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PubMed1993

Evidence of a hypercoagulable state in patients with acute lymphoblastic leukemia treated with low dose of E. coli L-asparaginase: a GIMEMA study.

Blood coagulation abnormalities induced by administration of E. coli L-asparaginase were investigated in 25 patients with acute lymphoblastic leukemia treated according to the GIMEMA ALL 0288 trial. Dosage of L-asparaginase was relatively low (6,000 U/m2/day for 7 days total dose 42,000 U/m2) as compared to the conventional dosages (120,000-140,000 U/m2 over 10-14 days). A significant decrease in fibronogen, plasminogen, alpha2-antiplasmin and antithrombin III was observed from day IV of L-asparaginase and it was maximum on day VIII, with return to the baseline levels on day XV. Protein C levels had only a borderline reduction, while no modification of protein S or factor VII was observed. Two of the patients investigated developed thrombosis. The presence of a prothrombotic state induced even by this low dosage of E. coli L-asparaginase was suggested by a significant increase of sensitive markers of hypercoagulability such as fibrinopeptide A, thrombin-antithrombin complexes, and prothrombin fragment F1 + 2.

Adolescent↗
PubMed1986

Hypercoagulable states and venous thrombosis.

Many factors predispose patients to thromboembolic disease. A young person presenting with idiopathic deep venous thrombosis may never have its etiology elucidated, despite exhaustive testing. On the other hand, hypercoagulability is no mystery in an obese, bedridden, postoperative patient with a malignancy. Invasive or noninvasive testing should be performed in all suspicious cases. Patients with positive results should be treated promptly; those with negative findings should not be subjected to anticoagulation. The length of anticoagulation depends on the length of time the patient remains at risk of thrombosis and may vary from months to a lifetime. Patients over 40 should receive prophylactic minidose heparin for abdominal and thoracic surgery. Patients undergoing hip surgery require some form of anticoagulation--be it heparin, warfarin, aspirin, or dihydroergotamine-heparin. Because of lower morbidity and superior long-term efficacy, transvenous devices are favored over surgical techniques for inferior vena caval interruption.

Blood Coagulation Disorders↗
PubMed2006

Pulmonary hypertension in thalassemia: association with platelet activation and hypercoagulable state.

The pathogenesis of pulmonary hypertension (PAH), a serious complication in thalassemia, is not well understood. Thromboembolism has been postulated as one of the causative factors; however, there are currently limited specific data on its role. To examine whether increased platelet activation and hypercoagulability are linked to PAH, 25 beta-thalassemia major and beta-thalassemia intermedia patients were evaluated with Doppler echocardiograms for estimation of pulmonary artery pressure and with laboratory assays for indications of a prothrombotic state. The association of clinical variables and abnormal coagulation assays with PAH was determined. PAH was identified in 17 (68%) patients; mean pulmonary artery systolic pressure was 39.8 +/- 5.4 mm Hg. PAH was significantly associated with prior splenectomy, older age, and evidence for chronic hemolysis, diagnosed in both transfused (n = 10) and nontransfused (n = 7) patients. Increased platelet activation, measured by P-selectin, was significantly associated with PAH (P = 0.001). Increased thrombin-antithrombin III level was more prevalent in the presence of PAH, but increased fibrinolysis or low protein C levels were not. This study underscores the role of platelet activation in the development of PAH and stresses its occurrence even among patients who are regularly transfused, especially those who are older and have had splenectomies.

Adolescent↗
PubMed1997

The hypercoagulable state. Who, how, and when to test and treat.

Patients with a family history of thrombosis, early-onset or recurring thrombosis, thrombosis at unusual sites, or warfarin-induced skin necrosis should be investigated for a possible underlying inherited hypercoagulable disorder. These include AT-III deficiency, protein C and S deficiencies, and APC resistance. Many patients should also be evaluated for the antiphospholipid syndrome, an acquired disorder. Functional assays are more useful than immunologic assays for diagnosing AT-III deficiency, protein C and S deficiencies, and APC resistance. A molecular probe is now available for the abnormal factor V most often responsible for APC resistance. Testing for the antiphospholipid syndrome involves assays for the lupus anticoagulant and anticardiolipin antibodies. AT-III and protein C concentrates are now available for short-term therapy. Long-term prophylactic administration of warfarin may have to be considered for some symptomatic patients with proven abnormalities, especially after more than one thrombotic event. While the management of asymptomatic persons remains controversial, the use of prophylactic anticoagulation should be anticipated for trauma, surgery, pregnancy, or other high-risk situations.

Anticoagulants↗
PubMed2002

Association of hypercoagulable states and increased platelet adhesion and aggregation with bacterial colonization of intravenous catheters.

Bacterial adherence to intravenous catheters may be mediated, in part, by adherence to coagulation proteins and platelets. The possibility that catheter infection is associated with gene polymorphisms that cause hypercoagulability or increased platelet stickiness was examined. Among patients with infected catheters, there was no increase in the frequency of polymorphisms that increase coagulability, including factor V Leiden R506G, factor II (prothrombin) G20210A, and methylenetetrahydrofolate reductase C677T, compared with control subjects. The incidence of polymorphisms of the platelet beta(3) integrin among patients with infected catheters was also similar to that among control subjects. The C/D heterozygote of the variable number tandem repeat polymorphism and the C/T heterozygote of the KO polymorphism of glycoprotein Ibalpha were more frequent among patients with infected catheters than they were among control subjects. In a small proportion of patients, a genetic predisposition to platelet stickiness may be associated with infection of intravenous catheters, but in the majority, a recognized genetic tendency to hypercoagulability or platelet stickiness does not underlie infection.

Antigens, Human Platelet↗
PubMed1999

[Persistence of hypercoagulability state after hip and knee arthroplasty: what is the optimal duration of antithrombotic guidelines in this surgery?].

Among 79 patients candidates to hip (53) and knee (26) replacement an evaluation was made of the influence of a two-week program with LMWH on the evolution of hypercoagulability markers: D-D, TAT, and F1 + 2. Measurements were performed by ELISA preoperatively and on days 1, 7 and about 45 postoperatively; in the latter, two extraction intervals were considered: < or = 45 days and > 45 days. With both surgical modalities, D-D and F1 + 2 peaked at 7th day postoperatively, whereas TAT peaked on day 1. Among D-D and F1 + 2 values quantitated on day 7th and the extraction interval < or = 45 days, no significant differences were obtained (Z < 2.64). The hypercoagulative chronicity exhibited by D-D and F1 + 2 during the first month and a half after this surgery, might require in some cases a more prolonged thromboprophylaxis.

Aged↗
PubMed1993

A chronic hypercoagulable state and life-long platelet activation in beta thalassemia major.

Increased frequency of thromboembolic events has been recently observed in patients with thalassemia major (TM), causing hypoxemia and cor pulmonale. Autopsy findings demonstrated "old" and recent pulmonary and renal infarcts as well as premature atherosclerosis. Studies to determine hypercoagulability showed: impaired platelet aggregation, increased circulating platelet aggregates, shortened platelet survival, enhanced excretion of urinary metabolites of thromboxane A2 (TXA2) and prostacyclin and decreased plasma levels of Protein C, Protein S or anti-thrombin III. Erythrocytes from TM patients enhanced thrombin formation in a "prothrombinase" assay (using a chromogenic substrate). Chronic anti-thrombotic therapy may be indicated in thalassemic patients to prevent the cardiac and pulmonary complications.

Blood Platelet Disorders↗
PubMed1999

Lipid-lowering therapy corrects endothelial cell dysfunction in a short time but does not affect hypercoagulable state even after long-term use in hyperlipidemic patients.

Lipid-lowering therapy reduces cardiac events to an extent that is disproportionate to the small degree of regression of coronary atherosclerosis observed among hyperlipidemic patients. We prospectively investigated the effects of lipid reduction using simvastatin on the endothelial dysfunction and hypercoagulability found in hyperlipidemic patients. We measured levels of coagulation factors [factor VII (FVII) coagulant activity (FVIIc), FVII antigen (FVIIAg), activated FVII (FVIIa), and fibrinogen], and markers of coagulation activation [prothrombin fragment 1 + 2 (F1 + 2)] and endothelial cell dysfunction [von Willebrand factor (vWF)] in 20 hyperlipidemic patients, 20 hypertensive patients, and 20 normotensive normolipidemic controls. The levels of FVIIa, FVIIc, FVIIAg, F1 + 2, and vWF were all higher in hyperlipidemic patients, but only FVIIa, F1 + 2, and vWF levels were higher in hypertensive patients than in controls. We measured the above parameters in 13 hyperlipidemic patients before and after 1, 3, 6, 12 and 24 months of simvastatin therapy and compared these values with those in 15 hypertensive patients at baseline and after 12 and 24 months. The median (25th-75th percentile) level of total cholesterol was decreased from 259 (255-278) to 206 (176-220) mg/dl after 1 month of simvastatin therapy and this reduction persisted for 2 years. The plasma level of vWF [136% (113-158%)] was not changed after 1 month of administration of simvastatin [132% (115-153%)], but was decreased after 3 months of treatment [114% (96-128%), P<0.01]. This decrease also persisted for 2 years during simvastatin therapy and both of these reductions were significant, compared with levels in hypertensive patients. In contrast, levels of fibrinogen, FVIIc, FVIIAg, FVIIa, and F1 + 2 did not change throughout the 2 years of simvastatin therapy. We conclude that lipid reduction using simvastatin corrects endothelial cell dysfunction but not hypercoagulability in hyperlipidemic patients. The improvement in endothelial cell function brought about by lipid-lowering therapy might contribute to the reduction in cardiac events within a relatively short time period in hyperlipidemic patients.

Blood Coagulation↗
PubMed1999

Hypercoagulability state in hip and knee surgery: influence of ABO antigenic system and allogenic transfusion.

It is well know that people with blood group O have a lower risk for venous thromboembolic disease (VTED) than does the general population. Moreover blood transfusion has been identified as a risk factor for VTED in patients with major trauma. The aim of this work is to investigate the behaviour of several markers of hypercoagulability before and after substitutive surgery of hip and knee in order to evaluate the relationship between the plasmatic levels of these markers, the ABO antigenic system and the allogenic blood transfusion. The plasmatic levels of D dimer (D-D), thrombin-antithrombin complex (TAT), and fragment 1 + 2 of prothrombin (F1 + 2) have been determined by the ELISA method in 79 patients subject to substitutive surgery of hip or knee one day before and one day after surgery. The 41 patients with blood groups different from O had presurgical levels of F1 + 2 higher than those of group O (p = 0.004), while no differences could be found for D-D and TAT. The 28 patients who received allogenic blood presented higher levels of D-D one day after surgery than non-transfused patients (p = 0.043); the practice of transfusion did not modify significantly the levels of TAT and F1 + 2 after surgery. In accordance with these results we suggest that blood group and transfusion are risk factors for hypercoagulability, and therefore we advise for a restrictive policy of transfusion practice. New therapies such as aprotinin should be assayed in order to minimize blood loss.

ABO Blood-Group System↗
PubMed1986

Hypercoagulable state induced by cytostatic drugs in stage II breast cancer patients.

An increased incidence of thromboembolic complications occurring in cancer patients during chemotherapy was recently reported. In view of this report, a study in 49 patients receiving adjuvant chemotherapy for Stage II breast cancer was begun in order to determine the effect of antineoplastic drugs on coagulation factors and platelet function. Among the coagulation factors, a significant decrease of thrombin time and partial prothrombin time was observed, whereas platelet function tests were unchanged. This finding suggests a trend towards hypercoagulability induced by chemotherapy. This effect should be considered when chemotherapy is employed in advanced cancer patients at high risk for thrombosis.

Adult↗
PubMed2002

Induction of a hypercoagulability state and endothelial cell activation by granulocyte colony-stimulating factor in peripheral blood stem cell donors.

In June, 1997, we initiated a prospective study to analyze the effect of granulocyte colony-stimulating factor (G-CSF) on coagulation system in peripheral blood stem cells (PBSC) donors following G-CSF administration. Since, 25 consecutively healthy donors received G-CSF (filgrastim) to mobilize and collect PBSC and 20 donors were finally included in the study. Blood samples were collected immediately before starting G-CSF and prior to PBSC collection to analyze the following parameters: prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, hypercoagulability markers (D-dimer, TAT complex, F1 + 2), natural anticoagulants (antithrombin, protein C, protein S), endothelial activation markers [von Willebrand factor antigen (vWF:Ag) and angiotensin converting enzyme (ACE)], and resistance to activated protein C. We found a significant increase in F1 + 2 and D-dimer while a significant decrease of antithrombin and protein C activity was evidenced. Regarding endothelial cell activation markers, a significant increase of vWF:Ag with a slightly significant decrease of ACE were also observed. Therefore, in PBSC donors receiving G-CSF our results reveal activation of both coagulation and endothelial cells that could favor the developing of thrombotic events. In consequence, a careful monitoring should be considered in those cases with risk factors for thrombosis.

Adolescent↗
PubMed1995

Hypercoagulable state indicates an additional risk factor for atherosclerosis in Werner's syndrome.

To assess the risk factors for atherosclerosis in Werner's syndrome (WS), coagulation/fibrinolytic system parameters and lipid levels were investigated in 9 non-smoker patients with WS and compared with normal control values (N). The levels of thrombin antithrombin III complex (p < 0.05), D-dimer (p < 0.05), tissue plasminogen activator (p < 0.005) and PA inhibitor 1 (p < 0.01) were significantly increased, while the level of thrombomodulin (p < 0.005) in the fasting plasma was significantly decreased in the WS cases compared with N. Lipid profiles confirmed that 8 of the 9 patients were of hyperlipidemia type IIb, 7 had hyperinsulinemia and 5 fulfilled the criteria for clinical diabetes mellitus. The hypercoagulable condition suggested the existence of multiple risk factors for atherosclerosis in WS in addition to the previously reported hyperinsulinemia and hyperlipidemia.

Adult↗
PubMed2002

Hypercoagulable state leading to paraplegia in a middle-aged man.

A 37-year-old man presented with an unusual thrombotic disorder characterized by acute paraplegia and the absence of palpable pulses due to extensive arterial thrombosis of the aorta and its distal branches. The patient had an extremely complicated course that necessitated multiple revascularization procedures over a 1.5-year period. This case is unusual not only because of its complexity but also because of the patient's relatively young age, his lack of risk factors for vascular disease, and the presence of a neurologic deficit that improved when circulation was restored. More unusual, however, is the fact that all diagnoses were excluded except for a high lipoprotein(a) level. To our knowledge, this is the 1st reported case in which aortic thrombosis has been related to hypercoagulability.

Acute Disease↗
PubMed2003

Measurement of tissue factor messenger RNA levels in leukocytes from patients in hypercoagulable state caused by several underlying diseases.

In a preliminary study, we have demonstrated that tissue factor (TF) is immunohistochemically stained in monocytes from patients with disseminated intravascular coagulation (DIC) but not from healthy volunteers, and that leukocytes from DIC patients induce enhanced activated factor X (FXa) generation in the presence of a mixture of FVIIa, FX and Ca(2+). Then, TF mRNA levels in leukocytes were measured to evaluate the role of TF in the pathophysiology of various diseases. TF mRNA levels in leukocytes were low in healthy volunteers but they were significantly increased in various diseases, especially in patients with infectious diseases, solid cancer, and hematopoietic tumors. TF mRNA levels in leukocytes were significantly higher in patients with high levels of C reactive protein (CRP) than in those with low CRP. TF mRNA levels were significantly higher in patients with DIC than in those without DIC. TF mRNA levels were well correlated with TF antigens in plasma and leukocytes. These findings suggest that the expression of TF mRNA in leukocytes is increased in various diseases and that this may play an important role in hypercoagulability or DIC.

Adult↗
PubMedDate not supplied

Evaluation of the hypercoagulable state by measuring protein C and antithrombin III levels in nephrotic syndrome and in familial Mediterranean fever-related amyloidosis.

The levels of protein C (PC) and antithrombin III (AT III) antigens (ag) were measured in the plasma of 39 patients with various histologic types of primary nephrotic syndrome (NS) and in 12 patients with amyloidosis secondary to familial Mediterranean fever (FMF). The controls comprised 15 healthy children. Normal or elevated PC levels were observed in primary NS patients (mean 64%, range 36-98%) and in amyloidosis patients (mean 58%, range 48-70%). There was no difference found between PC ag levels in primary NS and in amyloidosis patients. In addition, no correlation existed between protein selectivity and the PC ag levels in the primary NS patients. Normal and decreased levels of AT III were observed (mean 29 mg/dl, range 11.1-39 mg/dl) in the patients with primary NS and amyloidosis (mean 31 mg/dl range, 21-39 mg/dl). The AT III ag levels of these two groups did not differ and no correlation was found between protein selectivity and AT III levels in primary NS patients. These results suggest that in patients with primary NS, or amyloidosis secondary to FMF, hypercoagulability is not related to a deficiency in PC ag levels due to a dynamic balance between urinary losses, increased rate of hepatic synthesis, catabolism and the distribution of PC in the body compartments. Patients with low AT III levels may be more susceptible to thromboembolic complications than patients with normal levels.

Adolescent↗
PubMed1996

Postoperative hypercoagulable state followed by hyperfibrinolysis related to wound healing after hepatic resection.

BACKGROUND: Coagulative disorders may result from a breakdown in the balance between coagulation and fibrinolysis. It is important to assess the relative physiologic states of coagulation and fibrinolysis related to operation. STUDY DESIGN: A prospective study of 16 patients who underwent hepatic resection was performed. Coagulative and fibrinolytic activities were examined for comparison with those of patients having total thoracoesophagectomy or colorectal resection. In addition, mice underwent hepatic resection, and histologic analysis was conducted to detect local fibrinolysis. RESULTS: In patients who underwent hepatic resection, circulating levels of thrombin-antithrombin III complex were significantly elevated during operation, whereas the levels of plasmin-alpha 2-plasmin inhibitor complex, fibrin-fibrinogen degradation products, and D-dimer were slightly elevated. After operation, the values of thrombin-antithrombin III complex decreased but plasmin-alpha 2-plasmin inhibitor complex peaked on the third postoperative day and both fibrin-fibrinogen degradation products and D-dimer increased again to reach maximum levels on postoperative day 7. Immediately after operation, the ratio of thrombin-antithrombin III complex to plasmin-alpha 2-plasmin inhibitor complex was significantly greater and the ratio of tissue-type plasminogen activator to plasminogen activator inhibitor-1 was significantly lower in patients who underwent hepatic resection than comparable ratios in patients who underwent colorectal resection. In the murine model, fibrin-like products with immunostaining of plasminogen activator inhibitor-1 were broadly deposited at the edge of the residual liver on postoperative day 5, then disappeared by postoperative day 14. CONCLUSIONS: These findings indicate that immediately after operation the stress of hepatic resection led to extensive hypercoagulation and hypofibrinolytic activity, as compared with colorectal resection, and suggest that fibrinolysis without hypercoagulation in the late postoperative period might be caused by local fibrinolysis in the healing wound.

Aged↗
PubMed1984

Use of antiplatelet agents in pediatric hypercoagulable states.

Many diseases in children are associated with thrombotic tendencies either as a complication or as part of the pathophysiologic process. Disorders in which platelet consumption and/or activation occur include myeloproliferative syndromes, sickle cell disease, cardiac prostheses, arteriovenous shunts, vasculitis, diabetes mellitus, and hemolytic-uremic syndrome and other renal diseases. Platelet involvement can be demonstrated by several indicators, including an increase in platelet release product levels in the plasma (beta-thromboglobulin, platelet factor 4, and thromboxane B2). The agents that have the greatest success in thrombotic disorders where platelet involvement is prominent include the prostaglandin pathway cyclo-oxygenase inhibitors aspirin and sulfinpyrazone, as well as dipyridamole. Although indications and dosages for the use of antiplatelet agents in children can be suggested, the treatment of each patient should be individualized in light of current knowledge.

Adolescent↗
PubMed2000

Plasma levels of activated protein C-protein C inhibitor complex in patients with hypercoagulable states.

Plasma levels of activated protein C (APC)-protein C inhibitor (PCI) were significantly increased in patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), acute myocardial infarction (AMI), pulmonary embolism (PE), or deep vein thrombosis (DVT) and in patients undergoing hemodialysis (HD). Plasma levels of APC-alpha(1)-antitrypsin (AT) complex were significantly increased in patients with DIC and in those with TTP. Plasma levels of PCI were significantly decreased in patients with DIC, non-DIC, or TTP and in those undergoing HD. In the pre-DIC stage, the plasma levels of APC-PCI complex were significantly increased but not those of APC-alpha(1)-AT complex. These data suggest that measurements of APC-PCI complex and APC-alpha(1)-AT complex may be useful for the diagnosis of DIC. After treatment of DIC, the plasma levels of APC-PCI complex and APC-alpha(1)-AT complex were significantly decreased, but not those of PCI. Plasma levels of thrombin-antithrombin complex (TAT), plasmin-alpha(2)-plasmin complex (PPIC), D-dimer, and soluble fibrin monomer (SFM) were markedly increased in patients with DIC or pre-DIC and were moderately increased in patients with non-DIC, TTP, AMI, PE, or DVT and in those undergoing HD. The receiving operating characteristic (ROC) analysis showed that SFM and the APC-PCT complex are useful markers for diagnosis of DIC. The specificity of plasma TAT and PPIC levels was low. The positive rate of APC-PCI complex was higher than 90% with DIC, TTP, AMI, PE, and it was higher than 60% with DVT and HD. Since the APC-PCI complex was elevated not only in patients with venous thrombosis but also in those with arterial thrombosis, components of the protein C pathway might be useful markers for the diagnosis of arterial thrombosis.

Antithrombin III↗