Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “hypercoagulable state”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 955 records · Page 53Linked to original sources
PubMed2004

Ischemic pituitary apoplexy associated with the lupus anticoagulant.

PURPOSE: To report a case of ischemic pituitary apoplexy secondary to a hypercoagulable state following elective orthopedic surgery. DESIGN: Observational case report. METHODS: A 48-year-old Caucasian man underwent an uneventful, left-sided total hip replacement and corrective osteotomy of the proximal femur. Two days post-operative, he developed a frontal headache and blurred vision in both eyes. RESULTS: Ophthalmic examination revealed right VIth cranial nerve palsy. Imaging studies indicated pituitary apoplexy with a large hypodense pituitary lesion with widening of the sella turcica. Laboratory findings included positive lupus anticoagulant, a normal prothrombin time (PT), and an elevated activated partial thromboplastin time (aPTT). Five days after the initial symptoms, a transsphenoidal pituitary resection was performed. At a 6 months follow-up, the VIth nerve paresis was completely resolved. CONCLUSIONS: This case describes ischemic pituitary apoplexy associated with a pre-operatively elevated aPTT and positive lupus anticoagulant. This is the first report, to our knowledge, of atypical apoplexy concurrent with antiphospholipid (aPL) antibodies following an uneventful surgery. The results we obtained on this patient suggest that an associated hypercoaguable state may increase the risk of thrombosis following elective orthopedic surgery.

Antibodies, Antiphospholipid↗
PubMed2004

Large-artery stroke in a young patient with Crohn's disease. Role of vitamin B6 deficiency-induced hyperhomocysteinemia.

An increased incidence of ischemic stroke has been reported in patients with Crohn's disease. Cerebral infarcts are usually considered as a complication of the hypercoagulable state associated with this inflammatory bowel disease (IBD). The association between Crohn's disease, hyperhomocysteinemia and large-artery stroke of the young has rarely been reported. A 39-year-old woman, with prior medical history of Crohn's disease and hypertension, presented with an ischemic stroke of the left internal carotid artery (ICA) territory. Etiological workup disclosed bilateral high-grade ICA stenosis and atheroma of the subclavian and vertebral arteries. Exhaustive search for prothrombotic factors showed inflammation, with an increased level of fibrinogen and factor IX, and a marked hyperhomocysteinemia. Both vitamin B1 and vitamin B6 plasmatic levels were decreased. Heterozygous C677T methylene-tetrahydrofolate reductase gene mutation was present. This observation highlights the combined proatherogenic effect of vitamin B deficiency-induced hyperhomocysteinemia and inflammation leading to large-artery stroke of the young in the setting of Crohn's disease. Our case report stresses the importance of vitamin deficiency screening in patients with IBD in terms of stroke prevention.

Adult↗
PubMed2007

Deep cerebral vein thrombosis associated with iron deficiency anaemia in adults.

Cerebral venous thrombosis (CVT) is rare and has a wide spectrum of symptoms, therefore it is difficult to diagnose. Thrombosis of the deep cerebral veins occurs very rarely: it has been reported that approximately 6% of patients with CVT have deep CVT, and the prognosis for patients with this condition is poor. CVT has been reported in association with dehydration, a hypercoagulable state, mastoiditis, tumour invasion of a venous sinus, use of oral contraceptives, pregnancy, puerperium, head trauma, vasculitis, and intracranial and systemic infections. However, in the literature, there are few reported cases of CVT in association with iron deficiency anaemia, especially in adults. We present here two patients with bilateral thalamic and basal ganglionic lesions due to thrombosis of the deep cerebral veins. Both of our patients had severe hypochromic microcytic anaemia due to iron deficiency, and both had a good prognosis after 2 months.

Adolescent↗
PubMed2005

The influence of weather and environment on pulmonary embolism: pollutants and fossil fuels.

Previous publications have highlighted seasonal variations in the incidence of thrombosis and pulmonary embolism, and that weather patterns can influence these. While medical risk factors for pulmonary thrombo-embolism such as age, obesity, hypercoagulable states, cancer, previous thrombo-embolism, immobility, limb paralysis, surgery, major illness, trauma, hypotension, tachypnoea and right ventricular hypokinesis are not directly implicated regarding environmental factors such as weather, they could be influenced indirectly by these. This would be especially relevant in polluted areas that are associated with a higher pulmonary embolism risk. Routine nuclear medicine lung ventilation/perfusion studies (V/Q scans) of 2071 adult patients referred to the nuclear medicine department of the Royal Surrey County Hospital in Guildford, UK, between January 1998 and October 2002 were reviewed and 316 of these patients were classified as positive for pulmonary embolism with high probability scan on PIOPED criteria. The occurrence of positive scans was compared to environmental factors such as temperature, humidity, vapour pressure, air pressure and rainfall. Multiple linear regression was used to establish the significance of these relations. The incidence of pulmonary embolism was positively related to vapour pressure and rainfall. The most significant relation was to vapour pressure (p=0.010) while rainfall was less significant (p=0.017). There was no significant relation between pulmonary embolism and air pressure, humidity or temperature. It is postulated that rainfall and water vapour may be contributary factors in thrombosis and pulmonary embolism by way of pollutants that are carried as condensation nuclei in micro-droplets of water. In particular, fossil fuel pollutants are implicated as these condensation nuclei. Pollutants may be inhaled by populations exposed to windborne vapour droplets in cities or airports. Polluted vapour droplets may be absorbed by the lung to hasten coagulation cascades in the blood. This may lead to thrombosis and increased pulmonary embolism under high vapour pressure conditions. With combined factors such as pre-existing ill health or immobility on long flights, the risk of thrombosis and consequent embolism might increase substantially.

Adult↗
PubMed2006

Anticoagulant effects of a Cannabis extract in an obese rat model.

Blood coagulation studies were conducted to determine the possible anti-/prothrombotic effect of an organic cannabis extract and the three major cannabinoids, THC, CBD and CBN. The in vitro effect of the cannabis extract on thrombin activity produced an IC50 value of 9.89 mg/ml, compared to THC at 1.79 mg/ml. It was also found that the extract, THC and CBN showed considerable inhibition of thrombin-induced clot formation in vitro with IC50 values of 600, 87 and 83 microg/ml for the extract, THC and CBN respectively. In an in vivo model used to determine clotting times of lean and obese rats treated with a cannabis extract, 50% clotting times were found to be 1.5 and 2 fold greater than their respective control groups, supporting the results obtained in the in vitro model. The study thus shows that Cannabis sativa and the cannabinoids, THC and CBN, display anticoagulant activity and may be useful in the treatment of diseases such as type 2 diabetes in which a hypercoagulable state exists.

Animals↗
PubMed2004

Plasma levels of plasminogen activator inhibitor type 1, factor VIII, prothrombin activation fragment 1+2, anticardiolipin, and antiprothrombin antibodies are risk factors for thrombosis in hemodialysis patients.

Patients with end-stage renal disease are prone to hemorrhagic complications and simultaneously are at risk for a variety of thrombotic complications such as thrombosis of dialysis blood access, the subclavian vein, coronary arteries, cerebral vessel, and retinal veins, as well as priapism. The study was devised for the following purposes: (1) to identify the markers of thrombophilia in hemodialyzed patients, (2) to establish a role for antiphospholipid antibodies in thrombosis of the vascular access, (3) to characterize phospholipid antibodies in hemodialysis patients, and (4) to study the effects of dialysis on coagulation cascade. A group of 20 hemodialysis patients with no thrombotic complications (NTC) and 20 hemodialysis patients with thrombotic complications (TC) were studied along with 400 volunteer blood donors. Patients with systemic lupus erythematosus and those with nephrotic syndrome were excluded. All patients underwent a screening prothrombin time, activated partial thromboplastin time, fibrinogen (Fg), coagulation factors of the intrinsic and extrinsic pathways, antithrombin III (AT-III), protein C (PC), protein S (PS), resistance to activated protein C, prothrombin activation fragment 1+2 (F1+2), plasminogen, tissue type plasminogen activator (t-PA), plasminogen tissue activator inhibitor type-1 (PAI-1), anticardiolipin antibodies type M and G (ACA-IgM and ACA-IgG), lupus anticoagulant antibodies, and antiprothrombin antibodies type M and G (aPT-IgM and aPT-IgG). The study showed that PAI-1, F 1+2, factor VIII, ACA-IgM, and aPT-IgM levels were increased significantly over controls both in TC and NTC, however, they could distinguish patients with thrombotic complications from those without, being increased maximally in the former group. The novelty of the study is represented by the significant aPT increase that was observed in non-systemic lupus erythematosus hemodialysis patients, and particularly in those with thrombotic events. In addition, there was a reduction of factor XII during the treatment. It is possible to assume in the TC group and, to a lesser extent, also in the NTC group that endothelial cells liberate PAI-1 in the vascular lumen, which causes hypofibrinolysis. In addition, an excess of factor VIII is activated by endothelial dysfunction with subsequent activation of the coagulation cascade as shown by increased F1+2 and fibrinogen. ACA-IgM, in turn, is capable of interfering with the system of protein C, a potent anticoagulant factor that inactivates cofactors Va and VIIIa. They also induce the expression of procoagulant factors on the surface of the endothelial cells. In conclusion, the hypercoagulable state caused by alterations of coagulation and fibrinolytic factors is a cause of vascular access dysfunction and thrombosis of other vessels.

Antibodies↗
PubMed2004

Changes in intracranial pressure, coagulation, and neurologic outcome after resuscitation from experimental traumatic brain injury with hetastarch.

BACKGROUND: In a model of traumatic brain injury (TBI), 2 protocols compared changes in intracranial pressure (ICP), coagulation, and neurologic outcome after intravenous fluid (IVF) resuscitation with either Hextend (HEX, 6% hetastarch in lactated electrolyte injection) or standard of care, crystalloid plus mannitol (MAN). METHODS: In the nonsurvivor protocol, swine (n = 28) received a fluid percussion TBI and hemorrhage (27 +/- 3 mL/kg). At 30 minutes, resuscitation began with lactated Ringer's (LR) or HEX. After 60 minutes, MAN (1 g/kg) or placebo was given plus supplemental IVF to maintain cerebral perfusion pressure (CPP) > or = 70 mm Hg for 240 minutes. Swine in the survivor group (n = 15) also underwent TBI and hemorrhage, and resuscitation with HEX was compared to that of normal saline (NS)+MAN. Neurologic outcome and coagulation were evaluated for 72 hours. RESULTS: In the nonsurvivor protocol, HEX, LR+MAN, and HEX+MAN attenuated the time-related rise of ICP and prevented ICP >20 mm Hg versus LR alone (P < .05). HEX alone maintained CPP (relative to baseline) and decreased total IVF by 50% versus LR +/- MAN (P < .05). MAN had no additive effect with HEX. Coagulation, measured by thromboelastograph reaction time (R), was 11 +/- 1 and 9 +/- 1 minutes at baseline and after TBI (before randomization). At 240 minutes after HEX or LR+MAN, R was 6 +/- 1 or 7 +/- 2 minutes, which indicates a hypercoagulable state, but there was no difference between treatments. In the survivor protocol, ICP and CPP were similar with NS+MAN versus HEX, but IVF requirement was 161 +/- 20 versus 28 +/- 3 mL/kg (P < .05). Motor scores were higher on days 2 and 3 with HEX (P < .05). At 72 hours, R was 28 +/- 14 versus 26 +/- 6 minutes with NS+MAN versus HEX, which indicates a hypocoagulable state, but there was no difference between treatments. CONCLUSIONS: Hextend as the sole resuscitation fluid after severe TBI reduces fluid requirement, obviates the need for mannitol, improves neurologic outcome, and has no adverse effect on the coagulation profile relative to the crystalloid plus mannitol standard of care.

Animals↗
PubMed2003

Thrombogenesis and endothelial damage/dysfunction in peripheral artery disease. Relationship to ethnicity and disease severity.

Peripheral artery disease (PAD) and intermittent claudication are common in men aged over 55 years. Once the diagnosis has been made, very few patients suffer from a deterioration of the disease. Those that do deteriorate tend to do so due to thrombosis of an affected artery. It is apparent that the disruption in the vessel wall accounts for some of the cause of the thrombosis but blood constituents also play a role. We hypothesized that levels of soluble P-selectin (sP-sel, a marker of platelet activation), von Willebrand factor (vWf, an index of endothelial damage/dysfunction), tissue factor (TF, a coagulation protein involved in the 'extrinsic' coagulation pathway) and fibrinogen would be abnormally elevated in relation to disease severity and correlated with each other, and related to ethnicity, in a multiethnic population of patients with PAD. To test this hypothesis, we studied 234 patients (80% white, 7% Indo-Asian, 13% Afro-Caribbean) with confirmed PAD [ankle brachial pressure index (ABPI)< or =0.8] and 50 healthy controls. All of the indices studied were increased in patients over controls (p<0.05). None of the indices of the hypercoagulable state were significantly different between the three ethnic groups studied. Patients with ischaemic rest pain were shown to have higher levels of plasma fibrinogen (p<0.001) although none of the other prothrombotic markers were increased in this group. Furthermore, fibrinogen was higher in cases whose ABPI was below the median (<0.52) when compared to those less severely affected, with an inverse correlation between fibrinogen and ABPI (Spearman, r=-0.178, p=0.009). In conclusion, we found a prothrombotic state in patients with PAD with increased levels of markers of endothelial damage/dysfunction, platelet activation and thrombosis, which may contribute to the pathogenesis of this condition. However, disease severity was only related to plasma fibrinogen levels.

Aged↗
PubMed2003

Thrombosis in children with acute lymphoblastic leukemia. Part II. Pathogenesis of thrombosis in children with acute lymphoblastic leukemia: effects of the disease and therapy.

At diagnosis, there is evidence of increased thrombin generation in children with acute lymphoblastic leukemia (ALL), the etiology of which is unclear. However, thromboembolism (TE) in children with ALL is most commonly reported after the initiation of antileukemic therapy indicating a possible interaction of the disease and therapy. Antileukemic therapy influences the haemostatic system either by direct effect of the chemotherapeutic agents or indirectly through the effect of supportive care, e.g. central venous line (CVL) or infectious complications secondary to immunosuppression. Asparaginase and steroids are shown to induce hypercoagulable state by suppression of natural anticoagulants, especially AT and plasminogen, and by elevations in F VIII/vWF complex, respectively. In addition, steroid therapy causes hypofibrinolytic state by dose-dependent increase in plasminogen activator inhibitor 1 (PAI-1) levels. Combination of these effects coupled with increased thrombin generation may be responsible for the increased incidence of TE observed with concomitant administration of asparaginase and steroids. Further studies to delineate the mechanism of increased thrombin in generation children with ALL and effects of various chemotherapeutic agents, in isolation and in combination, on haemostatic system are needed.

Adolescent↗
PubMed2004

Anticoagulant therapy for the thrombotic complications of the antiphospholipid antibody syndrome.

Patients with antiphospholipid antibodies (APLA) are at risk of arterial thromboembolism (ATE) or venous thromboembolism (VTE). The true strength of the association between APLA and first TE is unknown as there are no prospective studies of a large, well-characterized inception cohort of matched patients with and without APLA. Thus, evidence-based treatment recommendations for primary prophylaxis of TE in such patients cannot be made. Optimal therapy of patients with recent TE and APLA remains controversial; although there is no doubt that some such patients have a malignant hypercoagulable state characterized by resistance to "usual intensity" anticoagulation; recent evidence suggests that most such patients are adequately treated with "usual therapy". After warfarin discontinuation, such patients appear to be at increased risk of recurrent TE, as demonstrated in a series of studies of discontinuation of secondary TE prophylaxis in patients with APLA and venous TE (VTE). Because of this increased risk of recurrent TE, after anticoagulants are discontinued, most "experts" recommend extended duration therapeutic dose warfarin for such patients. This paper will briefly review this evidence.

Anticoagulants↗
PubMed2004

Libman-Sacks endocarditis associated with antiphospholipid syndrome and infection.

INTRODUCTION: Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated not only with a hypercoagulable state and recurrent fetal loss but with many diverse clinical manifestations including heart involvement, neurological manifestations, as well as skin, kidney and hematologic abnormalities. Cardiac manifestations include coronary by-pass graft and angioplasty occlusions, cardiomyopathy, cyanotic congenital heart disease, intracardiac thrombus and complications of cardiovascular surgery. The valvular heart disease was defined as Libman-Sacks nonbacterial endocarditis. Previously, we have shown a linear subendothelial deposition of anti-cardiolipin/beta2 glycoprotein I (beta2GPI) antibodies in the valve specimens derived from APS patients. The involvement of complement C3c in the pathogenesis was documented. We assessed the beta2GPI-related target epitope recognized by the anti-beta2GPI Abs on the valves. MATERIALS AND METHODS: In order to find the beta2GPI-related target epitopes recognized by the anti-beta2GPI antibodies on the valves, we used beta2GPI-related synthetic peptides. The presence of anti-beta2GPI Abs on the studied valves was detected by anti-idiotypic antibody, followed by immunoperoxidase analysis. Biotin attached to the N-terminal of beta2GPI-related synthetic peptides and control peptide were used to identify the epitope addressed by the anti-beta2GPI Abs deposited on the patient's valve. The binding was probed by streptavidin-peroxidase and appropriate substrate. The specificity was confirmed by competition assays with control peptide and anti-idiotypic antibody. RESULTS: Among the beta2GPI-related synthetic peptides, two peptides were found in previous studies to mimic common pathogens either bacteriae or viruses, which raised a possible infectious origin for APS. One of these peptides, TLRVYK, is a specific target for anti-beta2GPI Abs deposited on the APS valves. This synthetic peptide was able to displace the anti-anti-beta2GPI anti-idiotypic Abs for binding the anti-beta2GPI Abs on the valve by a competition assay. CONCLUSION: We point to the possibility that Libman-Sacks nonbacterial endocarditis may have an infectious origin.

Antibodies, Anticardiolipin↗
PubMed2005

Relationship between hemoconcentration and blood coagulation responses to acute mental stress.

BACKGROUND: Acute mental stress elicits reliable changes in blood coagulation factors. We studied whether stress-related changes in coagulation measures are associated with concomitant hemoconcentration. METHODS: Twenty-two men (mean age 47+/-8 years) underwent the Trier Social Stress Test (TSST) combining 13 min of task preparation, job interview, and mental arithmetic. Venous blood was obtained immediately before the preparation phase and immediately after stress to determine seven measures of coagulation and three measures of hemoconcentration. RESULTS: Clotting factor VII activity (FVII:C; 99.5+/-21.9 vs. 104.5+/-23.7 IU; p=0.016), FVIII:C (96.3+/-18.1 vs. 105.1+/-25.7 IU; p=0.008), FXII:C (95.8+/-26.7 vs. 102.6+/-26.4 IU; p=0.002), and von Willebrand factor antigen (vWF; 103.3+/-36.3 vs. 110.1+/-43.3 IU; p=0.009) all increased from baseline to poststress, with a similar statistical trend observed for d-dimer (177.6+/-85.5 vs. 180.5+/-83.9 ng/ml; p=0.058). The absolute increases in fibrinogen and in soluble tissue factor were not significant. Hematocrit (40.8+/-2.5 vs. 42.7+/-2.8; p<0.001) and hemoglobin (14.5+/-0.81 vs. 15.2+/-0.97; p<0.001) increased, and plasma volume (59.2%+/-2.5 vs. 54.6+/-4.2%; p<0.001) decreased from baseline to poststress. Unlike with heart rate (HR) and blood pressure (BP) reactivity, there emerged no significant relationship between change scores in any hemoconcentration and coagulation measure (all r values<0.4, all p values>0.05). CONCLUSION: We corroborated significant changes in coagulation measures in response to acute mental stress compatible, with the notion that stress may elicit a hypercoagulable state. However, stress hemoconcentration appears not to explain a substantial proportion in coagulation changes elicited by acute mental stress.

Adult↗
PubMed2004

Coagulation status and complications of pregnancy.

INTRODUCTION: There is much interest in the relationship between coagulation status and complications of pregnancy. The thrombelastograph (TEG) has been proposed as a useful, inexpensive tool to screen for patients with hypercoagulable states. MATERIALS AND METHODS: We investigated 588 unselected pregnant women at booking, obtaining blood samples for TEG and thrombophilia investigation. Pregnancy outcome data was recorded. RESULTS: We found significant correlations between TEG parameters and the Prothrombin time (PT) and Activated Partial Thromboplastin time (APTT) (p<0.01) and with plasma Antithrombin level (p<0.01). There was no correlation between TEG and other thrombophilic defects (protein C, protein S, Factor V Leiden mutation, Prothrombin G20210A mutation, MTHFR C677T mutation and Lupus Anticoagulant). There was a significant association of TEG parameters with mid-trimester loss (MTL) but not with other adverse pregnancy outcomes. CONCLUSIONS: The correlation between TEG and PT, APTT and antithrombin level supports its value in providing a global measure of haemostasis. Coagulation status at booking is associated with increased risk of MTL but not with complications occurring later in pregnancy.

Adolescent↗
PubMed2005

Transforming growth factor beta-1 released from platelets contributes to hypercoagulability in veno-occlusive disease following hematopoetic stem cell transplantation.

BACKGROUND: Hepatic veno-occlusive disease (VOD) is one of the most disastrous complications after allogeneic hematopoetic stem cell transplantation (HSCT). Thrombocytopenia with refractoriness to platelet transfusions suggests an increased platelet consumption in these patients. Interactions between platelets and endothelial cells might contribute to the hypercoagulable state at the sinusoidal endothelium as a central mechanism in the pathogenesis of VOD. STUDY DESIGN: The influence of activated platelets on cultured human endothelial cells was investigated in vitro. We focused on the release of plasminogen activator inhibitor-1 (PAI-1) from endothelial cells which has earlier been found to be significantly elevated in plasma of VOD patients. Endothelial cells isolated from human umbilical cords (HUVEC) were incubated with activated platelets. The release of PAI-1 in the presence or absence of specific antibodies was determined by ELISA technique. Tissue factor (TF) expression on endothelial cells was observed by flowcytometric analysis. RESULTS: HUVEC incubated with activated platelets were found to release significantly more PAI-1 compared to untreated cultures. The endothelial PAI-1-secretion after incubation of HUVEC with activated platelets was completely inhibited by an IgG monoclonal antibody against human transforming growth factor beta-1 (TGF beta-1). In contrast, PAI-1 production was not suppressed after inhibition of HUVEC-platelet-interaction by an IgG monoclonal antibody against CD154 (CD40L) expressed on the surface of activated platelets. An increased release of PAI-1 and an increased expression of tissue factor (TF) on the endothelial cell surface were observed after stimulation with TGF beta-1. CONCLUSION: TGF beta-1 released from activated platelets contributes to the hemostatic imbalance at the sinusoidal endothelium in patients with hepatic VOD by increase of endothelial cell PAI-1 production and TF expression. As a potent profibrotic cytokine, TGF beta-1 might further be involved in phlebosclerosis and sinusoidal fibrosis occurring in VOD.

Blood Platelets↗
PubMed2005

Thromboembolic complications in the nephrotic syndrome: pathophysiology and clinical management.

Patients with the nephrotic syndrome are at increased risk of developing venous and arterial thromboembolism, the most common of which is renal vein thrombosis. There are several unanswered or controversial issues relating to the nephrotic syndrome and thromboembolism, which include the mechanism of thromboembolism, and optimal diagnostic and anticoagulant management strategies. This review will discuss several of these issues: the epidemiology and clinical spectrum of thromboembolic disease occurring in patients with the nephrotic syndrome; the pathophysiology of the hypercoagulable state associated with the nephrotic syndrome; the diagnosis of renal vein thrombosis in the nephrotic syndrome; and the evidence for prophylactic and therapeutic anticoagulation strategies in such patients.

Anticoagulants↗
PubMed2005

Hemostatic abnormalities and leukocyte activation caused by infection in patients with malignant lymphoma during chemotherapy.

Hemostatic parameters were examined before and during 102 courses of chemotherapy in 42 patients with malignant lymphoma with high risk for infection. The white blood cell count was significantly reduced in all patients at days 1 and 3, but significantly increased at days 7 and 9, compared to before chemotherapy. At day 7 of chemotherapy, tissue factor (TF) mRNA levels in leukocytes were significantly increased in all patients, especially those with infection. Plasma concentrations of granulocyte elastase derived-XDP (GE-XDP) levels correlated with D-dimer levels during chemotherapy in patients with malignant lymphoma, suggesting that the elevated D-dimer is fibrin products degraded by granulocyte elastase. GE-XDP, C-reactive protein (CRP), GE-XDP and D-dimer were significantly higher in patients with infection, disseminated intravascular coagulation (DIC) and acute respiratory distress syndrome (ARDS) than those without. In patients with DIC or ARDS, TF mRNA correlated with D-dimer, and GE-XDP correlated with leukocyte count, CRP and D-dimer, suggesting that inflammatory changes due to thrombosis may cause the activation of leukocytes in patients with malignant lymphoma during chemotherapy. Activated leukocytes and granulocyte elastase may elicit a hypercoagulable state and ARDS in patients with malignant lymphoma during chemotherapy.

Aged↗
PubMed1998

Hypofibrinolysis in atrial fibrillation.

BACKGROUND: There is a high incidence of systemic embolism in patients with chronic atrial fibrillation. A hypercoagulable state has been demonstrated, but the fibrinolytic system is rarely studied. METHODS: Plasma levels of modified antithrombin III (ATM), tissue plasminogen activator (TPA), its inhibitor (PAI-1), TPA-PAI-1 complexes and plasmin-antiplasmin complexes (PAP), d -dimer, and fibrinogen were measured in plasma from 36 patients with chronic atrial fibrillation. Fifteen patients had rheumatic mitral stenosis and 21 had nonrheumatic atrial fibrillation. Levels were compared with those found in the plasma of 20 healthy subjects. Transthoracic echocardiographic studies were done. RESULTS: Patients with atrial fibrillation had higher plasma levels of ATM, d -dimer, PAI-1, and TPA-PAI-1 complexes than controls (P <.001). The rheumatic atrial fibrillation group also showed elevated levels of fibrinogen (P <. 05). No significant differences were found in TPA and PAP. There were no differences between rheumatic and nonrheumatic atrial fibrillation. CONCLUSIONS: Atrial fibrillation shows a hypofibrinolytic state caused by elevated PAI-1 levels with no increase in PAP complex concentration. Elevated plasma d -dimer levels suggest increased intravascular thrombogenesis. This may contribute to increased risk of thrombosis.

Aged↗
PubMed2003

Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events.

Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in IE patients with and without embolic events by measuring the plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasminogen activator inhibitor-1, beta-thromboglobulin, and platelet factor 4. The study included 76 consecutive patients with definite IE according to the Duke criteria. Among them, 13 (17.1%) had major embolic events. Plasma concentrations of prothrombin fragment 1 + 2 (3.2 +/- 1.3 vs 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/L, p <0.001, respectively) and thrombin-antithrombin (7.3 +/- 1.5 vs 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p <0.001, respectively) were elevated in patients with embolic events compared with both patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-thromboglobulin (63.3 +/- 10.9 vs 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p <0.001, respectively) and platelet factor 4 (106.0 +/- 28.7 vs 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p <0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher plasminogen activator inhibitor-1 levels than both nonembolic patients and healthy subjects (14.4 +/- 6.4 vs 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). In conclusion, IE patients with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state that may contribute to the increased risk of thromboembolic events in this particular group.

Adolescent↗