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PubMed1995

Transient protein S deficiency associated with cerebral venous thrombosis in active ulcerative colitis.

Cerebral venous thrombosis is an uncommon complication of ulcerative colitis. We report the case of a 29-yr-old female with a recent diagnosis of ulcerative colitis who suffered stroke secondary to thrombosis of the veins of Galen and straight sinus. A search for a hypercoagulable state revealed a nonfamilial transient protein S deficiency. Possible involvement of C4b-binding protein in this hypercoagulable state is discussed.

Acute Disease↗
PubMed2002

Upper extremity deep venous thrombosis.

Upper extremity deep venous thrombosis (UEDVT) makes up approximately 1-4% of all episodes of deep venous thrombosis (DVT). Risk factors for UEDVT include central venous catheterization, strenuous upper extremity exercise or anatomic abnormalities causing venous compression, inherited thrombophilia, and acquired hypercoagulable states including pregnancy, oral contraceptive use, and cancer. Unexplained or recurrent UEDVT should prompt a search for inherited hypercoagulable states or underlying malignancy. Clinical presentations include arm, neck, and shoulder pain; edema; skin discoloration; tenderness; and venous distension. Because UEDVT is frequently asymptomatic until complications ensue, a high index of suspicion is required for patients with one or more risk factors for thrombosis. Pulmonary embolism and post-thrombotic syndrome are the most common sequelae of UEDVT. Early detection and treatment of UEDVT decrease complications, morbidity, and mortality. Compressive ultrasonography is an effective and economical means of confirming the clinical diagnosis in most patients. Traditional anticoagulant therapy of UEDVT is giving way to a multimodal approach involving transcatheter thrombolytic therapy followed by a minimum of 3 months of warfarin sodium anticoagulant therapy, venous decompression as needed, and balloon angioplasty with stenting for treatment of residual stricture. Low-dose anticoagulant therapy can safely and effectively mitigate the increased risk of UEDVT associated with the use of central venous catheters.

Arm↗
PubMed2000

Role of thrombotic vascular risk factors in inflammatory bowel disease.

Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). It is recognized that a hypercoagulable state exists in IBD which involves all components of the clotting system. It has been suggested that this hypercoagulable state is closely linked to the disease pathogenesis. Recent studies have shown that genetic defects such as factor V Leiden mutation and C677T methylenetetrahydrofolate reductase polymorphism associated with hyperhomocysteinemia seem to interfere in the thrombotic manifestations of IBD. Acquired factors such as antiphospholipid antibodies could also participate in the development of the thrombotic process. Deficiencies of other anticoagulant factors play a less important role in the thrombosis, and therefore it is not surprising that the results on these factors in IBD are contradictory. In conclusion the resultant gene-gene and gene-environment interactions between risk factors are the key to the understanding of why an IBD patient develops thrombosis at a specific point in time.

Antibodies, Antiphospholipid↗
PubMed1999

A prospective coagulation study including resistance to activated protein C and mutations in factors V and II in venous leg ulcers.

Hypercoagulable states have been reported to be associated with venous leg ulcers. In an attempt to investigate the prevalence of hypercoagulable states in patients with venous leg ulcers, we performed a prospective case-control study for the presence of coagulation defects in such patients, including resistance to activated protein C (APC), factor V Leiden mutation and a newly described mutation in factor II. Results were compared with those obtained in a control group. APC resistance was found in four of 33 patients tested, but only one was found to be heterozygous for the factor V Leiden mutation. Factor II mutation was found in two of 30 patients tested. Our findings show that the prevalence of coagulation abnormalities is not different in patients with venous leg ulcers from controls in our study, suggesting that only selected patients with venous ulcers and a history of recurrent deep venous thrombosis should be investigated for the presence of coagulation defects.

Activated Protein C Resistance↗
PubMed2005

Hypercoagulability is most prevalent early after injury and in female patients.

BACKGROUND: Hypercoagulability after injury is a major source of morbidity and mortality. Recent studies indicate that there is a gender-specific risk in trauma patients. This study was performed to determine the course of coagulation after injury and to determine whether there is a gender difference. We hypothesized that hypercoagulability would occur early after injury and that there would be no difference between men and women. METHODS: This was a prospective cohort study. Inclusion criteria were admission to the intensive care unit, Injury Severity Score > 4, and the ability to obtain consent from the patient or a relative. A Thrombelastograph (TEG) analysis was performed and routine coagulation parameters and thrombin-antithrombin complexes were measured within 24 hours of injury and then daily for 4 days. RESULTS: Sixty-five patients met criteria for entry into the study. Their mean age was 42 +/- 17 years and their mean Injury Severity Score was 23 +/- 12. Forty patients (62%) were men. The prevalence of a hypercoagulable state by TEG was 62% on day 1 and 26% on day 4 (p < 0.01). Women were significantly more hypercoagulable on day 1 than men as measured by the time to onset of clotting (women, 2.9 +/- 0.7 minutes; men, 3.9 +/- 1.5 minutes; p < 0.01; normal, 3.7-8.3 minutes). Mean platelet counts, international normalized ratios, and partial thromboplastin times were within normal limits throughout the study. Thrombin activation as measured by thrombin-antithrombin complexes decreased from 34 +/- 15 microg/L on day 1 to 18 +/- 8 microg/L (p < 0.01) on day 4, consistent with the prevalence of hypercoagulability by TEG. CONCLUSION: Hypercoagulability after injury is most prevalent during the first 24 hours. Women are more hypercoagulable than men early after injury. The TEG is more sensitive than routine coagulation assays for the detection of a hypercoagulable state.

Adult↗
PubMed1991

[A new advance in theory of blood coagulation and fibrinolysis and its practical application].

New trends in tests for coagulation and fibrinolysis and advances in diagnosis for the hypercoagulable state and utilization of immunological techniques such as various polyclonal and monoclonal antibodies are reported. We discussed (1) the new markers for hypercoagulable states, (2) differential diagnosis of disseminated intravascular coagulation (DIC) and abnormalities of coagulation in liver cirrhosis (LC), and (3) new markers for fibrinolysis and vascular function. Thrombin-antithrombin III complex (TAT) levels were higher in thrombotic diseases than in healthy controls. Therefore, TAT should be a good marker for hypercoagulation as fibrinopeptide A (FPA) and soluble fibrin monomer complex (SFMC). Measurement of TAT, plasma-alpha 2 plasmin inhibitor complex (PIC), and D dimer were useful for differential diagnosis of DIC and liver cirrhosis. t-PA-PAI complex correlated well with t-PA, but not with fibrinolytic parameters such as PIC. The t-PA-PAI complex may be a good marker for the function of the vascular endothelium.

Antithrombin III↗
PubMed2001

Portal vein thrombosis associated with antiphospholipid syndrome.

Portal vein thrombosis is a rare occurrence, and often an underlying hypercoagulable state can be found. Recently, there has been growing interest and recognition of the antiphospholipid syndrome in association with acquired hypercoagulable state. This syndrome consists of the association of lupus anticoagulant or antiphospholipid antibodies with arterial or venous thrombosis, thrombocytopenia, and spontaneous abortion. We report a case of portal vein thrombosis associated with the antiphospholipid syndrome. In our patient, chronic liver disease, hepatobiliary infection, abdominal malignancies, myeloproliferative disorders, and inherited coagulation disorders were excluded. This case report suggests that serum antiphospholipid antibodies should be investigated in patients with portal vein thrombosis of unexplained etiology.

Aged↗
PubMed1999

Laboratory diagnosis of the thrombophilic state in cancer patients.

Perturbations of coagulation in cancer patients have been described for a long time. In up to 90% of cancer patients "routine" blood tests are abnormal leading to a hypercoagulable state in these patients. Among these tests are an increase in clotting factors, fibrinogen, fibrinogen/fibrin degradation products, and thrombocytosis. Markers of the activation of coagulation have been developed, and levels of FPA, F1+2, TAT, and D-Dimer have been found higher in cancer patients. More specific procoagulant activities in cancer (CP and TF) have also been described and can be measured but none of them have any predictive value for the occurrence of venous thromboembolism in these patients. Consistent with this hypercoagulable state in cancer is the finding that most cancer patients have reduced plasma levels of inhibitors of coagulation. These complex abnormalities are clinically expressed as thrombosis, low-grade or fulminant DIC which can be assessed by different laboratory tests, and as hemorrhage when the fibrinolysis system is impaired. However, no studies have shown to date a relationship between these abnormalities of the coagulation tests and the clinical expression in any single individual. Because these patients are at high risk for thrombosis in special conditions such as surgery or during chemotherapy, prophylaxis with various forms of heparin are recommended.

Blood Coagulation↗
PubMed1994

Causes and mechanisms of territorial and nonterritorial cerebellar infarcts in 115 consecutive patients.

BACKGROUND AND PURPOSE: Territorial cerebellar infarcts have mainly a thromboembolic mechanism. Cerebellar infarcts less than 2 cm in diameter have recently been reported as nonterritorial infarcts, but it is not clear whether they are low-flow or embolic infarcts. The aim of the present study was to compare the characteristics and causes of territorial and nonterritorial infarcts in a prospective series of 115 patients. METHODS: We collected data from 115 consecutive patients with cerebellar infarcts (79 territorial and 36 nonterritorial [ie, less than 2 cm]), using magnetic resonance imaging (88 patients) and computed tomography. RESULTS: Patients with territorial infarcts and those with nonterritorial infarcts had similar vascular risk factors and clinical presentations and an equal frequency of cardiac source of embolism (32% versus 42%; P = NS) and of large artery occlusive disease (23% versus 19%; P = NS). Occlusive lesions of large arteries at angiography occurred at the level of one cerebellar artery (5% versus 0%; P = NS) and proximal to the ostia of the cerebellar arteries (18% versus 19%; P = NS). Infarcts distal to occlusive lesions were subdivided into unilateral vertebral artery occlusive disease (presumed artery-to-artery embolic mechanism; 18% versus 5%; P = NS) and low-flow state distal to bilateral vertebral or basilar artery occlusion (presumed hemodynamic mechanism; 0% versus 14%; P = .004). Patients with nonterritorial infarcts had more frequent hypercoagulable state (17% versus 1.25%; odds ratio, 15.6 [95% confidence interval, 1.8 to 135]). For the remaining patients, the mechanism of the infarct was unknown (34% versus 22%; P = NS). CONCLUSIONS: Cerebellar infarcts less than 2 cm in diameter (ie, nonterritorial) have the same high rate of embolic mechanism as territorial infarcts (47% versus 49%; P = NS), have more frequent hypercoagulable state, and sometimes have a hemodynamic mechanism.

Arterial Occlusive Diseases↗
PubMed2000

Coagulation and cancer: implications for diagnosis and management.

Coagulation disorders are a common problem in neoplastic patients and many factors contribute to increase the risk of thromboembolic events in these patients. An hypercoagulable state is induced by malignant cells interacting directly with hemostatic system and activating the coagulation cascade. More sensitive tests to assess an hypercoagulable state in cancer patients have been developed; even though these tests are always altered in cancer patients, none of them possess a clinical significance in terms of predictive value for the occurence of thromboembolism and disease prognosis in the individual patient. The most frequent thromboembolic complications in cancer patients are deep vein thrombosis of the lower extremities and pulmonary embolism; therefore, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura or haemolytic uremic syndrome are special manifestations of neoplastic disease. Diagnosis of idiopathic deep vein thrombosis, in the absence of other risk factors, could indicate the presence of occult malignant disease; however, the need for an extensive work-up to detect malignancy is still controversial. Neoplastic patients showing a thromboembolic event should be treated with unfractioned heparin or, alternatively, with low molecular weight heparins. In order to prevent recurrence, the administration of heparin should be associated and followed by an oral anticoagulant drug. In recent years new approaches in anti-aggregation therapy have been studied, such as COX-inhibitors, cicaprost and ReoPro; further studies are needed to determine the usefulness of these molecules in treatment of malignancies.

Antineoplastic Agents↗
PubMed1999

Coagulation/fibrinolysis disorder in patients with severe preeclampsia.

We investigated coagulation/fibrinolysis parameters in 50 patients with severe preeclampsia. The coagulation and clinical indices in patients with severe preeclampsia were 1.595 and 1.414, respectively. These indices show a strong correlation between the clinical status and coagulation/fibrinolysis abnormalities. Among patients with severe preeclampsia, a significant decrease in antithrombin (AT) (p = 0.002) and a significant increase in plasmin inhibitor complex (PIC) (p = 0.002), D-dimer (p < 0.05), and thrombin-antithrombin complex (TAT) (p = 0.001) were observed in cases terminated by cesarean section compared with those cases of vaginal delivery. There was no significant difference in platelet count (Plt), however, deltaPlt (the difference between platelet counts in early gestation and before delivery) was significantly larger (p < 0.05) in cases that ended in cesarean section. Furthermore, among cases terminated by cesarean section, a significant increase in PIC (p < 0.01) was observed when pregnancies were terminated because of maternal factors compared with those terminated because of fetal factors. These results suggest that (1) even in patients with severe preeclampsia, vaginal deliveries can be successful when they display a less hypercoagulable state; (2) a decrease in Plt during pregnancy may be a predictive marker for the termination of pregnancy; and (3) an excessive hypercoagulable state in patients with severe preeclampsia may be associated with the termination of pregnancy, especially when there is an aggravation of maternal factors.

Adult↗
PubMed1994

[A new cause of familial thrombophilia: resistance to the effect of activated protein C].

An examination of the cascade of events leading to coagulation emphasizes the importance of protein inhibitors. Deficiencies in these proteins have been implicated as playing a possible causal role in familial thrombo-embolic diseases. Recently the discovery of a probable deficiency in protein C cofactor, different from protein S, stimulated much research in this area. Protein C is a 461 amino acid vitamin K-dependent protein with a molar mass of 62,000 Daltons. After transduction the precursor protein is modified into an active form. Circulating protein C is then activated by proteolysis on the endothelial surface under the control of thrombomodulin-bound thrombin. Thus thrombin affects both procoagulation by activating factors V and VIII (and XI) and anticoagulation after being bound to thrombomodulin. Inactivation of factors V and VIII requires calcium, phospholipids and a C-protein cofactor, protein S. On the basis of clinical observations, it was hypothesized then confirmed that deficiency in a non-identified cofactor of protein C could explain resistance to the anticoagulating action of activated protein C. Purification of the plasma fraction carrying the cofactor activity led to the isolation of a protein which has all the biochemical properties of factor V. In addition, adding factor V to affected plasma has been shown to correct for resistance to activated protein C. But paradoxically, patients with resistance to the action of activated protein C have a normal level of factor V. The mutation responsible for activated protein C resistance was found to be a Gln for Arg mutation at position 506 of factor V. The implication of this mutation has been very recently confirmed and led rapidly to the development of molecular biology methods allowing its identification. At present, this new cause of familial hypercoagulable states can thus be identified with polymerase chain reaction and denaturing gradient gel electrophoresis. These advances have increased the number of identifiable hypercoagulable states, yet further work is needed since currently less than 10% of these diseases can be explained by deficiencies in one of the inhibitor proteins, antithrombin III, protein C or protein S.

Factor V↗
PubMed1980

Hypercoagulability in patients with mitral stenosis -- from the viewpoint of the behavior of plasma antithrombin III and alpha2-plasmin inhibitor.

The concentration of plasma antithrombin III (AT III) and the biological activity of plasma alpha2-plasmin inhibitor (alpha 2-PI) were measured in cases of mitral stenosis (MS) and rheumatic heart disease (RHD) without MS. Cases of MS showed the findings of the low levels of plasma AT III and normal or a little higher levels of plasma alpha 2-PI, that was not recognized in RHD without MS. This finding was interpreted to be hypercoagulable because of the acceleration of coagulation and of little or slight retardation of fibrinolysis. Besides, the influence of atrial fibrillation and chronic congestive heart failure on hypercoagulability in cases of MS was detected clearly, but the influence of them in cases of non-RHD was obscure. As the results, the severer the degree of MS, the clearer the hypercoagulable state. Therefore, the prethrombotic state existed in cases of MS, combined with blood flow disturbance due to atrial fibrillation or chronic congestive heart failure, endocardial damage resulted from rheumatic fever in an early stage and hypercoagulable state mentioned above in the present study. There was no significant difference between cases with and without thrombi in the degree of hypercoagulability in subjects with MS shown in the present work. It was concluded that the consumption of AT III caused the low levels of it in cases of MS, and that the low production of AT III in the liver rather than consumption caused the low levels of it in cases of non-RHD.

Adult↗
PubMed2005

[Clinical significance of detection of thrombus precursor protein in severe sepsis].

OBJECTIVE: To evaluate the significance of the changes in plasma thrombus precursor protein (TPP) in severe sepsis. METHODS: Enzyme linked immunoadsorbent assay (ELISA) was used in the determination of plasma TPP in 22 patients with severe sepsis group. Prothrombin time (PT), activated partial thromboplastin time(APTT), fibrin(Fib), D-Dimer were also determined and the values were compared with those obtained from 10 patients with infection and 8 healthy normal controls. At the same time, scores of sepsis related organ failure assessment(SOFA), simplified acute physiology score (SAPSII), Marshall criteria were made respectively in patients with severe sepsis on 1,3,5 days after admission to the ICU. Analysis of correlation between TPP and scores was done. RESULTS: (1)The concentration of TPP and positive rate of D-Dimer in severe sepsis were obviously higher than that in the ordinary infection group and normal control group (all P<0.05). But there were no differences in levels of PT, APTT, and Fib among three groups. (2)The concentration of TPP rose continuously in nonsurvivors due to severe sepsis, and it was positively correlated with scores of SOFA, SAPSII, Marshall criteria. CONCLUSION: TPP levels showed a higher specificity and sensitivity in detecting hypercoagulability state in severe than D-Dimer, PT, APTT, Fib assay. It can be used as a diagnostic and prognostic parameter for early hypercoagulability states and outcome of severe sepsis.

Adolescent↗
PubMed1995

Carcinoma of the thyroid: a cause of hypercoagulability?

A case of metastatic papillary carcinoma of the thyroid is described in which internal jugular vein thrombosis was the initial sign. Local factors, such as compression and invasion, were excluded as causes. A hypercoagulable state associated with deep vein thrombosis is known to accompany some types of adenocarcinomas or autoimmune diseases. We propose that carcinoma-induced hypercoagulability was the course of thrombogenesis in our patient. This is to the best of our knowledge the first report of an association between adenocarcinoma of the thyroid and a hypercoagulable state.

Blood Coagulation↗
PubMed2002

Cancer and the prothrombotic state.

Thrombosis is a frequent complication of cancer, so it follows that the presence of a tumour confers a prothrombotic state. Indeed, in patients with cancer, each of the three components of Virchow's triad that predispose for thrombus formation have abnormalities, thus fulfilling the requirement for a prothrombotic or hypercoagulable state. The many signs and symptoms of the prothrombotic state in cancer range from asymptomatic basic abnormal coagulation tests to massive clinical thromboembolism, when the patient may be gravely ill. Many procoagulant factors, such as tissue factor and cancer procoagulant, are secreted by or are expressed at the cell surface of many tumours. Platelet turnover and activity are also increased. Damaged endothelium and abnormalities of blood flow in cancer also seem to play a part, as does abnormal tumour angiogenesis. Some studies have even suggested that these abnormalities may be related to long-term prognosis and treatment. We briefly describe the various clinical manifestations of thrombosis in cancer and discuss the evidence for the existence of a prothrombotic or hypercoagulable state associated with this disease. Further work is needed to examine the mechanisms leading to the prothrombotic state in cancer, the potential prognostic and treatment implications, and the possible value of quantifying indices of hypercoagulability in clinical practice.

Angiography↗
PubMed1996

The role of anticoagulation in pylephlebitis.

BACKGROUND: Pylephlebitis may complicate any intra-abdominal infection and carries a high mortality rate. Acute cases are usually anticoagulated to prevent thrombus extension and enteric ischemia; however, the role of anticoagulation has not been clearly defined. METHODS: Over a 3-year period, pylephlebitis was diagnosed in 44 patients with portal vein thrombosis on computed tomography scan with fever, leukocytosis, and/or positive blood cultures. The charts were reviewed for etiology, extent of venous thrombosis, and method and results of treatment. RESULTS: Eighteen patients were hypercoagulable, due to clotting factor deficiencies (6), malignancy (8), or AIDS (4). Fifteen patients had mesenteric vein involvement. Thirty-two patients were not anticoagulated, and 5 died (3 with hypercoagulable states and 2 with normal clotting function). Twelve patients were anticoagulated, and none developed subsequent bowel infarction or died. CONCLUSION: Patients with pylephlebitis and a hypercoagulable state due to neoplasms or clotting factor deficiencies should be anticoagulated. Patients with normal clotting function and mesenteric vein involvement may also benefit. We believe anticoagulation in patients with thrombus isolated to the portal vein and normal clotting function may be unnecessary.

Adolescent↗
PubMed1998

Significance of elevated IgG anticardiolipin antibody levels in patients with Budd-Chiari syndrome.

OBJECTIVES: Budd-Chiari syndrome (BCS) is characterized by hepatic venous outflow obstruction. Though hypercoagulable states are implicated in the causation of BCS, the etiology remains unknown in most cases. Presence of anticardiolipin antibodies (aCL) is a known cause of hypercoagulable state. We therefore studied the frequency of IgG aCL in BCS. METHODS: Sera were obtained from 19 patients with BCS, 50 healthy controls, 18 age- and gender-matched patients with cirrhosis, and 15 patients with acute viral hepatitis. IgG aCL levels were measured using a solid-phase enzyme immunoassay. Values exceeding mean + 2 SD of healthy controls were taken as abnormal. RESULTS: Mean +/- SD IgG aCL levels (GPL units) in the four groups were: healthy controls, 6.3 +/- 4.4; BCS, 13.8 +/- 13.3 (p < 0.05, compared with healthy controls); cirrhosis, 15.1 +/- 14.9 (p < 0.05, compared with healthy controls and p = ns, compared with BCS patients); and acute viral hepatitis, 5.0 +/- 2.5 (p = ns, compared with healthy controls). The levels in BCS and cirrhosis patients were similar (p = ns). The number of patients with elevated aCL was: healthy controls, 3/50; BCS, 6/19; cirrhosis, 7/18; and acute viral hepatitis, 0/15. The number of patients with elevated IgG aCL was significantly higher among patients with BCS and cirrhosis, compared with controls (p = 0.03 and p = 0.002, respectively). CONCLUSIONS: Patients with BCS had higher IgG aCL levels than healthy controls. However, as aCL levels were also elevated in patients with cirrhosis, the pathogenetic role of IgG aCL in the causation of BCS is doubtful.

Acute Disease↗