Fibrinolysis and fibrinogenolysis in patients with thrombotic disease.

In order to assess the fibrinolytic state in thrombotic disease, plasma levels of fibrin degradation products (FbDP) and fibrinogen degradation products (FgDP) were measured in 126 patients with a variety of thrombotic diseases. Mean plasma concentrations of both FbDP and FgDP were significantly elevated in patients with thrombotic disease as compared with healthy subjects. Plasma concentrations of FgDP were positively correlated with FbDP (r = 0.667, P less than 0.001). When analysed according to the disease categories, the magnitude of elevations of FbDP and FgDP was most prominent in venous thrombotic disease such as deep vein thrombosis and pulmonary embolism. These findings indicate that fibrinolysis is accelerated in patients with thrombotic disease and that fibrinolysis is frequently accompanied by some fibrinogenolysis in these patients.     

Predictive Value of Inflammatory and Coagulation Parameters in the Course of Severe Ulcerative Colitis

Alterations in markers of coagulation have been found in patients with inflammatory bowel disease. Our aim was to study the predictive value of coagulation and inflammatory parameters in the course of severe ulcerative colitis. Twenty-seven patients were included. The disease course was followed for one year. Sensitivity, specificity, negative predictive value, positive predictive value, and likelihood ratio, as well as the clinical predictive value of laboratory variables were calculated. Inflammatory variables, such as ESR, CRP, and leukocyte and platelet count showed poor diagnostic accuracy. Several coagulation parameters, such as fibrinogen and fibrin(ogen) degradation products, were increased in patients with active ulcerative colitis, whereas coagulation factor XIII was decreased. No significant relationship between clinical course and coagulation parameters was demonstrated, though both inflammatory and coagulation parameters were useful in the assessment of disease activity in patients with active ulcerative colitis.     

Molecular markers of coagulation and fibrinolysis as indicators for the disease activity of rheumatoid arthritis

Pathological roles of coagulation and fibrinolytic system are suggested in the progressive and destructive articular lesions of rheumatoid arthritis (RA). In the present study, we simultaneously and serially determined recently available molecular markers of coagulation (thrombin-antithrombin III complex; TAT) and fibrinolysis/fibrinogenolysis [fibrin/fibrinogen degradation products (FDP),d-dimer and FDP-E], and compared their circulating levels with conventional indicators for the disease activity of RA in 31 patients. Either TAT,d-dimer or FDP-E levels well correlated with Lansbury activity index (LAI), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels. Compared with CRP levels, these hemostatic markers more strongly associated with LAI. In addition, the molecular marker levels correlated with each other in RA patients. The hemostatic markers were further determined on at least two different occasions in 14 RA patients. Percentage changes of thed-dimer level significantly associated with those of LAI, as observed between LAI and ESR or CRP levels. Our results clearly indicate excessive coagulation and fibrinolysis in active RA patients. Among the molecular markers determined,d-dimer was considered to be especially useful as a clinical indicator for disease activity of RA.     

Fibrinolysis and fibrinogenolysis in liver disease

Patients with liver disease frequently have hemostatic abnormalities which include accelerated fibrinolysis. In order to assess the fibrinolytic state in liver disease, plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP), and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 36 patients with liver disease (six patients with acute hepatitis, seven with chronic hepatitis, ten with liver cirrhosis, 11 with hepatocellular carcinoma, and two with intrahepatic cholestasis). As compared with healthy subjects, mean plasma levels of FbDP (1,083 +/- SD 1,254 vs. 236 +/- 100 ng/ml, P = 0.005) and TDP (1,773 +/- 1,814 vs. 669 +/- 212 ng/ml, P = 0.001) were significantly elevated in patients with liver disease, whereas FgDP was normal (389 +/- 202 vs. 396 +/- 132 ng/ml, P = 0.87). Plasma FbDP correlated very well with TDP (r = 0.986, P less than 0.00001) in liver disease. In addition, FbDP and TDP but not FgDP correlated with plasma concentrations of thrombin-antithrombin III complex. When plotted by the disease categories, the magnitude of elevations of FbDP and TDP was the most prominent in acute hepatitis followed by hepatocellular carcinoma. These findings indicate that activation of fibrinolysis occurs following thrombin generation, but increased primary fibrinogenolysis is rare in liver disease.     

凝血和纤溶状态的变化对炎症性肠病疾病活动性的影响

目的评价炎症性肠病患者及正常对照者之间凝血和纤溶状态的差异及其和疾病活动性的关系。方法队列研究271例炎症性肠病患者和正常对照者的凝血和纤溶状态,性别分层分析凝血和纤溶状态的改变和炎症活动性的关系。结果炎症性肠病患者血小板、血小板分布宽度、凝血酶原时间、纤维蛋白原和活化部分凝血活酶时间显著高于正常对照者（P〈0.05）,但平均血小板体积显著低于正常对照组（P〈0.05）。多元回归分析显示纤维蛋白原是男性溃疡性结肠炎患者ESR（β=1.316,P=0.000）和CRP（β=1.233,P=0.015）的线性相关因子;血小板（β=0.436,P=0.037）和凝血酶原时间（β=0.810,P=0.000）是女性克罗恩病患者克罗恩病活动指数的线性相关因子。结论炎症性肠病患者凝血和纤溶状态异常和疾病活动性相关,纤维蛋白原、血小板和凝血酶原时间是炎症活动性的预测因素。     

Molecular markers of coagulation and fibrinolysis as indicators for the disease activity of rheumatoid arthritis

Abstract

Pathological roles of coagulation and fibrinolytic system are suggested in the progressive and destructive articular lesions of rheumatoid arthritis (RA). In the present study, we simultaneously and serially determined recently available molecular markers of coagulation (thrombin-antithrombin III complex; TAT) and fibrinolysis/fibrinogenolysis [fibrin/fibrinogen degradation products (FDP),d-dimer and FDP-E], and compared their circulating levels with conventional indicators for the disease activity of RA in 31 patients. Either TAT,d-dimer or FDP-E levels well correlated with Lansbury activity index (LAI), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels. Compared with CRP levels, these hemostatic markers more strongly associated with LAI. In addition, the molecular marker levels correlated with each other in RA patients. The hemostatic markers were further determined on at least two different occasions in 14 RA patients. Percentage changes of thed-dimer level significantly associated with those of LAI, as observed between LAI and ESR or CRP levels. Our results clearly indicate excessive coagulation and fibrinolysis in active RA patients. Among the molecular markers determined,d-dimer was considered to be especially useful as a clinical indicator for disease activity of RA.     

Thrombin activation and increased fibrinolysis in patients with chronic liver disease

The respective roles of intravascular coagulation (DIC) and fibrinolysis were assessed in severe chronic liver disease by measuring thrombin-antithrombin (TAT) complexes, tissue-type plasminogen activator antigen (tPA Ag) and fibrinogen and fibrin degradation products (FgDP and FbDP respectively) in 66 patients with liver disease caused by cirrhosis (n = 34) or chronic hepatitis (n = 32) as compared to findings in a control group (n = 30). There was a significant increase of TAT complexes (P less than 0.01), tPA Ag (P less than 0.002), FDP and FbDP (P less than 0.001) in patients as compared to controls. FbDP increase was more evident in patients with cirrhosis than in those with hepatitis (P less than 0.01). Significant correlations between these parameters with some liver function tests were also demonstrated. Thus, in patients with severe liver disease, an increased thrombin activity, as demonstrated by high TAT levels; followed by hyperfibrinolysis suggest that a low grade DIC may occur.     

Elevated plasma von Willebrand factor levels in patients with active ulcerative colitis reflect endothelial perturbation due to systemic inflammation

AIM: To evaluate the plasma von Willebrand factor (vWF) levels in patients with ulcerative colitis (UC) and to investigate their relationship with disease activity, systemic inflammation and coagulation activation. METHODS: In 46 patients with ulcerative colitis (active in 34 patients), clinical data were gathered and plasma vWF levels, markers of inflammation (ESR, CRP, and fibrinogen) and thrombin generation (TAT, F1+2, and D-dimers) were measured at baseline and after 12 wk of treatment. Plasma vWF levels were also determined in 52 healthy controls (HC). The relationship of plasma vWF levels with disease activity, disease extent, response to therapy, acute-phase reactants (APRs) and coagulation markers (COAGs) was assessed. RESULTS: The mean plasma vWF concentrations were significantly higher in active UC patients (143.38±63.73%) than in HC (100.75±29.65%, P = 0.001) and inactive UC patients (98.92±43.6%, P = 0.031). ESR, CRP and fibrinogen mean levels were significantly higher in active UC patients than in inactive UC patients, whereas there were no significant differences in plasma levels of D-dimers, F1+2, and TAT. UC patients with raised APRs had significantly higher mean plasma vWF levels than those with normal APRs (144.3% vs 96.2%, P = 0.019), regardless of disease activity. Although the mean plasma vWF levels were higher in UC patients with raised COAGs than in those with normal COAGs, irrespective of disease activity, the difference was not significant (141.3% vs 118.2%, P = 0.216). No correlation was noted between plasma vWF levels and disease extent. After 12 wk of treatment, significant decreases of fibrinogen, ESR, F1+2, D-dimers and vWF levels were noted only in UC patients with clinical and endoscopic improvement. CONCLUSION: Our data indicate that increased plasma vWF levels correlate with active ulcerative colitis and increased acute-phase proteins. Elevated plasma vWF levels in ulcerative colitis possibly reflect an acute-phase response of the perturbed endothelium due to inflammation. In UC patients, plasma vWF levels may be another useful marker of disease activity or response to therapy.     

血常规检查对炎症性肠病活动性判断价值

目的 探讨血常规检查能否作为国人活动性炎症性肠病的评价方法.方法 112例炎症性肠病患者和58例健康人纳入研究.所有患者均进行血常规、C反应蛋白和血沉检测.克罗恩病和溃疡性结肠炎分别依据克罗恩病疾病活动指数和Truelove-witts标准进行疾病活动状态的评价.结果 活动期克罗恩病的血红蛋白、红细胞压积、平均血小板体积明显低于缓解期患者和健康对照,差异有统计学意义（P〈0.05）,而红细胞体积分布宽度、白细胞、中性粒细胞、血小板计数则高于缓解期和健康对照,差异有统计学意义（P〈0.05）.活动期溃疡性结肠炎的血红蛋白、红细胞压积、平均血小板体积亦显著低于缓解期和健康对照,差异有统计学意义（P〈0.05）,而血小板计数高于缓解期患者,差异有统计学意义（P〈0.05）,红细胞体积分布宽度、白细胞计数高于健康对照,差异有统计学意义（P〈0.05）.白细胞、血小板计数与血沉、C反应蛋白呈正相关性（P〈0.05）,而平均血小板体积与血沉、C反应蛋白呈负相关性（P〈0.05）.结论 血常规的多项指标随疾病活动状态改变而变化,并与目前公认的反应炎症指标呈明显相关性,提示血常规可以作为判断炎症性肠病活动度的方法.     

活动期溃疡性结肠炎凝血功能分析

背景：血栓栓塞是溃疡性结肠炎（UC）较严重的并发症之一,了解活动期UC凝血状态,可为治疗提供参考依据。目的：分析UC活动期患者凝血功能的变化,探讨其与疾病活动性和严重程度的关系。方法：选取2006年1月～2012年11月上海中医药大学附属普陀医院收治的UC患者162例。检测患者血小板计数（PLT）、平均血小板体积（MPV）、凝血酶原时间（胛）、活化部分凝血活酶时间（APTr）、纤维蛋白原（FIB）、凝血酶时间（r丌）、D-二聚体（D-D）、红细胞沉降率（ESR）、C反应蛋白（CRP）,评估患者临床活动性指数（CAI）和Baron内镜下评分。比较PLT、MPV、PT、APTT、FIB、Tr、D-D在UC不同疾病活动性和不同严重程度间的差异,分析UC活动期PLT、MPV、PT、FIB、D-D与ESR、CRP、CAI、Baron评分的相关性。结果：UC活动期组与缓解期组、正常对照组的PLT、MPV、FIB、D-D相比差异有统计学意义（P〈0．05）。轻、中、重度UC间D-D相比差异有统计学意义（P〈0．05）。Spearman等级相关分析显示,UC活动期患者PLT和D-D与ESR、CAI、Baron评分呈正相关,MPV与ESR、Baron评分呈负相关,PT和D-D与CRP呈正相关,FIB与ESR、CRP、Baron评分呈正相关（P〈0．05）。多元回归分析结果显示,UC活动期患者MPV与Baron评分呈负相关,FIB与ESR和CRP呈正相关,D-D与ESR和CRP呈正相关（P〈0．05）。结论：PLT、MPV、PT、FIB、D-D可作为评价UC活动性的指标,D-D可作为评价UC严重程度的指标。     

Dynamics of blood coagulation factor XIII in ulcerative colitis and preliminary study of the factor XIII concentrate

Summary Blood coagulation studies were performed in twenty patients with ulcerative colitis (UC). At the active stage of UC, a marked increase in platelet count and fibrinogen concentration, and a marked decrease in Factor XIII activity level were observed. At the active stage of UC, four patients were treated with Factor XIII concentrate leading to reduction of pain, bleeding and endoscopic findings.     

溃疡性结肠炎患者凝血功能的改变

目的分析活动期溃疡性结肠炎患者的凝血功能。方法以我院60例活动性溃疡性结肠炎及20例健康对照为检测对象,检测指标包括外周血血小板计数、部分凝血活酶时间及纤维蛋白原定量。结果与健康对照组比较,溃疡性结肠炎组血小板计数、纤维蛋白原定量均明显增高,差异具有统计学意义（P〈0．05）,在轻度、中度、重度之间,上述三个检测指标无差异（P〉0．05）。结论活动性溃疡性结肠炎患者处于高凝状态,疾病的严重程度与凝血功能无关。     

活动期溃疡性结肠炎患者体内血小板激活状态的评价

目的 探讨血小板激活和活动期溃疡性结肠炎的关系。方法 对32例活动期溃疡性结肠炎、11例缓解期溃疡性结肠炎、30例肠易激综合征（IBS）患者和正常对照组27例用SH－93智能血液凝聚仪检测血小板聚集率，用酶联免疫法检测P－选择素和血栓素B2（TXB2）。同时评价43例溃疡性结肠炎内镜下表现和结肠黏膜活检情况。结果 32例活动期溃疡性结肠炎患者平均1min血小板聚集率和最大血小板聚集率均明显高于IBS组和正常对照组（P＜0．01）；32例活动期溃疡性结肠炎P－选择素和TXB2明显高于IBS组和正常对照组，差异有显著性（P＜0．01或P＜0．05）。缓解期溃疡性结肠炎的P－选择素也高于正常对照组。结论 活动期溃疡性结肠炎患者体内存在血小板激活，血小板可能直接参与结肠黏膜的急性炎症反应。其中P－选择素是溃疡性结肠炎的特异性指标，而血小板聚集率和TXB2与疾病的活动度有关。抗血小板药物可能对溃疡性结肠炎有一定的治疗效果。     

Fibrin and fibrinogen degradation products with an intact D-domain C- terminal gamma chain inhibit an early step in accessory cell-dependent lymphocyte mitogenesis

Although the low molecular weight degradation products of fibrinogen (FgDP) and fibrin (FbDP) are known to inhibit lymphocyte blastogenesis, the effect of purified macro-molecular FgDP and FbDP (molecular weight, 90 to 200 Kd) is unclear. We have examined the effect of these latter FgDP and FbDP and find that products that contain the D domain inhibit lymphocyte proliferation in response to T-cell mitogens, allogeneic mononuclear leukocytes, and anti-CD3 in vitro. Plasmic digestion of D1 in the absence of calcium with removal of the C-terminal end of the gamma chain or disruption of the gamma-gamma C-terminal cross-link site of D-dimer (DD) by puffadder venom (PAV-D) abrogates their inhibitory potential. Prior incubation of monocytes with DD or D1 inhibits subsequent lymphocyte transformation. Binding studies with radiolabeled DD and PAV-D confirm that monocytes interact only with DD. This specific binding may be competitively inhibited by monoclonal antibodies to CD11b/CD18 or by peptide analogues of the C-terminal gamma chain of fibrinogen that mimic the adhesion recognition site of integrins. We postulate that DD and D1 bind to CD11b/CD18 on adherent monocytes and modulate lymphocyte activation. These products are typically present in the plasma of patients with disseminated intravascular coagulation with sepsis and could therefore influence inflammatory processes in vivo.     

Mean platelet volume: a useful marker of inflammatory bowel disease activity

OBJECTIVES: We investigated whether the mean platelet volume would be a useful marker in the evaluation of inflammatory bowel disease activity. METHODS: Complete blood count, C-reactive protein, erythrocyte sedimentation rate, serum thrombopoietin and erythropoietin, plasma beta-thromboglobulin, and platelet factor 4 were measured in 93 patients with ulcerative colitis, 66 patients with Crohn's disease, and 38 healthy blood donors. Disease activity was assessed by the Clinical Colitis Activity Index in patients with ulcerative colitis and by the Crohn's Disease Activity Index in patients with Crohn's disease. RESULTS: Mean platelet count was increased in patients with active compared to inactive ulcerative colitis (p < 0.05), and in patients with active compared to inactive Crohn's disease (p = 0.0002) or healthy controls (p < 0.0001). On the other hand, mean platelet volume was significantly decreased in patients with active compared to inactive ulcerative colitis (p = 0.02) or healthy controls (p < 0.0001), and in patients with active compared to inactive Crohn's disease (p = 0.0005) or healthy controls (p < 0.0001). Mean platelet volume was inversely correlated with the white blood cell count (r = -0.17, p = 0.02), C-reactive protein (r = -0.46, p = 0.009) and erythrocyte sedimentation rate (r = -0.28, p = 0.008). No significant correlations were found between mean platelet volume and serum thrombopoietin or erythropoietin levels; however, a strong negative correlation between mean platelet volume and beta-thromboglobulin (r = -0.34, p < 0.0001) and platelet factor 4 (r = -0.30, p = 0.0002) was observed. CONCLUSIONS: Mean platelet volume is significantly reduced in active inflammatory bowel disease and is negatively correlated with the known inflammatory bowel disease activity markers and the platelet activation products. We propose that mean platelet volume provides a useful marker of activity in inflammatory bowel disease.     

Platelet (dys)function and plasma plasminogen levels in hemodialysis patients

The factors contributing to platelet dysfunction in hemodialysis patients are still not completely known. We explored whether the fibrinolytic system influences platelet function in hemodialysis patients. We measured standard fibrinolytic parameters and markers of fibrinolysis/coagulation activation, and correlated them to platelet aggregation in 15 hemodialysis patients. Fifteen healthy age-matched volunteers served as controls. Hemodialysis patients had significantly decreased levels of plasminogen (0.76 [0.64-0.86] vs. 0.98 [0.87-1.08] rel, P < 0.001), and increased levels of fibrinogen (4.6 [3.9-5.5] vs. 4.0 [3.4-4.6] g/L, P < 0.05), whereas tissue-type plasminogen activator antigen and plasminogen activator inhibitor (PAI)-1 antigen and PAI activity were comparable to controls. Furthermore, elevated levels of markers of fibrinolysis/coagulation were found in hemodialysis patients: D-dimer (280 [170-460] vs. 135 [120-150] ng/mL, P < 0.01), prothrombin fragments 1 + 2 (1.7 [1.4-1.9] vs. 1.1 [1.0-1.2] nmol/L, P < 0.001), and thrombin-antithrombin complexes (5.2 [4.2-17.7] vs. 0 [0-4.2]microg/L, P < 0.01). The aggregation of platelets (induced by adenosine diphosphate) was slightly impaired in patients compared to controls (72 [43-79] vs. 83 [73-88]%, P = 0.08). Analysis showed that platelet aggregation positively correlated with plasminogen levels (r = 0.48, P < 0.01). No correlation with other fibrinolytic parameters or markers of activation was found. In hemodialysis patients platelet (dys)function appears to be associated with both the fibrinolytic and coagulation systems. We found that platelet aggregation significantly correlates with plasma plasminogen levels. This relation, which has not been hitherto described, seems to be causal and clinically important. Further exploration of this may help us to better understand the mechanisms of platelet dysfunction in hemodialysis patients.     

An overlooked indicator of disease activity in ulcerative colitis: Mean platelet volume

Many non-invasive tests have been studied for diagnosis and determining the activation degree of inflammatory bowel disease (IBD). Nevertheless, an ideal test has not been found yet. Mean platelet volume (MPV) is influenced by the inflammation. In a few study, decreased platelet volume have been reported in IBD. The aim of this study is to determine whether platelet volume would be useful in ulcerative colitis (UC) activity. Additionally we have analyzed overall accuracy of MPV in disease activity and compared with other inflammatory markers. A total of 61 UC patients (male/female : 41/20), and 27 healthy subjects (male/female : 18/9) were enrolled into the study. For all subjects following tests were performed; ESR, CRP, white blood cell count and mean platelet volume. A statistically significant decrease in MPV was noted in patients with UC (8.29 ± 1.02fL) compared with healthy controls (8.65 ± 0.79 fL). MPV of active UC (8.06 ± 1.19 fL) patients were significantly lower than that of inactive UC (8.45 ± 0.87 fL). Overall accuracy of MPV in determination of active UC was 71% (with sensitivity 67%, specificity 73%). A negative correlation was found between MPV and endoscopic activity index (r : -0.358 p : 0.005). In UC, MPV did not correlate with ESR, CRP and white blood cell. Our study showed that MPV reduced in UC, particularly in patients with active UC. Decreased MPV may be an indicator for increased disease activity in patients with UC.     

Red Cell Distribution Width for Assessment of Activity of Inflammatory Bowel Disease

Background Impaired iron absorption or increased loss of iron was found to correlate with disease activity and markers of inflammation in inflammatory bowel disease (IBD). Red cell distribution width (RDW) could be a reliable index of anisocytosis with the highest sensitivity to iron deficiency. Aim The importance of RDW in assessment of IBD disease activity is unknown. In this study, we aimed to determine if RDW could be useful in detecting active disease in patients with IBD. Materials and methods A total of 74 patients with ulcerative colitis (UC) and 22 patients with Crohn’s disease (CD) formed the study group with 20 age- and sex-matched healthy volunteers as the control group. CD activity index higher than 150 in patients with CD was considered to indicate active disease. Patients with moderate and severe disease according to the Truelove-Witts scale were accepted as having active UC. In addition to RDW, serum C-reactive protein (CRP) and fibrinogen levels, erythrocyte sedimentation rates (ESR), leukocyte, and platelet counts were measured. Results Fourteen (63.6%) of the patients with CD and 43 (58.1%) of the patients with UC had active disease. RDW, fibrinogen, CRP, ESR, and platelet counts were all significantly elevated in patients having active IBD compared with those without active disease and controls (P < 0.05). The study subjects were further classified into two subgroups: cases with active and inactive UC and those with active and inactive CD. A subgroup analysis indicated that for an RDW cutoff of 14, the sensitivity for detecting active UC was 88% and the specificity was 71% (area under curve [AUC] 0.81, P = 0.0001). RDW was the most sensitive and specific parameter indicating active UC. However, the same was not true for CD since CRP at a cutoff of 0.54 mg/dl showed a sensitivity of 92% and a specificity of 63% (AUC 0.92, P = 0.001), whereas RDW at a cutoff of 14.1 showed 78% sensitivity and 63% specificity to detect active CD. Conclusion Among the laboratory tests investigated, including fibrinogen, CRP, ESR, and platelet counts, receiver operating characteristic (ROC) curve analysis indicated RDW to be the most significant indicator of active UC. For CD, CRP was an important marker of active disease.     

Intravenous magnesium does not influence the activity of the coagulation cascade.

Experimental arterial thrombus formation is reduced during intravenous magnesium infusion. It is well documented that magnesium reduces platelet reactivity, but the antithrombotic effect could also originate from anticoagulant properties or increased fibrinolysis. We therefore evaluated the effect of intravenous magnesium on prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III complex (TAT) concentrations, and fibrin degradation products (FbDP) in a randomized, cross-over study in 14 healthy volunteers. Citrated blood samples were collected at 0, 30, and 180 min. An additional in vitro study on magnesium's effect on the activity of different coagulation factors was carried out. A transient increase was seen in F1 + 2 and TAT after 30 min but without any significant difference between the placebo and magnesium period. FbDP did not change significantly between the two treatments. Increasing concentrations of magnesium dose-dependently decreased binding of activated factor X to activated factor VII (FVIIa), but the decrease was slight and probably without any significance for coagulation at the concentrations tested. No effect was observed on the activity of FVIIa or activated factor VIII. In conclusion, no significant differences were observed on markers of coagulation or fibrinolytic activity during intravenous magnesium infusion. These results indicate that the observed antithrombotic effect of magnesium is more likely to arise from the previously observed platelet inhibition.