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PubMed1992

[A clinical study on hemostatic fluctuation during and after cardiopulmonary bypass using hemostatic molecular markers].

Heparin is indispensable anticoagulant for cardiopulmonary bypass, but the dose of heparin is even now under discussion. In this study, hemostatic fluctuation was analyzed during and after the bypass using hemostatic molecular markers. The subjects were 16 adult cases of open heart surgery, 12 males, 4 females. The average age was 55.0 year. Operations were aortocoronary bypass in 12, valvular surgery in 3 and ASD patch closure in one with moderate hypothermic cardiopulmonary bypass. At the beginning of cardiopulmonary bypass, 3 mg/kg heparin was administered and the equivalent amount of protamine sulfate was used for neutralization at the end of the bypass. Platelet count, hematocrit, antithrombin III (ATIII), beta-thromboglobulin, platelet factor 4, fibrinopeptide A, thrombin antithrombin III complex, FDP, D dimer FDP, plasmin alpha 2 plasmin inhibitor complex, tissue plasminogen activator (t-PA), and thrombomodulin (TM) were measured through the operation up to two weeks after surgery. ATIII decreased to 50% of control value all through the bypass. Platelet markers increased immediately, and the activated state continued 3 hours after the bypass. Coagulation markers increased markedly after the aortic declamping, and reached at its peak by three times as control value, immediately after the protamine neutralization and continued for 3 hours. During the bypass, fibrinogenolysis caused by t-PA which was stimulated by non-physiological circulation and stimulating substances, was observed. Fibrinolysis occurred following the hypercoagulability after the neutralization. TM was within normal range before the aortic declamping. But increased gradually after the declamp, and reached twice as much as the base line. It could be concluded that hypercoagulability and high platelet activation might play a role of perioperative thrombosis. Hypercoagulability and increase of serum TM would be related to reperfusion of the lung. The increasing of TM would reflect broad injury of vessel walls after the bypass, because plasma TM increased following the generalized injury of endothelial cells.

Adult↗

PubMed1994

Analysis of platelet abnormalities in uremia with and without Glanzmann's thrombasthenia.

Uremia causes a bleeding tendency associated with platelet dysfunction, and previous studies have shown abnormalities of platelet glycoprotein (GP) Ib or GPIIb/IIIa and a tendency for platelet activation in uremia. The present study compared the abnormalities of platelet function in uremia with (n = 1) or without (n = 18) associated Glanzmann's thrombasthenia. There was a significant difference between ristocetin-induced agglutination of platelets from the uremic patients without Glanzmann's thrombasthenia and platelets from healthy controls (n = 15). In addition, a reduction of GPIb expression by uremic platelets along with normal GPIIb/IIIa expression was confirmed using flow cytometry. Many coagulation markers were increased in the uremic patient with Glanzmann's thrombasthenia, suggesting that the coagulation was enhanced and the platelets were prone to activation. However, the thrombasthenic platelets actually showed little increase in the binding of a monoclonal anti-CD63 antibody directed against lysosomal integral membrane protein (which is expressed after platelet activation), while uremic platelets showed a marked increase. In addition, the expression of GPIb by thrombasthenic platelets was normal, while that of GPIIb/IIIa was markedly decreased. Our results suggest that thrombasthenic platelets are resistant to activation and to the degradation of GPIb under uremic condition and that this difference from 'ordinary' uremic platelets be related to the difference in GPIIb/IIIa.

Adult↗

PubMed2002

Pathological haemostasis and "prothrombotic state" in Behçet's disease.

Behçet's disease (BD) is a widespread occlusive-type vasculitis with life-threatening manifestations. The vasculopathy of BD is unique and any type of vessel can be involved. Moreover, vascular lesions in BD represent an occlusive nature suggesting a hypercoagulable/prothrombotic state. The data concerning the genetic defects of the coagulation cascade are expanding. There is evidence of universal activation of haemostatic system in BD. Procoagulant markers of thrombosis are elevated reflecting intravenous excessive thrombin formation. Defective fibrinolysis with impaired fibrinolytic kinetics may have a role in the hypercoagulable/prothrombotic state of BD. Endothelial cell injury and/or pathological activation is well documented in BD. The aim of this paper is to review current literature knowledge and our experience regarding the unresolved complicated issues of genetic thrombotic defects, in vivo haemostatic markers, coagulation inhibitors, impaired fibrinolysis, and endothelial injury/dysfunction of the hypercoagulable/prothrombotic state of BD. The clinical aspects of vascular thrombosis, the genetic basis of coagulation, coagulation inhibitors, fibrinolysis inhibitors, and endothelial dysfunction are reviewed. Challenges and future prospects regarding the prothrombotic state of BD are discussed together with new promising antithrombotic and antiplatelet treatment strategies. Better understanding of the exact pathogenesis of the hypercoagulable/prothrombotic state of this disease may help to develop novel therapeutic approaches offering a better outcome for Behçet's patients with thrombosis.

Behcet Syndrome↗

PubMed1998

Mechanisms of cerebrovascular events as assessed by procoagulant activity, cerebral microemboli, and platelet microparticles in patients with prosthetic heart valves.

BACKGROUND AND PURPOSE: Cerebrovascular events (CVE) in patients with prosthetic heart valves (PHV) have remained a severe and frequent complication despite oral anticoagulation with or without aspirin. We studied the possible pathophysiological involvement of platelet-derived microparticles (PMP) as a contributing factor for the increased incidence of CVE in patients with PHV. METHODS: We compared in a retrospective, case-control study the clinical outcome after the implantation of the PHV with several different independent morphological and functional methods, including simultaneous transcranial Doppler monitoring of both middle cerebral arteries, PMP detection by flow cytometry with use of platelet-specific antibodies, coagulation markers, and determination of the procoagulant activity by Russell's viper venom time, a phospholipid-dependent coagulation assay. RESULTS: Eight of 26 patients with PHV had 9 CVE during 136 person-years of observation. Transcranial Doppler monitoring revealed an increased frequency of microembolic signals recorded over a 30-minute period in patients with CVE (75+/-25; median, 55; range, 27 to 248) compared with those without CVE (23+/-12; median, 7; range, 0 to 153; P<0.05) or with control subjects (0; P<0.001). Flow cytometry analysis showed increased levels of PMP in patients with compared to those without CVE (4.1+/-0.6% versus 2.4+/-0.4% of all fluorescence-positive events gated; P<0.05). Increased procoagulant activity was documented by the shortened Russell's viper venom time expressed as an increased level of platelet equivalents per microliter of plasma in patients compared with control subjects (+24.7+/-14.9%; P<0.01). Subgroup analysis revealed that patients with CVE had a higher excess of platelet equivalents per microliter of plasma than patients without CVE in relation to the controls (+68.7+/-36.7%; P<0.05). Mildly elevated thrombin-antithrombin III complexes (2.9+/-0.7; median, 2.3; normal, <2.0 microg/L) suggested incompletely suppressed thrombin formation, and fibrin generation (fibrinopeptide A) was in the upper normal range (2.1+/-0.2; median, 1.8; normal, <2.0 ng/mL), despite adequate anticoagulation (INR=3.6+/-0.1). CONCLUSIONS: Our data show increased microembolic signals, platelet microparticles, and procoagulant activity in symptomatic patients with PHV and provide a potential pathophysiological explanation of CVE.

Antithrombin III↗

PubMed2002

Effect of modified ultrafiltration on the inflammatory response in paediatric open-heart surgery: a prospective, randomized study.

Modified ultrafiltration (MUF) is often used in conjunction with paediatric cardiac surgery with cardiopulmonary bypass (CPB) and is thought to improve clinical outcome. It is unclear whether these improvements (if any) are due to the removal of inflammatory mediators. In this prospective study, 18 children aged 12-24 months undergoing uncomplicated cardiac surgery with methylprednisolone added in the pump prime were randomized to receive CPB with (n = 10) and without (n = 8) MUF. Cytokines (TNFalpha, IL-6, IL-1beta, IL-10, IL-1ra), complement split products (C3d, C4d) and coagulation system activation (F1 + 2, ATIII) were measured pre-, peri- and up to 48 h postoperatively. For clinical outcome, the alveolar-arterial oxygen (A-a) gradient, transfusion requirement, drain loss, mean blood pressure and requirement for inotropic support were registered up to 24 h postoperatively. Our results show an improvement in postoperative oxygenation as well as a tendency towards decreased drain loss and improved haemodynamics in the MUF group. There were no intergroup differences detectable for TNFalpha, IL-1beta, IL-1ra, complement and coagulation markers. We conclude that MUF in itself does not significantly influence TNFalpha, IL-1beta, IL-1ra and the complement and coagulation profiles in children undergoing cardiac surgery with CPB. Despite this, there was some evidence for improved clinical outcome. Our results do not support that MUF improves postoperative organ function by modulation of the measured markers of inflammation.

Biomarkers↗

PubMed2004

The effects of perioperatively administered crystalloids and colloids on concentrations of molecular markers of activated coagulation and fibrinolysis.

To explore whether intravenous administration of routinely used crystalloid or colloid solutions differently affects the coagulation system, we investigated orthopaedic patients. Since crystalloid solutions might cause hypercoagulability, we here present our results on molecular markers of coagulation and fibrinolysis. Patients undergoing knee replacement surgery randomly received isovolemic amounts of lactated Ringer's solution, 6% hydroxyethyl starch 200/0.5 or 4% modified gelatine. Arterial blood samples for determination of specific molecular markers of activated coagulation (thrombin/antithrombin complex, D-dimer, prothrombin fragment F1 + 2), fibrinolysis (plasmin/alpha 2-antiplasmin complex, tissue plasminogen activator, plasminogen activator inhibitor-1), and concentrations of coagulation factor XIII were obtained at baseline, before tourniquet release, at the end of surgery and 2 h after operation. During the observation period, thrombin/antithrombin complex increased from 4.8 to 54.7 microg/l, D-dimer increased from 0.3 to 6.0 mg/ml, prothrombin fragment F1 + 2 increased from 1.7 to 5.9 nmol/l, tissue plasminogen activator decreased from 7.3 to 6.7 ng/ml, plasminogen activator inhibitor-1 increased from 68.4 to 71.0 ng/ml, plasmin/alpha 2-antiplasmin complex increased from 281.5 to 884 microg/l and factor XIII decreased from 89.0 to 58.5%. All parameters changed significantly but without any detectable difference in the response profile between the groups receiving different intravenous fluids. During knee replacement surgery a pronounced activation of the coagulation/fibrinolytic system was observed, regardless of whether patients received crystalloid or colloid fluids. Thus, these results cannot confirm the hypothesis that crystalloid fluids per se cause hypercoagulability in vivo.

Aged↗

PubMed2004

Hemostatic function and progressing ischemic stroke: D-dimer predicts early clinical progression.

BACKGROUND AND PURPOSE: Early clinical progression of ischemic stroke is common and is associated with increased risk of death and dependency. We hypothesized that activation of the coagulation system is an important contributor in some cases of deterioration. We aimed to characterize alterations in circulating hemostatic markers in patients with progressing stroke. METHODS: Consecutive acute ischemic stroke admissions were recruited. Progressing stroke was defined by deterioration in components of the Scandinavian Stroke Scale. Hemostatic markers (coagulation factors VIIc, VIIIc, and IXc, prothrombin fragments 1+2 [F1+2], thrombin-antithrombin complexes [TAT], D-dimer, fibrinogen, von Willebrand factor [vWF] and tissue plasminogen activator) were measured within 24 hours of symptom recognition. RESULTS: Fifty-four (25%) of the 219 patients met criteria for progressing stroke. F1+2 (median 1.28 versus 1.06 nmol/L, P=0.01), TAT (5.28 versus 4.07 microg/L, P<0.01), D-dimer (443 versus 194 ng/mL, P<0.001) and vWF (216 versus 198 IU/dL, P<0.05) levels were higher in these patients than in stable/improving patients. In logistic regression analysis, with all important clinical and laboratory variables included, only natural log D-dimer (odds ratio [OR]: 1.87; 95% confidence interval [CI]: 1.38 to 2.54; P=0.0001) and mean arterial blood pressure (OR: 1.26 per 10 mm Hg change; 95% CI: 1.05 to 1.51; P=0.01) remained independent predictors of progressing stroke. CONCLUSIONS: There is evidence of excess thrombin generation and fibrin turnover in patients with progressing ischemic stroke. Measurement of D-dimer levels can identify patients at high risk for stroke progression. Further research is required to determine whether such patients benefit from acute interventions aimed at modifying hemostatic function.

Aged↗

PubMed2003

Fresh frozen plasma reduces thrombin formation in newborn infants.

BACKGROUND: Newborn infants undergoing intensive care are at risk of bleeding and thrombotic complications. Fresh frozen plasma (FFP) is used in hope of preventing these complications, despite poorly defined effects on the coagulation system and lack of proven clinical efficacy. OBJECTIVES AND METHODS: We prospectively evaluated coagulopathy and the effect of standardized amount of FFP transfusion (10 mL kg-1 + 4 mL in 2 h) on various coagulation markers in 33 newborn infants during the first 24 h of intensive care. RESULTS: Increased levels of prothrombin fragment F1+2, thrombin-antithrombin complexes (TAT), and d-dimer were found prior to the transfusion in 97%, 81%, and 100% of the patients, respectively. FFP transfusion was associated with a decrease in F1+2 level in 26/32 (81%) of the patients. The extent of F1+2 decrease correlated with the pretransfusion F1+2 level (R = 0.65, P < 0.0001). The patient series was divided into two groups according to increasing pretransfusional F1+2 level: Group 1 (preFFP F1+2 > or = 2.35 nm, n = 16), Group 2 (F1+2 <2.35 nm, n = 16). In Group 1, F1+2 decreased on average 1.58 nm (P < 0.01) from the baseline during FFP transfusion but no significant change in the level of F1+2 during the transfusion was observed in Group 2. Pretransfusional levels of individual factors or prothrombin time (PT) did not correlate with the FFP-associated decrease in F1+2 level. CONCLUSIONS: In the patients with the highest pretransfusional thrombin formation, FFP had an acute thrombin-reducing effect. Pretransfusion thrombin generation markers, rather than PT or individual pro- and anticoagulants, may be helpful in identifying the patient who will have measurable coagulational effects induced by FFP.

Biomarkers↗

PubMed2004

Activation of fibrinolysis and coagulation in non-occlusive intestinal ischaemia in a pig model.

The present study was carried out to explore the dynamics of the fibrinolytic and coagulation systems during non-occlusive intestinal ischaemia in a porcine model. Nineteen pigs underwent laparotomy. The inferior mesenteric artery and the collateral vessels to the rectum were ligated. The superior mesenteric artery (SMA) was isolated at its origin from the aorta, and constriction and flowmeter devices were applied. The blood flow of the SMA was reduced to cause ischaemia in the distal colon within the pHi interval 6.9-7.1. Fibrinogen, soluble fibrin, D-dimer, tissue plasminogen activator/plasminogen activator inhibitor-1 (tPA/PAI-1) complex and albumin were measured. Corrections for pig D-dimer and albumin were performed. Fibrinogen decreased significantly after laparotomy (P < 0.0001) and further after constriction of the SMA (P < 0.05), whereas soluble fibrin increased significantly (P < 0.005) after constriction of the SMA. The tPA/PAI-1 complex increased significantly after laparotomy (P < 0.05) and, after constriction of the SMA, the values first tended to decrease (P = 0.06) and then to increase (P = 0.056). The need to calibrate assays of human plasma proteins when applying them to experimental pig models was demonstrated. After constriction of the SMA, there was a rapidly reversed peak in the coagulation marker soluble fibrin and a strong tendency of alteration of the fibrinolytic marker tPA/PAI-1 complex.

Animals↗

PubMed2003

Double blind, randomized study of estradiol replacement therapy on markers of inflammation, coagulation and fibrinolysis.

Estrogen replacement therapy (ERT) has been found to be associated with increased cardiovascular risk in the first year after initiation of ERT. We compared the effects of oral and transdermal estradiol (E2) replacement therapy on markers of inflammation, coagulation and fibrinolysis in a randomized double-blind trial. Forty-three healthy women were randomized 6 weeks after surgically induced menopause to receive treatment with either oral or transdermal E2 over a period of 28 weeks. At baseline and after 28 weeks, levels of serum lipids and lipoproteins, and markers of coagulation, fibrinolysis and inflammation were determined. Among fibrinolytic parameters, oral E2 shortened euglobulin clot lysis time (P<0.05) and reduced tissue type plasminogen activator antigen (P=0.01) and plasminogen activator inhibitor activity (P<0.05). Among coagulation parameters, both routes of E2 replacement decreased fibrinogen levels (P=0.002 for oral and P=0.007 for transdermal E2). Oral E2 resulted in an increase in C-reactive protein (CRP) from 2.15 (0.71-4.05) to 3.41 (1.12-5.92) mg/l (P=0.04), while transdermal E2 showed no effect. Levels of serum amyloid A (SAA), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) did not change significantly after oral and transdermal E2. Oral E2 significantly improved the lipid profile, while transdermal E2 had a less pronounced effect. Both oral and transdermal E2 significantly reduced fasting glucose. Oral E2 was associated with a pro-inflammatory response, but at the same time improved fibrinolytic capacity, showed no pro-coagulatory effects, and acted beneficially on lipids and lipoproteins. There was no influence of transdermal E2 on markers of coagulation activation, fibrinolysis and inflammation, but it decreased fibrinogen levels significantly. Further studies are needed to explore the clinical relevance of these observations.

Administration, Cutaneous↗

PubMed1998

Mechanisms of hypercoagulation in malignancy and during chemotherapy.

Patients with cancer are at increased risk for thromboembolic disease. Commonly they present with abnormalities of one or more circulating markers of haemostatic system activation, underlying a 'hypercoagulable state'. Despite numerous investigations which have identified alterations in all of the haemostatic components (i.e. coagulation, fibrinolysis, endothelium, platelets and monocytes), no firm conclusions have been reached regarding the clinical utility of any of these coagulation markers for predicting thrombosis in cancer patients. The predictive value of one or more of these tests could help to identify safe and effective methods for prophylaxis against thrombotic complications in these patients. Plasma clotting abnormalities are usually exacerbated by chemotherapy. The mechanisms by which the haemostatic system is activated in malignancy (and chemotherapy) are reviewed.

Antineoplastic Agents↗

PubMed2005

The effects of oral and transdermal hormone replacement therapy on C-reactive protein levels and other inflammatory markers in women with high risk of thrombosis.

INTRODUCTION: In the estrogen in venous thromboembolism (EVTET) study of 140 women with a history of venous thromboembolism (VTE), oral hormone replacement therapy (HRT) was associated with strong activation of coagulation markers and increased risk of recurrent VTE. No such associations were observed in the estrogen women atherosclerosis (EWA) study of 118 women with established coronary artery disease who were given transdermal HRT. OBJECTIVES AND METHODS: The aim of the present study was to evaluate the effects of oral and transdermal HRT on levels of C-reactive protein (CRP), which was assayed with a highly sensitive method. We also evaluated the effects on other inflammatory markers and the influence of possible confounding factors. RESULTS: Oral HRT was associated with a significant increase in CRP after 3 months as compared with placebo (median 79% [95% confidence interval 36-119%] versus -4% [-13 to 10%], p = 0.001). These changes sustained after 12 months. Among those allocated HRT, the median increase in CRP was higher in women who subsequently developed recurrent thrombosis (median 328%, n = 5, versus 54%, n = 60). TNF-alpha levels decreased significantly by mean -10% [-15 to -5%] versus 3% [-4 to 10%], p=0.004. Soluble VCAM-1 decreased in the HRT group compared to the placebo group (mean -13% [-18 to -8%] versus 1%, [-3 to 5%], p < 0.001). There were no significant changes in levels of IL-6, TGF-beta or P-selectin. On transdermal HRT no significant changes in CRP were observed after 3 and 12 months of treatment. CONCLUSIONS: Our findings substantiate that oral HRT containing estradiol is associated with a marked and rapid increase in CRP, whereas transdermal treatment is not. However, this increase on oral treatment was associated with no increases of other inflammatory markers.

Administration, Cutaneous↗

PubMed2001

Hemostatic risk factors for atherothrombotic disease: an epidemiologic view.

A number of prospective epidemiologic studies have now tested the hypothesis that plasma measures of hemostatic factors measured in initially healthy subjects may predict the future onset of atherothrombotic events. Epidemiologic evidence is very strong that plasma fibrinogen is a risk marker, if not a causal factor, for atherothrombotic events. Evidence is mixed on whether factor VII, factor VIII, von Willebrand factor, or other coagulation markers predict incident atherothrombosis. D-dimer is emerging as a strong risk marker, as are several fibrinolytic markers such as tPA antigen--but not PAI-1. Despite suggestive studies, no genetic polymorphism influencing hemostatic factor levels has emerged as a consistent and strong risk factor for atherothrombosis. Thus, prospective epidemiologic studies have identified several potential hemostatic markers of atherothrombosis risk, but their causal role and clinical utility in risk prediction remain incompletely established.

Arteriosclerosis↗

PubMed2005

Evidence of endothelial dysfunction in patients with functionally univentricular physiology before completion of the Fontan operation.

INTRODUCTION: Postoperative thrombosis after a cavopulmonary connection has been widely described. Abnormalities in coagulation seem to occur early in the course of patients with functionally univentricular physiology, and may precede surgery. Endothelial abnormalities due to chronic hypoxia, and hyperviscosity, may contribute to this scene. The purpose of our study was to investigate if patients with a superior cavopulmonary connection have altered levels of endothelial and coagulative markers in the plasma. METHODS: We compared findings in 10 patients, aged from 4 to 19 years, with 6 age-matched normal controls. We measured levels of von Willebrand factor antigen, thrombomodulin, tissue-type plasminogen activator, plasminogen activator inhibitor-1 and d-dimer in the plasma using enzyme-linked immunosorbent assay. RESULTS: We found increased levels of von Willebrand factor antigen (p = 0.01), tissue-type plasminogen activator (p = 0.01), and decreased levels of thrombomodulin (p = 0.008) in the patients when compared to controls, while levels of plasminogen activator inhibitor-1 were not different. Values of d-dimer were within the reference range. Levels of tissue-type plasminogen activator had a positive correlation with von Willebrand factor antigen (r = 0.66, p = 0.008). CONCLUSIONS: Altered levels of endothelial markers in the plasma, in the presence of normal levels of d-dimer, suggest that endothelial dysfunction may precede the occurrence of intravascular coagulation and thrombosis in patients with functionally univentricular physiology. These observations may have therapeutical implications.

Adolescent↗

PubMed1999

Changes in coagulation and fibrinolysis markers in acute ischemic stroke treated with recombinant tissue plasminogen activator.

BACKGROUND AND PURPOSE: Shifts of the balance between coagulation and fibrinolysis play a crucial role in pathogenesis and treatment of cerebral ischemia. In this study, we characterized the kinetics of hemostatic abnormalities induced by acute ischemic stroke and its thrombolytic (recombinant tissue plasminogen activator [rtPA]) or anticoagulant (heparin) treatment. METHODS: Systemic generation of molecular markers of hemostasis (fibrin monomer, D-dimer, thrombin-antithrombin complex, and fibrinopeptide 1.2) was monitored in acute ischemic stroke, and the effects of thrombolytic and anticoagulant treatments were analyzed. RESULTS: Thrombolysis with rtPA induced a massive response of markers of coagulation activation and fibrin formation that peaked after 1 to 3 hours and persisted for up to 72 hours. In contrast, only minor hemostatic changes were induced by acute ischemic stroke itself. Administration of heparin did not significantly affect these hemostatic abnormalities. CONCLUSIONS: This first characterization of the coagulation activation induced by rtPA treatment for acute ischemic stroke and the failure to abolish such hemostatic abnormalities by heparin may be of value for further refinement of the currently discussed thrombolytic therapy and the controversial adjunctive anticoagulant prophylaxis in stroke patients.

Aged↗

PubMed2002

Persistent activation of coagulation and fibrinolysis after treatment of active ulcerative colitis.

OBJECTIVE: Haemostatic changes may be involved in the pathogenesis and progression of ulcerative colitis. We studied longitudinally inflammatory and haemostatic parameters in patients treated for severe ulcerative colitis. DESIGN AND SETTING: We carried out a descriptive study of longitudinal blood measurements in patients with severe ulcerative colitis from one large regional hospital. METHODS: Nineteen patients with severe ulcerative colitis were assessed by an endoscopic score and a patient score at baseline. Patients were assessed by patient scores during treatment at scheduled intervals. At each visit, inflammatory and haemostatic parameters were determined. RESULTS: At baseline, the erythrocyte sedimentation rate, C-reactive protein, leucocyte and granulocyte count, thrombin-antithrombin complexes, prothrombin fragment 1+2, fibrinogen and degradation products of fibrinogen and fibrin were increased in patients when compared with controls, whereas albumin concentration and factor XIII activity were significantly lower. Antithrombin activity was normal. During treatment, the median patient score diminished significantly from 12 to 4.5 points after 2 weeks, decreased further to 4 points after 4 weeks and remained below 4 points throughout the remaining study period. Inflammation parameters returned to within the reference range in two patients after 4 weeks, whereas the coagulation markers prothrombin fragment 1+2 and thrombin-antithrombin complexes returned to normal values after 8 weeks and 24 weeks, respectively. In contrast with markers of inflammation, slightly increased concentrations of the degradation products of both fibrinogen and fibrin were found for almost 1 year, which indicated low-grade activation of coagulation and fibrinolysis. CONCLUSIONS: These results are compatible with a condition of persistent hypercoagulation in patients with ulcerative colitis who are in clinical remission. Persistent hypercoagulation may contribute to the clinical course of ulcerative colitis.

Adult↗

PubMed2006

Risk factors for dysbaric osteonecrosis.

OBJECTIVES: Dysbaric osteonecrosis (DON) is a complication of ineffective decompression following exposure to high-pressure environments. This study was designed to determine risk factors for the occurrence of DON in divers. METHODS: Fifty-six male divers received skeletal examinations by radiography to assess the occurrence of DON. A questionnaire was used to obtain clinical and diving information, including diving experience and maximum diving depth. Blood samples were collected to analyse the levels of plasminogen activator inhibitor (PAI)-1, cholesterol, triglyceride, low-density lipoprotein, very low-density lipoprotein, high-density lipoprotein, apolipoprotein A1 and apolipoprotein B. RESULTS: Lesions of DON were detected in 31 of the 56 (55%) divers. Multivariate logistic regression analysis showed that high levels of PAI-1, a coagulation marker (odds ratio 4.281; P=0.0296) and great maximum diving depth (odds ratio 5.627; P=0.0231) were independent predictors of DON. CONCLUSIONS: This study has shown the presence of coagulation abnormality in divers with DON. This result suggests that a pharmacological approach incorporating the use of an anticoagulant may represent a potential strategy for the prevention of DON.

Adult↗

PubMed2004

Activation of the inflammation, coagulation, and fibrinolysis systems, without influence of abciximab infusion in patients with non-ST-elevation acute coronary syndromes treated with dalteparin: a GUSTO IV substudy.

BACKGROUND: In acute coronary syndromes, the inflammation and the coagulation systems are activated, implying an impaired outcome. In addition to platelet inhibition, recent evidence suggests that the glycoprotein IIb/IIIa receptor inhibitor abciximab attenuates inflammation and coagulation activity. METHODS: The Swedish Global Utilization of Strategies To open Occluded arteries-IV (GUSTO-IV) substudy included 404 patients with non-ST-elevation acute coronary syndromes. In addition to aspirin and dalteparin, all patients were randomized to receive abciximab infusion for 24 hours or 48 hours or corresponding placebo without early coronary revascularization. Plasma samples were obtained at baseline and 24, 48, and 72 hours. RESULTS: The median levels of the coagulation markers thrombin/antithrombin complex and soluble fibrin increased significantly from 3.1 to 3.7 ug/L (baseline to peak; P <.001) and from 20 to 23 nmol/L (P <.001), respectively. The fibrinolysis marker, tissue plasminogen-activator, also increased its median levels, from 11.7 to 17.5 ug/L (P <.001), whereas the median level of plasminogen-activator-inhibitor was unchanged. The inflammatory markers interleukin-6, C-reactive protein, and fibrinogen also increased their median levels (5.4-7.8 ng/L, P <.001; 4.4-8.7 mg/L, P <.001; 3.3-3.9 g/L, P <.001). However, there were no differences in median levels or in changes of median levels of any marker at any point between the placebo group and any of the abciximab groups. CONCLUSIONS: In non-ST-elevation acute coronary syndrome, there was a simultaneous activation of the inflammation, coagulation, and fibrinolysis systems, despite aspirin and dalteparin treatment. Prolonged treatment with abciximab had no influence of the activation of these systems.

Abciximab↗