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Results for “hypercoagulable state”

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At least 235 records · Page 13Linked to original sources
PubMed1978

The hypercoagulable state and pulmonary embolism in patients with ovarian carcinoma.

Fifty-nine patients with ovarian carcinoma were studied with particular reference to abnormalities of the coagulation mechanism. The notable findings were the high incidence of episodic thrombocytosis (73%) and the relation of these peaks of thrombocytosis to periods of expected maximum tumour break-down. The incidence of pulmonary embolism for the series was 44%, with the majority occurring in the group demonstrating significant thrombocytosis; in this latter group, pulmonary embolism constituted the major cause of death. The abnormalities in coagulation are discussed, together with pragmatic significance and methods of control.

Adenocarcinoma↗
PubMed1996

Hypercoagulable state in patients with antiphospholipid syndrome is related to high induced tissue factor expression on monocytes and to low free protein s.

Antiphospholipid antibodies (aPLs) are associated with thrombosis, but the mechanisms of this thrombotic tendency are unknown. We studied 56 patients 612 with systemic lupus erythematosus [SLE] and aPLs and previous thrombosis, 12 with SLE and aPLs but no thrombosis, 15 with SLE without aPLs or thrombosis, 11 with primary antiphospholipid syndrome with thrombosis, and 6 asymptomatic subjects with aPLs) to investigate the ability of aPLs to induce tissue factor (TF) expression on human normal monocytes. A double direct immunofluorescence technique (anti-CD14 and anti-TF) was used, and procoagulant activity in viable and disrupted cells was measured after plasma incubation for 6 hours at 37 degrees C with normal mononuclear cells. Hemostasis regulatory proteins, prothrombin fragment 1 + 2, and thrombin-antithrombin III complex levels were determined. Increased TF expression and procoagulant activity were observed using plasma samples from SLE patients with aPLs and thrombosis (P < .01) and from primary antiphospholipid syndrome patients (P < .01) but not from patients with SLE and aPLs but no thrombosis, patients with SLE without aPLs, or asymptomatic patients with aPLs. Purified aPL immunoglobulins from one primary antiphospholipid syndrome and two SLE patients added to normal plasma showed a significant increase in both TF expression and procoagulant activity (P < .05) compared with purified aPL from two SLE patients without thrombosis. The addition of nonspecific IgG from three SLE patients without aPLs and from three control subjects did not increase TF expression. Low free protein S was seen in eight patients. Increased TF expression and low free protein S correlated with thrombosis (P < .01) and with higher prothrombin fragment 1 + 2 and thrombin-antithrombin III values (P < .01). These observations may contribute to a further understanding of the thrombotic risk in aPL patients.

Antiphospholipid Syndrome↗
PubMed1992

Markers of a hypercoagulable state following acute ischemic stroke.

BACKGROUND AND PURPOSE: The nature of hematologic disorders in different stroke subtypes remains uncertain. The purpose of this study was to clarify the differences in the coagulation and fibrinolytic activities among ischemic stroke subtypes. METHODS: We performed sequential measurements of hematologic parameters in 21 patients with acute cardioembolic stroke, 10 patients with atherothrombotic stroke, 23 patients with lacunar stroke, and 20 age-matched controls. RESULTS: A marked elevation of plasma concentrations of the thrombin-antithrombin III complex and crosslinked D-dimer was observed only in cardioembolic stroke within 48 hours of onset (p less than 0.01), persisting for one month with a gradual decline. In atherothrombotic stroke, however, the level of crosslinked D-dimer was not elevated at the onset, but increased seven days after onset (p less than 0.01). No significant changes in these marker levels were observed in lacunar stroke. CONCLUSIONS: Our findings suggest that the nature of altered coagulation and fibrinolysis are different in various subtypes of ischemic stroke, and that an assessment of these hematologic parameters may be useful for the early classification of these subtypes.

Acute Disease↗
PubMedDate not supplied

Hypercoagulable state in patients with advanced gastrointestinal cancer: evidence for an acquired resistance to activated protein C.

AIMS AND BACKGROUND: Thromboembolic complications are common in patients with cancer and represent the second cause of death in patients with overt malignant disease. The aim of this study was to investigate the activated protein C pathway in cancer. METHODS: We studied the coagulation cascade, natural clotting inhibitors, fibrinolytic proteins and resistance to activated protein C in 20 patients with advanced gastrointestinal cancer and 84 volunteers by measuring PT, APTT, fibrinogen, AT III, PC, PS, APC resistance, fibrinolytic system (PLG, ANPL, PAI-1, and t-PA) and activation peptides (D-Dimers, prothrombin 0 fragment 1 + 2/F1 + 2). RESULTS: Laboratory tests confirmed coagulation abnormalities in cancer patients. Fibrinogen, D-Dimers and F1 + 2 were increased, while t-PA activity was significantly lower than that of controls. APC resistance was higher in cancer patients compared to the control group (55% vs 2%; P < 0.0001). Excess thrombin generation was manifested by increased F1 + 2 plasma levels in APC-resistant cancer patients. Genetic analyses showed that only one patient with a poor response to APC carried a factor V R506Q mutation in exon 10. CONCLUSIONS: Our findings show a high prevalence of APC resistance in cancer, compatible with an acquired defect in the APC pathway.

Adult↗
PubMed2003

Decreased protein Z concentrations complicating the hypercoagulable state of Behçet's disease.

Protein Z is a vitamin-K-dependent plasma protein that serves as a cofactor for the inhibition of factor Xa. Although the precise physiologic function of protein Z is still unknown, abnormal plasma protein Z concentrations have been associated with a number of thrombotic disease states. There is the evidence of universal activation of the hemostatic system in Behçet's disease (BD), which represents a hypercoagulable/prothrombotic state. Circulating protein Z levels in patients with BD were evaluated. Plasma protein Z concentrations were assayed in 24 patients with BD (male/female: 13/11, mean age 35.4 years) and in 24 healthy controls (males/females: 14/10, mean age 59.8 years). The disease duration was 10.6 years (range, 1-30 years). None of the subjects in either group had received anticoagulants within 3 weeks before the study, and none of them had liver dysfunction. Patients complicated with vascular disease were also excluded from the study. Mean plasma concentrations of protein Z were 141 ng/mL (range, 56.8-257) in healthy controls and 107.8 ng/mL (range, 21.2-202) in BD patients (p<0.05). There was a positive correlation between the disease duration and protein Z levels in the study group (p<0.05, r=0.448). Alterations of protein Z concentrations could complicate the pathobiology of the prothrombotic state of BD. Furthermore, the tendency of increment in the protein Z with the passage of time may reflect the diminution of the disease activity.

Adolescent↗
PubMed2006

Higher levels of serum fibrin-monomer reflect hypercoagulable state and thrombus formation in the left atrial appendage in patients with acute ischemic stroke.

BACKGROUND: It is sometimes difficult to make a diagnosis of cardioembolic stroke in the stroke care unit, because of the splashing and vanishing of the intracardiac source of the emboli on transesophageal echocardiography. Serum fibrin-monomer (FM) is a new marker for coagulation activity that is useful for identifying older individuals at increased risk of ischemic stroke. METHODS AND RESULTS: Two hundred and four patients with acute ischemic stroke were examined for serum coagulation and fibrinolytic activity on admission, and underwent transesophageal echocardiography within 7 days of onset. Serum levels of FM was significantly higher in patients with left atrial appendage (LAA) thrombus formation (n=24) than in those with no thrombus (88+/-52 vs 14+/-9 microg/ml, p<0.0001). On multivariate logistic regression analysis, FM was an independent predictor for LAA thrombus (RR 2.975, 95% confidence interval 1.114 to 4.820, p=0.0214). In patients with LAA thrombus negative group, cases with LAA emptying flow velocity at atrial systole that was absent or smaller than at early diastole had significantly higher FM levels as compared to cases with larger velocity (42+/-12 vs 8+/-5 microg/ml, p<0.0001). CONCLUSION: Higher levels of serum FM reflect LAA flow pattern alterations and thrombus formation in patients with acute ischemic stroke.

Aged↗
PubMed2003

Blood coagulation in patients with chronic heart failure: evidence for hypercoagulable state and potential for pharmacological intervention.

Incidence data on thromboembolism in patients with heart failure (which may include stroke, peripheral embolism, pulmonary embolism) are limited but provide a general population range from 1-5 cases per 1000 each year, increasing with age to more than 30 cases per 1000 each year among people aged 75 years or older. However, the incidence of thromboembolism varied depending very much on what was being investigated in each of these studies. Data from subgroup analysis of the larger heart failure trials would seem to support this incidence data, although there is very little true epidemiological data and no randomised, controlled trial has been designed to specifically investigate thromboembolism in patients with heart failure. The pathophysiology of heart failure is complex. There are many well recognised factors which are associated with thrombosis in heart failure patients, such as vascular abnormalities, increased coagulability and impaired blood flow. In the past 50 years many studies have been performed to investigate if oral anticoagulation is of benefit for the prevention of thromboembolism in patients with heart failure. The use of warfarin therapy for heart failure patients has been a controversial subject. Warfarin does have a role to play in patients with myocardial infarction and those with atrial fibrillation. Furthermore, in patients with congestive heart failure secondary to coronary artery disease, warfarin reduces the occurrence of nonfatal myocardial infarction and, therefore, may reduce the chances of progression to heart failure. It has also been shown that warfarin reduces the risk of thromboembolic strokes in patients recovering from myocardial infarction. At present, there is a lack of randomised data, and the incidence of bleeding complications in patients with heart failure has caused a decrease in the use of oral anticoagulants for the prevention of thrombosis. This review summarises the incidence, potential mechanism and therapeutic approaches for management of thromboembolism in heart failure.

Anticoagulants↗