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PubMed2001

Natural coagulation inhibitors (protein C, protein S, antithrombin) in patients with sickle cell anemia in a steady state.

BACKGROUND: Patients with sickle cell anemia (SCA) run the risk of having decreased levels of natural coagulation inhibitors. This may be due to either hemostatic abnormalities or hepatic dysfunction. This study is designed to evaluate coagulation profiles of patients with SCA in a steady state and to determine whether hypercoagulable state is present or not. METHODS: Seventeen children with SCA in a steady state were included in this study. The routine hematological evaluation was done with a coulter-counter. Reticulocyte percentage and blood coagulation tests were also determined. The coagulation inhibitors such as protein C (as activated partial thromboplastine time prolongation time), protein S (as Factor V inhibition) and antithrombin (colorimetric assay) were measured in all cases. RESULTS: In the coagulation profile, mean euglobuline lysis time and mean fibrin degradation product levels were both significantly higher in the patient group than in the control group (P<0.05), although other parameters were within normal limits. The values for aspartate aminotransferase (AST), alanine aminotransferase (ALT) and indirect reacting bilirubin were significantly higher in the patient group than in the control group (P<0.001, P<0.005, P<0.0001, respectively). The serum protein levels were normal. Mean factor V level was significantly lower and mean factor VIII level was found significantly higher in the patient group than in the control group (P<0.05 and P<0.005, respectively). Protein C and AT levels were lower in patients with SCA than in control subjects (P<0.001). Protein S levels were also lower in the patient group than in the control group, but the difference between the two groups was not significant (P>0.05). CONCLUSION: It is indicated that antithrombotic functions of patients with SCA are handicapped even in a steady state; and both hemostatic abnormalities and hepatic dysfunction contribute to low levels of natural coagulation inhibitors.

Adolescent↗
PubMed2003

Role of coagulation and fibrinolytic system in prostate cancer.

Patients with prostate carcinoma paradoxically have both a hypercoagulable state and a bleeding diathesis. Hypercoagulability manifested by venous and arterial thrombosis has been documented in several large clinical trials. However, many investigators have reported a high risk of postoperative bleeding in prostate cancer patients. Disseminated intravascular coagulopathy has also been commonly noted at different clinical stages of this indolent cancer. In this article we review clinical, laboratory, and experimental evidence for abnormalities of various components of the coagulation and plasminogen pathways and analyze their contribution in prostate cancer growth, progression, and angiogenesis. Finally, we propose potential therapeutic antiangiogenic strategies in patients with prostate cancer.

Blood Coagulation↗
PubMed2000

Thromboelastography identifies sex-related differences in coagulation.

UNLABELLED: Thromboelastography is an in vitro, point-of-care monitor of whole blood coagulation. Thromboelastography studies have demonstrated a hypercoagulable state during pregnancy. Perhaps the hypercoagulability is attributable to female sex hormones. The aim of the study was to determine if sex, in addition to pregnancy, affected thromboelastography variables by studying male and female (pregnant and nonpregnant) volunteers. Thromboelastography showed significant (P:<0.01) differences in sex, with a significant (P: < 0. 0001) trend of increasing whole blood coagulability from men through nonpregnant to pregnant women. The thromboelastograph, used as a diagnostic tool, shows that women have more whole blood coagulability than men. IMPLICATIONS: The thromboelastograph, used as a diagnostic tool, shows that women have more whole blood coagulability than men.

Adult↗
PubMed1999

Thrombotic risk factors associated with transurethral prostatectomy.

OBJECTIVE: To ascertain the potential thrombotic risk associated with transurethral prostatectomy (TURP). PATIENTS AND METHODS: The changes in coagulation variables were assessed in a prospective study of 40 patients undergoing TURP. RESULTS: There was a significant increase in thrombin-antithrombin complexes 6 h after TURP (anova, P=0.01) combined with a significant decrease in activated partial thromboplastin time (anova, P=0.006), suggesting a postoperative hypercoagulable state. The significant increase in d-dimer 24 h after TURP (anova, P=0.015) in the absence of any significant rise in tissue plasminogen activator antigen levels perioperatively (anova, P=0.737) suggests a physiological fibrinolytic response to the developing procoagulant state. The absence of any significant increase in plasminogen activator inhibitor-1 antigen perioperatively (anova, P=0.348) suggests the observed hypercoagulability is not due to a 'fibrinolytic shutdown' reported in other forms of surgery. CONCLUSION: TURP is associated with a hypercoagulable prothrombotic state; aspirin withdrawal perioperatively may be hazardous, and low-dose heparin prophylaxis for venous thrombosis should be considered.

Anticoagulants↗
PubMed2001

Recurrent thromboembolic disease following splenectomy for pyruvate kinase deficiency.

We report a case of recurrent thromboembolic disease and chronic pulmonary hypertension in an adult patient with pyruvate kinase deficiency who underwent splenectomy as a child. Thromboembolism has been reported as a complication following splenectomy for various hereditary chronic hemolytic anemias. To our knowledge, this association has not been described in patients specifically with pyruvate kinase deficiency. Our patient presented at age 37 with recurrent pulmonary emboli, 36 years after splenectomy for severe hemolytic anemia. Work-up for other hypercoagulable states was negative. The mechanism for hypercoagulability in this condition is unclear but may involve a quantitative or qualitative change in disrupted thrombogenic red blood cell membranes that would normally be removed by the spleen. Clinicians should have a high index of suspicion for thrombotic events in these patients, as early diagnosis and treatment can reduce morbidity and mortality, and chronic anticoagulation may help prevent the sequelae of repeated thromboembolic events.

Adult↗
PubMed1997

Thromboelastographic changes in healthy parturients and postpartum women.

Thromboelastography (TEG) using disposable plastic cups and pins was performed with native whole blood (native group) in 17 nonpregnant volunteers, 134 healthy term pregnant women (>36 wk gestation), and 69 postpartum women. Thromboelastography was also performed with celite-activated whole blood (celite group) in 15 nonpregnant female volunteers, 38 healthy term pregnant women, and 34 postpartum women. The thromboelastographic parameters r and K were significantly decreased in pregnant and postpartum women compared with nonpregnant women in both groups (P < 0.05). The maximum amplitude MA, elastic shear modulus, and alpha angles were significantly increased in pregnant and postpartum women compared with nonpregnant women in both groups (P < 0.05). The TEG coagulation index was significantly greater in pregnant and postpartum women compared with nonpregnant women in both groups. In this study, TEG showed that pregnancy is a hypercoagulable state and that postpartum women remain hypercoagulable through the first 24 h postdelivery. The use of celite in TEG accelerated the speed of TEG analysis.

Blood Coagulation↗
PubMed2004

[Budd-Chiari syndrome: updated treatment modalities].

Budd-Chiari Syndrome (BCS) refers to hepatic venous outflow obstruction, resulting in simultaneous occurrence of hepatic congestion and portal hypertension, leading to a typical clinical triad consisting of right upper quadrant pain, hepatomegaly and ascites. Contrary to Asia and Africa, where BCS is caused primarily by an obstructing membranous web, BCS in the western world is considered a thrombotic complication of an underlying hypercoagulable state. Recognition of the contribution of hypercoagulability as a causative factor in BCS, has led to acknowledgement of the importance of anti-coagulant therapy in BCS. Indeed, a conservative approach consisting of diuretics and anti-coagulant therapy is considered an appropriate treatment strategy for the BCS patient, in the absence of significant hepatic insult. However, once disease progression is noted, based on clinical symptoms, hepatic laboratory disturbance or histological evidence of irreversible hepatic damage, a definite invasive treatment should be applied. The specific procedure to be used is dependent upon the extent of hepatic insult and the anatomical characteristics of the venous obstruction in any individual patient. In the absence of significant hepatic damage, one may employ surgical shunting or invasive roentgenic measures, such as TransJugular Intrahepatic Porto-Systemic Shunt procedure, for the decompression of the portal system. Alternatively, in cases of a single localized obstruction, one may use balloon angioplasty with stent insertion. In contrast, upon evidence of significant hepatic damage, liver transplantation becomes necessary. To date, numerous studies report excellent results regarding the success of liver transplantation for patients with advanced BCS disease accompanied by significant hepatic damage.

Anticoagulants↗
PubMed1995

Hemostatic abnormalities and increased vascular endothelial cell markers in patients with red cell fragmentation syndrome induced by mitomycin C.

We examined red cell fragmentation syndrome (RCFS) induced by mitomycin C (MMC) (13 patients), by thrombotic thrombocytopenic purpura (TTP) (17 patients), and by disseminated intravascular coagulation (DIC) (15 patients). Plasma cytokine levels were increased in the TTP and DIC patients, but not in those whose RCFS was induced by MMC, suggesting that the activation of the immune system plays an important role in the pathogenesis of RCFS due to TTP and DIC but did not in RCFS due to MMC. Plasma thrombomodulin, tissue type plasminogen activator, and plasminogen activator inhibitor-I levels were increased in all RCFS patients, suggesting that RCFS, whether MMC induced, or due to TTP or DIC, might be associated with vascular endothelial cell injury. In TTP, von Willebrand factor (vWF) antigen and high molecular weight vWF multimer levels were reduced, possibly as a result of microthrombus consumption. The hemostatic data in this study showed that the TTP patients were in a hypercoagulable state without hyperfibrinolysis, and that DIC patients were in both a hypercoagulable and a hyperfibrinolytic state, whereas hemostatic abnormalities were slight in patients with MMC induced RCFS. These findings suggest that vascular endothelial cell injuries might be associated with RCFS, and that those injuries in MMC-induced RCFS might not be related to microthrombi or an activated immune system.

Adolescent↗
PubMed1997

[The appropriate use of clinical biological tests in hypercoagulability].

Biological markers who are associated with hypercoagulability are of two types: Markers of activation: among them, the most interesting are the D-dimers which are good tools of diagnostic for the deep venous thrombosis and the pulmonary embolism. Thanks to their high negative predictive value. Etiological factors of hypercoagulable states and thrombosis, in other words: the "hypercoagulability chek up". This one should never be systematic. We propose either to practice it one month after the end of the anticoagulant therapy or to make it with prophylactic doses of low molecular weight heparin and far from the thrombotic episode.

Biomarkers↗
PubMedDate not supplied

[Evaluation of hemostasis in venous thromboembolism pathology].

Thromboembolic disease results from an hypercoagulable state and multifactorial causes may lead to hypercoagulability. Thrombogenic risk factors can be acquired and/or inherited. For each thrombophilic patient, the main clinical features retained are: the patient age, the familial history, the recurrence of thromboembolic events, an unusual site of thrombosis. Anti-phospholipid antibodies, which are considered as acquired thrombogenic risk factors, can be detected with coagulation tests and/or Elisa methods. The association of antiphospholipid antibodies with thrombosis is defined as the anti-phospholipid syndrome. Last decades, genetic risk factors were identified. First of all, antithrombin, protein C and protein S deficiencies were described. These deficiencies are involved in about 10% of patients who develop thrombosis before the age of 50. In 1993, a new genetic risk factor was discovered: activated protein C resistance which is due to the Q506 mutation in factor V. This defect represents the most prevalent abnormality of inherited thrombophilia, affecting 20 to 40% of thrombophilic patients. Interestingly, hyperhomocysteinemia, known as potentially predisposing to arterial disease, was also recognized as a risk factor for venous occlusive disease. Several genes encoding homocystein metabolism enzymes, such as cystathionine beta-synthase or methylenetetrahydrofolate reductase are concerned. Establishment of a causal association between the presence of a biological abnormality and the occurrence of thrombosis may lead to an adapted prophylaxis whatever the risk situation.

Antiphospholipid Syndrome↗
PubMed2002

Hyperhomocysteinaemia, coagulation pathway activation and thrombophilia in patients with inflammatory bowel disease.

BACKGROUND: The 5,10-methylenetetrahydrofolate reductase (MTHFR) 677C-->T polymorphism encoding the thermolabile variant is, when present as homozygote type (TT variant), a known genetic cause of mild hyperhomocysteinaemia (HHCY). This polymorphism has been observed in increased numbers in patients with inflammatory bowel disease (IBD). Coagulation and fibrinolysis are activated in patients with active IBD, but it is not known whether raised plasma homocysteine (HCY) found in patients with IBD significantly contributes to this activation. The aim of this study was to investigate if HHCY or presence of the TT variant significantly induces a hypercoagulable state in IBD patients receiving anti-inflammatory therapy during active disease, and to study if genetic determinants for thromboembolic disease are more frequent in these patients. METHODS: The study was designed as a cross-sectional study in an outpatient clinic comprising 106 IBD patients receiving anti-inflammatory therapy. Markers of coagulation were measured in order to elucidate whether patients with HHCY or the MTHFR TT variant were hypercoagulant compared with patients with no impairment of HCY metabolism. In addition, markers of inflammation and acute-phase reactants were measured in order to compare activity during active disease and during remission. Genetic determinants of thromboembolic disease in patients with IBD and in relevant controls were investigated in the expectation of a more frequent occurrence of these markers of thrombophilia if hypercoagulability could be a primary or contributory factor in IBD. RESULTS: No significant difference could be found in coagulation activity, acute-phase reactants or inflammatory markers in IBD patients with the TT variant of the 677C-->4T polymorphism or high (>15 micromol/L) plasma HCY levels, compared with IBD patients with no impairment of HCY metabolism. In patients with IBD, the coagulation activity was significantly increased during active disease compared with a state of remission. As expected, a significant difference regarding interleukin 6, C-reactive protein and erythrocyte sedimentation rate was present in IBD, comparing active disease with a state of remission. No significant complement activation was present in either of the groups or during active disease. Neither of the allele frequencies of genetic determinants for thrombophilia (coagulation factor V 1691G-->A (factor V Leiden) and factor II 20210G-->A polymorphisms) in the background population differed significantly from that in IBD patients. CONCLUSIONS: This study found no correlation between the MTHFR TT variant or HHCY and a hypercoagulable state in IBD patients receiving anti-inflammatory treatment. This coagulation activity is high during exacerbations of disease, but a considerable reduction is seen in patients on anti-inflammatory therapy compared with non-treated patients. Coagulation activation in IBD is probably a consequence of the inflammatory nature of the disease. That thrombophilia could be a contributory or primary factor in the development of IBD is not supported by the present study, as the frequencies for the genetic determinants for thrombophilia are similar in IBD patients and controls.

Adolescent↗
PubMed2026

A Novel Complete F8 Tandem Duplication Causing Elevated Factor VIII Activity and Associated with Venous Thromboembolism.

Background Coagulation factor VIII (FVIII) is a critical component of the intrinsic coagulation pathway. While elevated FVIII levels are an established risk factor for venous thromboembolism (VTE), genetic variants in the F8 gene directly causing such elevations remain scarce. Here, we report a novel complete F8 tandem duplication identified in a female patient with splanchnic venous thrombosis (SVT). Methods We performed genetic testing using a thrombophilia panel targeting 35 genes involved in thrombosis and haemostasis to detect both point variants and copy number variations (CNVs). Family co-segregation analysis and phenotypic assays for FVIII and von Willebrand factor (VWF) were conducted. The structural basis of the identified F8 copy number gain was elucidated using optical genome mapping (OGM). Full-length F8 mRNA amplification, quantitative PCR, plasma FVIII Western blotting, and X-chromosome inactivation analysis were performed to assess the functional consequences of the duplication. Thrombin generation test (TGT) was employed to assess the hypercoagulable state. Results Genetic testing identified three copies of all 26 exons of the F8 gene in the proband, which was also detected in her mother (CNVs = 3) and son (CNVs = 2). One-stage clotting and chromogenic assays confirmed persistently elevated FVIII activity in the proband and her mother, accompanied by increased FVIII antigen levels. The OGM analysis confirmed a 229 kb tandem duplication including the F8 gene on one of the proband's X chromosomes. The junction regions exhibited high sequence homology and were rich in repetitive sequences, which precluded precise breakpoint mapping. Full-length F8 mRNA amplification revealed no aberrant transcripts, whereas quantitative PCR showed increased F8 mRNA expression in all carriers. Plasma FVIII Western blotting indicated FVIII heavy and light chains of expected molecular weights with increased band intensity in carriers. X-chromosome inactivation analysis in female carriers showed no significant skewing. TGT in two available carriers showed increased thrombin generation compared with a normal control at both low (1 pM) and high (5 pM) tissue factor concentrations. Conclusion We identified a novel complete F8 tandem duplication associated with increased FVIII expression and a hypercoagulable phenotype in a female patient with SVT. These findings support F8 gene dosage gain as a rare gain-of-function mechanism contributing to elevated FVIII levels and thrombophilia, while variation in VWF levels and acquired risk factors may modify thrombotic penetrance.

coagulation factor VIII↗
PubMed2005

Role of lipopolysaccharide and cecal ligation and puncture on blood coagulation and inflammation in sensitive and resistant mice models.

The hemostatic system is severely disturbed during endotoxemia, leading to a hypercoagulable state. However, it remains uncertain to what extent hypercoagulability is the critical factor in determining the clinical course rather than just the consequence of a severe systemic inflammatory response. To answer this question, we evaluated the evolution of hemostatic and inflammatory markers, as well as histological features, in mice sensitive and resistant to two models of endotoxemia: lipopolysaccharide-injection and cecal ligation puncture. Genetic (knockout mice) and pharmacological (PJ34) blockade of the nuclear enzyme PARP-1 was used to achieve resistance to the endotoxemia. In both models, endotoxemia resulted in antithrombin deficiency, decreased platelets, and fibrin deposition in organs, which were similar in all groups of mice. By contrast, proinflammatory mediators, inflammatory cell infiltration (especially that mediated by mononuclear cells), and organ degeneration were more intense in sensitive animals. Further studies supported a negative role for the triggering of the coagulation cascade in the mortality associated with the endotoxic shock. Hirudin had a minor effect on cell infiltration and organ damage, despite causing a potent inhibition of fibrin deposition. On the other hand, a sublethal dose of lipopolysaccharide yielded significant fibrin deposition but weak activation of the inflammatory response. Our results suggest that activation of coagulation by endotoxemia is severe and independent of the inflammatory response. However, such activation may act with fibrin deposition to have a minor influence on survival in sepsis.

Animals↗
PubMed1999

[Pulmonary thromboembolism in a female with resistance to activated protein C].

Primary or acquired hypercoagulable states favour thrombotic events. The identification of prothrombotic states is of immediate practical usefulness in the orientation, prophylaxis and treatment of pulmonary embolism. Detection of individuals resistant to activated protein C. the most frequent laboratory anomaly in the study of patients with venous thromboembolism, offers a better approach for these patients as well as a better prophylaxis and orientation of their direct relatives concerning thromboembolic events. The authors describe the clinical case of a young woman, previously healthy, who developed serious pulmonary thromboembolism, the resolution of which was difficult and the evolution unusual. Later, a state of resistance to activated protein C (aPCr) was identified. Concerning the case described, the authors reflect on hypercoagulable situations, especially "aPCr" states.

Activated Protein C Resistance↗
PubMed1995

Reduced fibrinolytic potential one year after kidney transplantation. Relationship to long-term steroid treatment.

Thromboembolic complications constitute an important risk in renal transplant patients, in whom a hypercoagulable state is associated with immunosuppressive treatment, and the presence of hypercoagulability and hypofibrinolysis specifically with cyclosporine. Hypercorticism secondary to steroid treatment has been associated with a thrombophilic state and the presence of a reduced fibrinolytic potential in particular. The aims of this study were to first evaluate the fibrinolytic potential by the venous occlusion (VO) test in 19 renal transplant (RT) patients, and then compare these findings with those obtained in similar groups of normal subjects and patients with Cushing's disease. The following tests were carried out before and after the VO test: euglobulin lysis time and t-PA and PAI-1 activities and antigen. Compared with normal controls, RT and Cushing's patients both showed a similar significant increase in PAI-1 activity and concentration. The VO test revealed a similar impairment in fibrinolytic potential in both the RT and Cushing groups. High and pathological PAI-1 levels before and after the VO test were consistent with a defective fibrinolytic potential due to the inhibitory effect of PAI-1 on plasminogen activation. A hypofibrinolytic state was found in 68.4% of RT patients. Our results suggest that an imbalance in the fibrinolytic system is a typical feature of RT patients one year after transplantation. Steroids appear to be the immunosuppressive drug mainly involved in determining thromboembolic risk after renal transplantation.

Adult↗
PubMed1996

Thrombelastographic evaluation of coagulation in transurethral prostatectomy.

OBJECTIVE: To assess the changes in overall coagulation status and define the degree of systemic fibrinolysis occurring in patients undergoing transurethral prostatectomy (TURP). PATIENTS AND METHODS: Thirty patients undergoing TURP, 23 for benign prostatic hyperplasia and seven for prostatic carcinoma, were studied prospectively. Serial venous blood samples were taken using the two-syringe technique. Samples were taken before, during and at intervals up to 72 h and 10-14 days after surgery. Thrombelastography (TEG) was performed on native whole blood samples. Peri-operative blood loss was assessed, until the catheter was removed, by photometric estimation of the haemoglobin content of the irrigant fluid and the measurement of clot volume. RESULTS: There was no evidence of fibrinolysis (TEG Percentage Clot Lysis Ly60 > 15%) in any patient over the whole peri-operative period. There was a significant change in the mean TEG variables towards hypercoagulation from 3 h until 10-14 days postoperatively, compared with the pre-operative values (P < 0.05). There was a significant correlation between blood loss and clot volume. CONCLUSION: These results question the role of systemic fibrinolysis in primary and secondary haemorrhage following TURP and thus the rationale of using antifibrinolytics in these patients. The persistent hypercoagulable state post-operatively indicates a possible role of hypercoagulability in clot retention.

Blood Coagulation↗
PubMed2002

Advances in deep vein thrombosis treatment.

Venous and arterial thromboses account for some of the most common causes of morbidity and mortality amongst patients in the United States and many other Western societies. Clotting disorders and hypercoagulable states are no longer just treated by hematologist, but by multiple specialties including internal medicine, family practice, critical care physicians and most recently, hospitalists. In more than 75% of cases, the cause of the thrombotic episodes can be identified. More than one-half of the patients with thrombosis harbor either congenital propensity to develop a thrombosis, or have an acquired event that precipitates a pro-thrombotic state.

Fibrinolytic Agents↗
PubMed1981

Thoracic aortic thrombi and hypercoagulability.

This unusual report shows the association between thoracic aortic mural thrombus formation and the hypercoagulable state without concomitant disseminated intravascular coagulation. The patient's hypercoagulability was reflected by laboratory results that included elevated Factor VIII and fibrinogen levels, along with a decreased level of antithrombin III. The underlying cause was probably acute peritonitis, a condition associated with coagulopathy.

Journal Article↗