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PubMedDate not supplied

[The search for clinical markers of abnormal hypercoagulable states among factors that trigger venous thromboembolic disease].

We proposed to search for markers of hypercoagulable states in function of age, sex or factors that trigger venous thromboembolic disease (VTD) in a group of patients so diagnosed. The following patient data were analyzed: age, sex and triggering factors of VTD categorized as associative-transient, permanent or unknown. In patients under age 55 years of age in whom the triggering factor of VTD was unknown, and in those who had a family and/or personal history of VTD, coagulability was assessed approximately three months after the episode of acute thrombosis and was repeated during follow-up. From April 1993 to July 1996 we saw 297 patients diagnosed of VTD and performed 187 coagulability tests (63%). Eighty-six were normal (46%) and 101 (54%) abnormal. No significant relations were found for age, sex or triggering factors and the results of follow-up coagulability testing. We conclude that factors known to trigger VTD are not the only ones relevant for indicating the need to order the assessment of coagulability, given that the presence of coagulopathy is not confined to patients with supposed clinical markers.

Biomarkers↗
PubMed2005

Extensive aortic thromboembolism due to acquired hypercoagulable state: an autopsy case report.

Aortic thrombosis rarely occurs without severe atherosclerosis, aneurysm, or cardiosurgical or traumatic state. Arterial thrombosis is commonly related to an inherited and/or acquired hypercoagulable state. A 50-year-old woman presented with diffuse abdominal pain. One day after her admission, she experienced bloody stools. Computed tomography showed multiple extensive thromboses in the aorta and superior mesentery arteries. She underwent a partial jejunoileostomy and colectomy for extensive bowel infarction. Following surgery, her condition deteriorated and she died on the fourth hospital day. At autopsy, gross examination showed 2 large thrombi (7 and 8 cm in length) in the proximal and descending (thoracic) aorta, with mild atherosclerosis. A mesenteric artery thromboembolus with extensive bowel infarction was present. Postmortem laboratory studies revealed an elevated anticardiolipin immunoglobulin G antibody level. The thrombotic state in this patient was considered multifactorial secondary to acquired risk factors, including obesity, mild aortic atherosclerosis with coronary artery disease, and presence of a high titer anticardiolipin antibody.

Aorta, Thoracic↗
PubMed1992

Hypercoagulable states. Their causes and management.

Recognition of patients who should be evaluated for either hereditary or acquired hypercoagulable states is important so that treatment may be instituted if necessary to prevent thrombosis. Close attention to the medical history, medications, family history, and circumstantial risk factors can help identify patients at risk so that morbidity and mortality may be reduced. Patients with hereditary thrombosis should receive lifelong anticoagulation.

Blood Coagulation Disorders↗
PubMed2005

Life-threatening hypercoagulable state following splenectomy in ITP: successful management with aggressive antithrombotic therapy and danazol.

A life-threatening hypercoagulable state (HCS) is reported that developed after splenectomy in idiopathic thrombocytopenic purpura (ITP). A 50-year-old active male was rejected for blood donation because of an incidental finding of low platelet counts, 40,000/uL. The diagnosis was ITP. Although asymptomatic, he underwent splenectomy because of poor response to steroids and intravenous (IV) gamma globulin. One month after splenectomy, he suffered pulmonary emboli without deep venous embolism (DVT), followed by bilateral DVT, threatening amputation of the legs. Emergency thrombolysis, insertion of stent, and IV heparin saved his legs. Extensive workup for HCS was negative. IV heparin was withheld for colonoscopy for possible gastrointestinal neoplasm, at which time DVT recurred, necessitating another thrombolysis and heparin infusion. He was discharged on enoxaparin, antiplatelet therapy, and danazol. Platelet hyperactivation, characterized by high platelet microparticles (PMP) and CD62P, was present throughout his course of active ITP, resolving when ITP went into remission with danazol therapy. ITP has remained in remission for 4 years after stopping enoxaparin and danazol. In vitro, his plasma in active ITP induced activation of normal platelets, generating PMP and inducing CD62p-positive platelets and platelet aggregates; his plasma from remission had no effect. This indicates the presence of a platelet activating factor, possibly anti-platelet antibodies. Splenectomy may have allowed procoagulant PMP to accumulate to high levels resulting in HCS. We advise awareness of thrombotic complications post-splenectomy in the subset of ITP patients who are largely asymptomatic and exhibit persisting platelet activation.

Blood Coagulation Disorders↗
PubMed1991

[Non-neoplastic hypercoagulability states].

Patients with proven recurrent venous or arterial thrombosis should be investigated for a predisposing cause corresponding to a hypercoagulable state. The latter is made up of two broad categories: the first consists of inherited thrombotic disorders; the second of a heterogeneous array of acquired clinical disorders, some of which are illustrated by clinical reports encountered in our department of internal medicine. Although the development and application of specific tests have provided valuable information about the pathogenesis of intravascular thromboses, these assays are currently able to provide aetiological diagnoses in fewer than 20 percent of young patients with recurrent venous thromboembolism.

Adolescent↗
PubMed2002

Laboratory evaluation of hypercoagulable states in patients with central retinal vein occlusion who are less than 56 years of age.

PURPOSE: To investigate whether hypercoagulability plays a role in thrombus formation in patients with central retinal vein occlusion (CRVO) who are less than 56 years of age. DESIGN: Prospective, observational case series with retrospective comparative controls. PARTICIPANTS AND CONTROLS: Participants included 55 consecutive patients with CRVO less than 56 years of age. The laboratory's age-matched control groups were used to compare results for the same tests. METHODS: Fifty-five patients with CRVO less than 56 years old (mean age, 44 years) underwent laboratory evaluation for homocysteine, activated protein C resistance, protein C activity, protein S activity, antithrombin III activity, antiphospholipid antibodies, and anticardiolipin antibodies. The results were compared with previously drawn age-matched control groups obtained by the same laboratory for statistical significance. MAIN OUTCOME MEASURES: Patients were considered to have a positive test if their results were outside the laboratory's established range. RESULTS: Fifteen of 55 patients (27%) had one positive test result suggesting hypercoagulability. Compared with the control groups, these patients less than 56 years old with CRVO had a higher incidence of coagulation abnormalities by laboratory testing. Among the parameters tested, hyperhomocysteinemia and circulating antiphospholipid antibodies were significantly more common in the CRVO patients (P < 0.05) compared with age-matched controls. CONCLUSIONS: Hypercoagulability may play a role in the pathogenesis of CRVO in patients less than 56 years old. The cause of CRVO remains multifactorial, and laboratory tests suggesting hypercoagulable states alone cannot account for the cause in most of these patients less than 56 years of age. The authors recommend examining blood pressure, intraocular pressure, complete blood count, glucose levels, and a lipid panel on all patients with CRVO. When tests for these common risk factors for CRVO are negative, consider ordering selected tests in young patients with CRVO to rule out thrombophilias, especially in patients with bilateral CRVO, a history of previous thrombosis, or family history of thrombosis.

Activated Protein C Resistance↗
PubMed1996

Lipoprotein (a), homocysteine, and hypercoagulable states in young men with premature peripheral atherosclerosis: a prospective, controlled analysis.

PURPOSE: Elevated lipoprotein (a) (Lp[a]) lipoprotein, total homocysteine, and hypercoagulable states (HCS) have all been implicated as risk factors for premature-onset atherosclerosis. This study was performed to determine the prevalence of these abnormalities in young men with chronic lower extremity ischemia (peripheral vascular disease [PVD]) and to determine their relative strengths as risk factors for premature peripheral atherosclerosis. METHODS: We analyzed 50 young white men (aged 45 years or younger at onset of symptoms) and compared them with 45 age-matched white male control subjects. RESULTS: Atherosclerotic risk factors were similar in both groups. The mean (+/- SEM) Lp(a) lipoprotein level was 36 +/- 6 mg/dl among the study patients, compared with 14 +/- 2 mg/dl among control subjects (p = 0.02, Mann-Whitney). Twenty (40%) study patients and seven (16%) control subjects had Lp(a) lipoprotein levels of 30 mg/dl or greater (atherosclerotic risk threshold) (p = 0.01, odds ratio = 3.62, confidence interval (CI) 1.4 to 9.5). Positive HCS panels (antiphospholipid antibodies or deficiencies in antithrombin III, protein C, or protein S) were nearly twice as prevalent in study patients (n = 15, 30%) as in controls (n = 8, 18%), but this difference did not achieve statistical significance. The mean total plasma homocysteine level among the study patients was 15.9 +/- 0.9 mumol/L, which was not significantly different from the mean control value of 14.7 +/- 0.7 mumol/L. Lp(a) lipoprotein was related to risk of premature PVD through a linear logistic relationship (p = 0.003, odds ratio per each 1 mg/dl Lp(a) change was 1.03, CI 1.0 to 1.1). Multivariate analysis with stepwise logistic regression selected two variables: Lp(a) lipoprotein > or = 30 mg/dl (p = 0.01, odds ratio = 3.6, CI 1.3 to 9.9) and family history (p = 0.07, odds ratio = 2.2, CI 0.9 to 5.3). Tests of interaction demonstrated no effect between Lp(a) lipoprotein, HCS, and homocysteine. CONCLUSIONS: Lp(a) lipoprotein of 30 mg/dl or greater is an independent risk factor for premature peripheral atherosclerosis in men. None of the other examined variables exhibited a significant association with premature PVD.

Adult↗
PubMed2004

Tissue factor messenger RNA levels in leukocytes compared with tissue factor antigens in plasma from patients in hypercoagulable state caused by various diseases.

We compared the levels of tissue factor (TF) mRNA in leukocytes with plasma TF antigens of patients in hypercoagulable state caused by various diseases. Flow cytometric analysis showed absence of TF antigen expression on neutrophils and monocytes in healthy subjects but strong expression in both cell types of patients with infections.TF mRNA levels in leukocytes were low in healthy subjects but they were significantly elevated in patients with underlying diseases of disseminated intravascular coagulation (DIC), especially in acute myeloid leukaemia (AML) and infections.TF mRNA levels in leukocytes were significantly high in patients with all diseases except those with thrombosis, and plasma TF antigen levels were significantly high in all diseases. TF mRNA in leukocytes and plasma TF antigen levels were significantly high in patients with overt-DIC, and TF mRNA/antigen ratio was significantly high in patients with overt-DIC. In patients with solid cancers, TF mRNA and TF mRNA/antigen ratio were significantly higher in patients with metastases than those without. TF mRNA levels in leukocytes and plasma levels of TF antigen did not correlate in normal subjects and all patients, but they tended to be correlated in patients with AML, infections or overt-DIC. Our analysis suggests that TF expression in leukocytes plays an important role in various diseases but the expression level does not always correlate with plasma levels of TF antigen.

Adult↗
PubMed1990

Postpartum Budd-Chiari syndrome with prolonged hypercoagulability state.

Budd-Chiari syndrome after pregnancy is an extremely rare disease. Reported here is a case of postpartum Budd-Chiari syndrome with unusual features of prolonged hypercoagulability state. The disease occurred 2 weeks after delivery and despite massive anticoagulation treatment the patient developed severe hepatic vein occlusion, renal vein thrombosis, inferior vena cava thrombosis, and femoral artery thrombosis.

Adult↗
PubMed2002

Hypercoagulable states and pregnancy.

Pulmonary thromboembolism is a major cause of maternal death in the developed world. Underlying this condition is the problem of deep venous thrombosis. These problems often reflect an underlying hypercoagulable state. Growing evidence implicates congenital and acquired thrombophilias in the pathophysiologic processes underlying not only venous thrombosis, but also miscarriage, intrauterine growth restriction, and preeclampsia, raising new possibilities for intervention.

Anticoagulants↗
PubMed1996

Acute-phase response and the hypercoagulable state in pulmonary tuberculosis.

In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.

Acute-Phase Reaction↗
PubMed2004

Hypercoagulable state associated with kidney-pancreas transplantation. Thromboelastogram-directed anti-coagulation and implications for future therapy.

BACKGROUND: The clinical consequences of type 1 diabetes mellitus (IDDM) include diabetic triopathy: retinopathy, nephropathy, and neuropathy, as well as microangiopathy, accelerated atherosclerotic disease, and hypercoagulability. The etiology of the hypercoagulability is multifactorial, involving various clotting factors or pathways (for example platelets, fibrinogen, individual components of the clotting system and/or fibrinolysis in different studies). The development of end-stage renal disease (ESRD), with the uremia-related platelet effect has the potential to protect from the existing hypercoagulable state. This has important implications for surgery, particularly simultaneous pancreas-kidney (SPK) transplantation, where the pancreas has historically been prone to thrombosis. This has led us to perform intra-operative thromboelastograms (TEG's) to evaluate the patient's current coagulation status. METHODS: A TEG was performed in 85 SPK recipients along with a control group of 54 non-diabetic kidney transplant (KT) recipients. RESULTS: For each of the 4 TEG coagulation parameters, the SPK recipients were significantly more hypercoagulable than the non-diabetic KT recipients. The use of intra-operative heparin is based on the degree of hypercoagulability by TEG and degree of operative hemostasis. There has been one PT lost to thrombosis (1%) in the first week following transplantation during this time. CONCLUSION: The use of TEG is a helpful adjunct to SPK surgery, demonstrating the patient's current coagulation status. Nearly all SPK recipients (type 1 IDDM with ESRD) have been demonstrated to be hypercoagulable. The TEG allows the judicious use of anti-coagulation at the time of surgery, and beyond.

Anticoagulants↗
PubMed1993

Phosphatidylserine in the outer leaflet of red blood cells from beta-thalassemia patients may explain the chronic hypercoagulable state and thrombotic episodes.

Investigation of red blood cells from beta-thalassemia patients by means of prothrombinase assay reveals phosphatidylserine in the outer leaflet of the plasma membrane. This might explain their elevated susceptibility to phagocytosis by macrophages and the chronic hypercoagulable state, frequent thrombotic events, and life-long platelet activation that are found in thalassemic patients.

Blood Coagulation Disorders↗
PubMedDate not supplied

Hypercoagulable state associated with a deficiency of protein C in a thoroughbred colt.

Protein C is a vitamin K-dependent serine protease with anticoagulant and profibrinolytic activity which is synthesized in the liver. Decreased protein C activity was detected in a Thoroughbred colt with clinical and histopathologic evidence of recurrent venous thrombosis. Although protein C activity was reduced, protein C antigen concentration was normal. Consumptive coagulopathies produce a decrease in both the functional and antigenic concentrations of protein C, thus a defect in protein C synthesis was suspected. Inhibition of gamma-carboxylation secondary to vitamin K antagonism results in the synthesis of a protein C molecule with antigenicity, but without biological activity. However, there was no evidence of vitamin K antagonism. The hypercoaguable state resulting from the reduced activity of protein C in this colt was associated with uncomplicated renal disease, rather than a protein C consumptive process such as endotoxemia. A primary hypercoagulable state due to a deficiency of protein C activity was diagnosed. Primary deficiencies of protein C activity have not been previously documented in horses.

Animals↗
PubMed2002

Effect of beta2-adrenergic receptor functioning and increased norepinephrine on the hypercoagulable state with mental stress.

BACKGROUND: Procoagulant stress responses may contribute to atherosclerosis development and acute coronary thrombosis. In the present study, we examined the role of beta2-adrenergic receptor function and plasma catecholamines in the stress-induced increase in the 2 hypercoagulability markers thrombin-antithrombin III (TAT) complex and fibrin D-dimer (DD). METHODS: Lymphocyte beta2-adrenoreceptor sensitivity and density were assessed at rest, and plasma levels of TAT, DD, epinephrine, and norepinephrine were measured at rest and in response to a standardized mental stress task in 19 normotensive and mildly hypertensive nonmedicated subjects (mean age 38 years, age range 29 to 48 years). RESULTS: The stressor elicited a significant increase in TAT (P =.024), DD (P =.026), and norepinephrine (P =.005). Resting beta2-adrenoreceptor sensitivity (isoproterenol-stimulated cyclic adenosine monophosphate production) plus the norepinephrine change scores (stress minus rest) accounted for 59% of the variance in the absolute TAT increase in response to stress (P =.001). Hypertension status and demographic variables such as sex did not influence the results. CONCLUSIONS: Acute mental stress may trigger a hypercoagulable state evidenced by increased thrombin activity and increased fibrin turnover. Beta2-adrenergic receptor sensitivity and plasma catecholamine activity may mediate the procoagulant response to acute stressors. These mechanisms may help explain the adverse impact of mental stress on the cardiovascular system.

Adult↗
PubMed1991

Essential thrombocythemia: a hypercoagulable state.

Essential thrombocythemia is an entity characterized by clonal proliferation of megakaryocytes and thrombocytosis. We have analyzed the presenting manifestation of 13 patients with Essential Thrombocythemia diagnosed in the last three years. The major findings include the frequent presence of symptomatology of a hypercoagulable state with prompt improvement of these symptoms once the thrombocytosis is controlled. Constitutional symptoms, organomegaly, modest Leukocytosis and eosinophilia were also often seen. No catastrophic events were detected with a mean follow up period of 17.5 months.

Adolescent↗
PubMed2005

Hepatocavopathy and isolated splenic vein thrombosis due to hypercoagulability state.

We report a patient with protein C and protein S deficiency and factor V Leiden mutation presenting with splenic vein thrombosis and with a web between the hepatic venous confluence and vena cava inferior. These two findings were thought to be due to the hypercoagulable state of the patient. Interestingly, there was no need for invasive procedures as the inferior accessory hepatic vein was patent. Hepatic venous flow was being maintained by the inferior accessory hepatic vein or a dominant collateral vein.

Anticoagulants↗
PubMed1994

Hypercoagulability state in patients with chronic obstructive pulmonary disease. Chronic Obstructive Bronchitis and Haemostasis Group.

Since there is some clinical evidence that the clinical course of patients with chronic obstructive pulmonary disease (COPD) may be complicated by thrombosis in the pulmonary vessels, we studied whether a hypercoagulability state (HS) does occur in COPD. Plasma levels of prothrombin F1 + 2 fragment, a marker of thrombin generation, D-dimer, a marker of in vivo thrombin and plasmin activation, and fibrinogen were measured in 37 COPD patients and in 30 controls matched for sex and age. COPD patients had significantly higher values of F1 + 2 (p = 0.0001) and fibrinogen (p = 0.0005) than healthy subjects. The difference persisted after excluding smoking patients. F1 + 2 was not correlated with PaO2 (r = 0.02, p > 0.05) and PaCO2 (p = 0.12, p > 0.05). In six patients with stable COPD and F1 + 2 greater than 1.65 nM (mean + 2 SD of controls) subcutaneous calcium-heparin therapy (5000 IU t.i.d. for 15 days) significantly reduced F1 + 2 (p = 0.03) and PaCO2 (p = 0.01). This study shows that COPD patients have an ongoing prothrombotic state which could potentially account for thrombosis occurring in pulmonary vessels. The effect of calcium-heparin treatment on clotting system activation and blood gas may suggest this treatment as potential candidate for prospective study in COPD patients.

Adult↗