Coma Scale (GCS), pupillary light reflex, distance of midline shift on brain computed tomography (CT), and Glasgow Outcome Score (GOS) in patients with trauma/non-trauma intracranial hemorrhage (ICH) are not consistent in studies. Ninety-eight traumatic and 59 non-traumatic ICH patients were studied. Pre-existing venous thrombosis, recent surgery, drug use (aspirin or coumadin), or malignancy, were excluded. D-dimer level was estimated within hours after acute insult, and statistical analyses were used for comparisons between groups. Traumatic ICH patients had higher D-dimer levels than controls (2984 vs. 256 ,g/l; P = 0.001). The GCS, midline shift on brain CT, pupillary reflex, and GOS at 3 months were significantly correlated with high D-dimer value in traumatic patients (individual P < 0.001), but not in the non-traumatic group. Using receiver-operating characteristic curve (ROC), the cutoff point was 1496 ,g/l, with sensitivity and specificity of 100% and 83%, respectively. D-dimer ,1496 ,g/l predicted a poor outcome [adjusted odds ratio (OR) 14.44, 95% CI 1.16,179.27; P = 0.038]. A high D-dimer level is associated with a poor outcome in patients with traumatic ICH. It can be used in addition to neurological assessment to predict the outcome. [source] Hemostatic Defect in Baboons Autotransfused Treated Plasma to Simulate Shed BloodJOURNAL OF CARDIAC SURGERY, Issue 6 2006C. Robert Valeri M.D. This study was done to determine how autotransfusion of nontreated plasma and plasma treated with urokinase with and without aprotinin affected hemostasis in healthy baboons. Methods: A 500-mL volume of blood was collected from the baboon, a 250-mL volume of plasma was isolated, and the RBCs were reinfused. Three baboons were autotransfused untreated plasma. Four baboons received plasma that had been treated with 3000 IU/mL urokinase at +37°C for 30 minutes. Eight baboons received plasma that had been treated first with urokinase 3000 IU/mL at +37°C for 30 minutes and then with aprotinin (1000 KIU/mL). Bleeding time, fibrinogen degradation products (FDP), D-dimer, and alpha-2 antiplasmin levels were measured. Results: During the 4-hour period following autotransfusion of the urokinase-aprotinin-treated plasma, the levels of D-dimer and FDP were significantly higher and fibrinogen and alpha-2 antiplasmin levels were significantly lower than those levels seen after the autotransfusion of nontreated plasma. FDP and D-dimer levels showed significant positive correlations with prothrombin time (PT) and activated partial thromboplastin time (aPTT). A significant negative correlation was observed between thrombin time (TT) and fibrinogen level. A significant positive correlation was observed between bleeding time and D-dimer level and a significant negative correlation between the bleeding time and the fibrinogen level. Conclusions: The infusion of a volume of urokinase or urokinase-aprotinin treated autologous plasma equivalent to 15% of the blood volume was not associated with a bleeding diathesis in healthy baboons. [source] High D-dimer levels increase the likelihood of pulmonary embolismJOURNAL OF INTERNAL MEDICINE, Issue 2 2008L. W. Tick Abstract. Objective., To determine the utility of high quantitative D-dimer levels in the diagnosis of pulmonary embolism. Methods., D-dimer testing was performed in consecutive patients with suspected pulmonary embolism. We included patients with suspected pulmonary embolism with a high risk for venous thromboembolism, i.e. hospitalized patients, patients older than 80 years, with malignancy or previous surgery. Presence of pulmonary embolism was based on a diagnostic management strategy using a clinical decision rule (CDR), D-dimer testing and computed tomography. Results., A total of 1515 patients were included with an overall pulmonary embolism prevalence of 21%. The pulmonary embolism prevalence was strongly associated with the height of the D-dimer level, and increased fourfold with D-dimer levels greater than 4000 ng mL,1 compared to levels between 500 and 1000 ng mL,1. Patients with D-dimer levels higher than 2000 ng mL,1 and an unlikely CDR had a pulmonary embolism prevalence of 36%. This prevalence is comparable to the pulmonary embolism likely CDR group. When D-dimer levels were above 4000 ng mL,1, the observed pulmonary embolism prevalence was very high, independent of CDR score. Conclusion., Strongly elevated D-dimer levels substantially increase the likelihood of pulmonary embolism. Whether this should translate into more intensive diagnostic and therapeutic measures in patients with high D-dimer levels irrespective of CDR remains to be studied. [source] Effect of oral melatonin on the procoagulant response to acute psychosocial stress in healthy men: a randomized placebo-controlled studyJOURNAL OF PINEAL RESEARCH, Issue 4 2008Petra H. Wirtz Abstract:, Acute mental stress is a potent trigger of acute coronary syndromes. Catecholamine-induced hypercoagulability with acute stress contributes to thrombus growth after coronary plaque rupture. Melatonin may diminish catecholamine activity. We hypothesized that melatonin mitigates the acute procoagulant stress response and that this effect is accompanied by a decrease in the stress-induced catecholamine surge. Forty-five healthy young men received a single oral dose of either 3 mg melatonin (n = 24) or placebo medication (n = 21). One hour thereafter, they underwent a standardized short-term psychosocial stressor. Plasma levels of clotting factor VII activity (FVII:C), FVIII:C, fibrinogen, D-dimer, and catecholamines were measured at rest, immediately after stress, and 20 min and 60 min post-stress. The integrated change in D-dimer levels from rest to 60 min post-stress differed between medication groups controlling for demographic and metabolic factors (P = 0.047, = 0.195). Compared with the melatonin group, the placebo group showed a greater increase in absolute D-dimer levels from rest to immediately post-stress (P = 0.13; = 0.060) and significant recovery of D-dimer levels from immediately post-stress to 60 min thereafter (P = 0.007; = 0.174). Stress-induced changes in FVII:C, FVIII:C, fibrinogen, and catecholamines did not significantly differ between groups. Oral melatonin attenuated the stress-induced elevation in the sensitive coagulation activation marker D-dimer without affecting catecholamine activity. The finding provides preliminary support for a protective effect of melatonin in reducing the atherothrombotic risk with acute mental stress. [source] Oral melatonin reduces blood coagulation activity: a placebo-controlled study in healthy young menJOURNAL OF PINEAL RESEARCH, Issue 2 2008Petra H. Wirtz Abstract:, Melatonin has previously been suggested to affect hemostatic function but studies on the issue are scant. We hypothesized that, in humans, oral administration of melatonin is associated with decreased plasma levels of procoagulant hemostatic measures compared with placebo medication and that plasma melatonin concentration shows an inverse association with procoagulant measures. Forty-six healthy men (mean age 25 ± 4 yr) were randomized, single-blinded, to either 3 mg of oral melatonin (n = 25) or placebo medication (n = 21). One hour thereafter, levels of melatonin, fibrinogen, and D-dimer as well as activities of coagulation factor VII (FVII:C) and VIII (FVIII:C) were measured in plasma. Multivariate analysis of covariance and regression analysis controlled for age, body mass index, mean arterial blood pressure, heart rate, and norepinephrine plasma level. Subjects on melatonin had significantly lower mean levels of FVIII:C (81%, 95% CI 71,92 versus 103%, 95% CI 90,119; P = 0.018) and of fibrinogen (1.92 g/L, 95% CI 1.76,2.08 versus 2.26 g/L, 95% CI 2.09,2.43; P = 0.007) than those on placebo explaining 14 and 17% of the respective variance. In all subjects, increased plasma melatonin concentration independently predicted lower levels of FVIII:C (P = 0.037) and fibrinogen (P = 0.022) explaining 9 and 11% of the respective variance. Melatonin medication and plasma concentration were not significantly associated with FVII:C and D-dimer levels. A single dose of oral melatonin was associated with lower plasma levels of procoagulant factors 60 min later. There might be a dose,response relationship between the plasma concentration of melatonin and coagulation activity. [source] Pregnancy outcome and fibrinolytic, endothelial and coagulation markers in women undergoing uterine artery Doppler screening at 23 weeksJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2009B. J. HUNT Summary.,Background:,Pre-eclampsia (PET) and/or fetal growth restriction (FGR) remain a major cause of maternal and fetal morbidity and mortality. In pregnancy, fibrinolysis is controlled by the maternal endothelium and placenta, both of which are central to the pathogenesis of PET/FGR. Clinically, uterine artery Doppler screening at 23 weeks is used to predict PET/FGR. An abnormal uterine artery Doppler finding is defined as early diastolic bilateral uterine artery notching (BN) in the waveform. However, about 50% of mothers with BN do not develop PET/FGR. Objectives:,We investigated fibrinolytic changes and uterine artery Doppler findings in the second trimester, and related them to pregnancy outcome; in particular assessing whether fibrinolytic markers could discriminate between normal and abnormal outcome in mothers with BN. Patients/methods:,Plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), plasminogen activator inhibitor-2 (PAI-2), plasmin-,2 antiplasmin (PAP), D-dimers and markers of endothelial dysfunction were measured with Doppler ultrasound at 23 weeks. Results:,Those with BN had decreased PAP and D-dimer levels, and raised PAI-1 and thrombomodulin levels. Mothers with BN and PET/FGR had significantly increased t-PA levels and reduced PAI-2 levels. Conclusions:,BN at 23 weeks of gestation is associated with increased PAI-1 levels. Within the BN group, mothers who developed PET/FGR had increased t-PA levels and decreased PAI-2 levels, although there was no net change in fibrinolysis as measured by D-dimer levels. No single fibrinolytic marker is helpful in determining pregnancy outcome in those with BN, but t-PA and PAI-2 are worthy of study in a multifactorial algorithm. [source] Common genetic variants associated with plasma fibrin D-dimer concentration in older European- and African-American adultsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2008L. A. LANGE Summary.,Background and Objectives:,D-dimer is a hemostasis marker that reflects ongoing fibrin formation and degradation. There is significant inter-individual and inter-population variability in D-dimer concentration, but whether genetic factors underlie these differences is largely unknown. We hypothesized that common coagulation gene variants contribute to differences in circulating D-dimer concentration. Methods:,The setting was European-American (EA; n = 1858) and African-American (AA; n = 327) unrelated older adults from the Cardiovascular Health Study (CHS), in which we genotyped SNPs in 42 genes related to blood coagulation and fibrinolysis. Results:,Several fibrinogen gene polymorphisms, including the Thr312Ala A, chain variant and the FGG-10034 C/T variant, were associated with ,20% higher plasma D-dimer levels in EA (false discovery rate < 5% for covariate-adjusted model). There was also some evidence that a Pro41Leu variant of the PLAU gene encoding urinary plasminogen activator and non-coding polymorphism of the plasminogen activator inhibitor type 1 gene (SERPINE1) were associated with higher plasma D-dimer in EA. There were no significant associations between the studied coagulation or fibrinolysis gene SNPs and plasma D-dimer levels in the smaller AA sample. However, each standard deviation increase in European ancestry assessed by ancestry-informative gene markers was associated with ,10% lower mean D-dimer levels in AA. Conclusions:,Together, common coagulation/fibrinolysis gene SNPs explained only ,2% of the variance in plasma D-dimer levels in EA. These findings suggest that the association of D-dimer with risk of vascular outcomes may be mediated largely by environmental factors, other genes, and/or genetic interactions. [source] D-dimer levels during delivery and the postpartumJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2005M. EPINEY Summary.,Background: D-dimer (DD) measurement has proved to be very useful to exclude venous thromboembolism (VTE) in outpatients. However, during pregnancy, the progressive increase as well as the interindividual variations of DD means that in this instance they are of poor value to rule out VTE. Only a few studies have reported measurements of DD levels in the postpartum. Objectives: To measure DD sequentially in the puerperium in order to determine when DD levels return to values obtained in non-pregnant women and can again be used in the exclusion of VTE. Patients and methods: After uncomplicated pregnancies, 150 women delivering at term either vaginally (n = 100) or by cesarean section (n = 50) were included. DD levels were measured immediately following delivery and next at days 1, 3, 10, 30 and 45. Results: There was a marked elevation of DD at delivery, especially when instrumental. All DD measurements were above 500 ng mL,1 at delivery, at day 1 and at day 3 postpartum. A sharp decrease in DD was observed between day 1 and day 3, followed by a slight increase at day 10. At day 30 and day 45, respectively, 79% and 93% of women in the vaginal delivery group and 70% and 83% in the cesarean group had levels below 500 ng mL,1. Bleeding, breastfeeding and heparin prophylaxis did not modify DD levels significantly. Conclusion: Using the Vidas DD new assay, our study provides reference intervals for DD in the postpartum period. Using a cut-off at 500 ng mL,1, DD measurement for ruling out VTE was found to be useful again 4 weeks after delivery. [source] Prospective study of hemostatic alterations in children with acute lymphoblastic leukemia,AMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2010Paola Giordano In a group of newly diagnosed acute lymphocytic leukemia (ALL) children we evaluated a number of hemostatic and inflammatory markers at diagnosis and at different time points during chemotherapy for the remission induction to identify alterations in the plasma levels of prothrombotic markers before and during the course of chemotherapy. The following plasma markers were evaluated: thrombin-antithrombin complex (TAT), D-Dimer, plasminogen activator inhibitor 1 (PAI-1), antithrombin, fibrinogen, von Willebrand factor (VWF) antigen and high molecular weight VWF (HMW-VWF) multimers, P-selectin, tumor necrosis factor alpha (TNF-,), and interleukin 6 (IL-6). Plasma samples were collected at the following time points: at T0 (baseline) and T1 (+24 days of therapy), T2 (+36 days therapy), and T3 (+64 days therapy). The results show that, at diagnosis, ALL children presented with laboratory signs of increased thrombin generation and fibrin formation (i.e. high TAT and D-dimer levels), fibrinolysis inhibition (i.e. high PAI-1 level), endothelial activation (i.e., high HMW-VWF and soluble P-selectin levels) and inflammation (i.e. high TNF-alpha and IL-6 levels). After starting induction therapy, the thrombin generation markers and inflammatory cytokines significantly decreased. To the opposite, PAI-1 and P-selectin significantly increased, suggesting an insult by chemotherapy on the vascular endothelium. These effects were more evident during steroid administration. Symptomatic venous thromboembolism (VTE) episodes developed in two cases during induction therapy, which did not allow the evaluation of the predictive value for VTE of laboratory markers. Am. J. Hematol., 2010. © 2010 Wiley-Liss, Inc. [source] Thrombin activatable fibrinolysis inhibitor activity, thrombin-antithrombin complex and D-dimer levels in preterm neonates with early respiratory distress syndromeAMERICAN JOURNAL OF HEMATOLOGY, Issue 1 2008Tugba Gursoy Intraalveolar fibrin deposition found in neonates with respiratory distress syndrome (RDS) is explained by the activation of the coagulation system and inefficient fibrinolysis. However, thrombin activatable fibrinolysis inhibitor activity (TAFIa), an inhibitor of fibrinolysis, and the ratio of D-dimer to thrombin,antithrombin complex (D-dimer/TAT), an index of fibrinolytic activity, have not been reported previously in neonatal RDS. Aim of this study is to evaluate the influence of plasma TAFIa levels on the fibrinolytic state in neonatal RDS. The RDS group (Group 1) consisted of 29 neonates, and 18 neonates served as the control group (Group 2). Plasma TAFIa levels and D-dimer/TAT ratios were evaluated in all neonates in the first 6 hr of life. Neonates in the RDS group were further divided into two subgroups; Group 1a consisted of 12 neonates with evidence of mild asphyxia (Apgar score at 5 min <7 and cord pH <7.26), and Group 1b consisted of 17 nonasphyxiated neonates. No significant difference was found in TAFIa levels and D-dimer/TAT ratios between Groups 1 and 2 [214% (56.2,361%) and 124.3 (4.4,3,921) in Group 1 and 201% (60.3,381%) and 147 (5.9,1,426) in Group 2]. There were negative correlations between cord pH and TAFIa levels in both groups. Increased TAFIa levels and decreased D-dimer/TAT ratios and platelet counts were detected in mildly asphyxiated neonates when compared with nonasphyxiated ones. TAFIa is not responsible for the hypofibrinolytic state reported in RDS. However, asphyxia influences TAFIa levels and increased TAFIa levels depress fibrinolysis. Am. J. Hematol., 2008. © 2007 Wiley-Liss, Inc. [source] Coagulopathy and embolic signal in cancer patients with ischemic strokeANNALS OF NEUROLOGY, Issue 2 2010Jin Myoung Seok MD Objective It has been reported that embolic signal (ES) detected by transcranial Doppler (TCD) has clinical significance, especially in patients with recent stroke attributable to arterial or cardiac embolism. Therefore, we conducted this study to determine whether the prevalence of ES is high in ischemic stroke patients with cancer and related to hypercoagulopathy. Methods We prospectively studied cancer patients with acute ischemic stroke within the middle cerebral artery (MCA) distribution on diffusion-weighted imaging. Conventional stroke mechanisms (CSMs) were determined using cardiologic and vascular studies. Additionally, the coagulation status was assessed based on the serum D-dimer levels, and TCD monitoring was performed on both MCAs for 30 minutes to detect ES. Clinical features including vascular risk factors, characteristics of ischemic stroke, and cancer and laboratory findings associated with the presence of ES were evaluated. Results A total of 74 patients were finally included in this study. ES was more commonly observed in patients without CSMs (22 of 38 patients, 57.9%) than in those with CSMs (12 of 36 patients, 33.3%) (p = 0.034). Moreover, ES was more commonly detected in patients with high D-dimer levels (p < 0.001), and D-dimer levels were significantly correlated with the number of ESs in patients without CSMs (r = 0.732, p < 0.001), but were poorly correlated in patients with CSMs (r = 0.152, p = 0.375). Higher levels of D-dimer (odds ratio [OR], 1.082 per 1,g/ml increase; 95% confidence interval [CI], 1.014,1.154) and adenocarcinoma (OR, 3.829; 95% CI, 1.23,13.052) were independently associated with the presence of ES. The use of anticoagulants dramatically decreased the D-dimer levels. Interpretation A high prevalence of ES was observed in cancer patients with ischemic stroke, especially in those without CSMs. Elevated D-dimer levels were independently associated with ES, and decreased dramatically with the use of anticoagulants. ANN NEUROL 2010;68:213,219 [source] Relationship between elevated cerebrospinal fluid levels of plasminogen activator inhibitor 1 and neuronal destruction in patients with neuropsychiatric systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 7 2009Jakub Kwieci Objective A homeostatic imbalance between coagulation and fibrinolysis might occur intrathecally in neuropsychiatric systemic lupus erythematosus (NPSLE). However, there are no published data on levels of fibrinolytic factors in the cerebrospinal fluid (CSF) of patients with NPSLE. The present study was undertaken to assess CSF levels of fibrinolytic molecules, including urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), D-dimer, and plasminogen activator inhibitor 1 (PAI-1), in SLE patients with clinically verified neuropsychiatric involvement and to compare these levels with those in SLE patients without neuropsychiatric involvement and in healthy subjects. Methods Levels of uPA, tPA, and PAI-1 were assessed in CSF from 94 patients with SLE (33 who had NPSLE, 56 who did not have NPSLE, and 5 who were positive for antiphospholipid antibody [not included in the NPSLE or non-NPSLE group]) and from 53 age-matched controls. Patients were evaluated clinically, with magnetic resonance imaging of the brain, analyses of neuronal/glial degradation products in CSF, and neuropsychiatric testing. Results In the group of patients with NPSLE, intrathecal PAI-1 levels were significantly elevated compared with levels in SLE patients without overt neuropsychiatric involvement (P < 0.05) and in healthy controls (P < 0.001). In contrast, intrathecal levels of uPA did not differ significantly. Intrathecal levels of PAI-1 correlated significantly with CSF levels of interleukin-6 (IL-6) (r = 0.34, P < 0.001) and IL-8 (r = 0.33, P < 0.001). Importantly, increased PAI-1 and D-dimer levels were observed in SLE patients who had pathologically elevated levels of glial fibrillary acidic protein, neurofilament triplet protein, and tau protein in CSF. Conclusion Intrathecal release of PAI-1 is increased in patients with NPSLE. This results in impaired fibrinolysis, which might contribute to neuronal and astrocytic damage in NPSLE. [source] C-reactive protein in the diagnosis of deep vein thrombosisBRITISH JOURNAL OF HAEMATOLOGY, Issue 2 2002Robert A. Bucek Summary. The role of C-reactive protein (CRP) in the diagnosis of suspected deep vein thrombosis (DVT) and a possible advantage of its additional evaluation with D-dimer has not been clearly evaluated. We therefore studied plasma CRP and D-dimer levels in 233 consecutive patients with suspected DVT; the final diagnosis was based on the results of colour duplex ultrasound or venography. DVT was diagnosed in 31·3%. CRP and D-dimer correlated significantly (r = 0·64, P < 0·01); both were increased significantly in patients suffering from DVT (P < 0·001). Multivariate analysis revealed a significant influence of the presence of DVT (P < 0·001), the presence of malignancy (P < 0·001) and the presence of inflammatory diseases (P = 0·009) on plasma CRP, while there was no significant influence of the duration of symptoms (P = 0·30). The sensitivity (75%vs 93%) to specificity (69%vs 55%) relationship showed inferior results for CRP compared with D-dimer; its additional evaluation did not improve the diagnostic value of D-dimer. We conclude that CRP can provide additional information neither for the diagnostic process in patients with suspected DVT nor for the differential diagnosis of DVT and inflammatory diseases. [source] Fibrinolytic risk factor clustering and insulin resistance in healthy male relatives of men with intermittent claudication,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2006D. J. Parry Background: Raised fibrinolytic factors predict cardiovascular risk in healthy subjects. The aim of this study was to measure fibrinolytic factors and insulin resistance in healthy male first-degree relatives of men with intermittent claudication younger than 65 years. Methods: The study compared 165 healthy first-degree relatives with 165 age-, sex- and race-matched control subjects free from a personal or family history of premature cardiovascular disease. Primary outcome measures were plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (tPA) and D-dimer levels. Insulin resistance was estimated by Homeostasis Model Assessment. Clinical and biochemical risk factors were measured and subjects genotyped for the PAI-1 4G/5G polymorphism. Results: First-degree relatives had significantly higher mean PAI-1 (10·23 versus 7·85 ng/ml; P = 0·024), tPA (9·98 versus 8·29 ng/ml; P < 0·001) and D-dimer levels (56·6 versus 46·1 ng/ml; P = 0·004). They also had significantly higher insulin resistance (1·85 versus 1·53; P < 0·001) and clustered multiple atherogenic risk factors. On multivariate analysis the association between both tPA and D-dimer levels and relative status was independent of other variables. Conclusion: Raised levels of PAI-1, tPA, D-dimer and estimated insulin resistance were present in the healthy male first-degree relatives of men with intermittent claudication. These data support the hypothesis of fibrinolytic risk factor clustering in this high-risk population. Copyright © 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Preliminary study of D-dimer as a possible marker of acute bowel ischaemiaBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2001Dr S. Acosta Background: Occlusion of the superior mesenteric artery (SMA) demands prompt recognition and diagnosis. No accurate diagnostic method is available. The aim of this study was to determine whether the fibrinolytic marker D-dimer is a useful early marker of acute bowel ischaemia. Methods: Fourteen patients suspected of having acute bowel ischaemia were analysed for an increase in plasma D-dimer level. Results: Six patients had embolic or thrombotic occlusion of the SMA and all had significantly higher D-dimer levels than those without thromboembolic occlusion (P < 0·05). Four patients with strangulation of the small bowel due to adhesions and one with a ruptured aortic aneurysm also had raised D-dimer values. Conclusion: In patients with suspected thromboembolic occlusive disease of the SMA, a raised level of D-dimer indicated the presence of acute bowel ischaemia, whatever the cause. A more extensive prospective study is needed to evaluate a potential survival benefit using the test as a marker of the need for urgent laparotomy. © 2001 British Journal of Surgery Society Ltd [source] Activation of the coagulation system occurs within rather than outside cutaneous haemangiomasACTA PAEDIATRICA, Issue 10 2001J Antovic Haemangiomas are the commonest tumours of infancy. They can become even more serious if followed by consumption coagulopathy and even life-threatening in cases of Kasabach,Merritt syndrome, with thrombocytopenia and haemorrhage. Data exist concerning systemic coagulation abnormalities in children with haemangiomas but to our knowledge there are no data on local consumption coagulopathy in haemangioma per se. We examined blood coagulation and fibrinolysis parameters in blood withdrawn from haemangioma blood vessels and blood withdrawn from the systemic vein in 14 children with cutaneous haemangiomas (3M, 11F; age range 3 mo to 10 y). Compared with controls, significant decreases in fibrinogen levels, FVII activity, antithrombin and plasmin inhibitor levels and increases in international normalized ratio (INR) and D-dimer levels were observed in the blood samples withdrawn directly from haemangioma blood vessels. Fibrinogen and antithrombin levels in samples withdrawn from systemic veins were reduced in relation to control values whilst INR values increased, but within normal ranges. D-dimer levels were increased in peripheral blood. The fibrinogen level was significantly lower and the INR and D-dimer levels were significantly higher in blood samples from haemangiomas compared to systemic blood. Clinical signs of systemic disseminated intravascular coagulation were not observed. Conclusions: Our results suggest a strong local activation and local consumption coagulopathy in haemangioma, along with less conspicuous but observable systemic changes in coagulation and fibrinolysis parameters, although without signs of consumptive coagulopathy. These systemic changes could be a reflection of intra-lesion coagulation activation although there is no evidence to suggest truly systemic disseminated intravascular coagulation. [source] | ||||||||||||||||||||||