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PubMed2003

Venous thrombosis and changes of hemostatic variables during cross-sex hormone treatment in transsexual people.

The incidence of venous thrombosis associated with estrogen treatment in male-to-female (M-->F) transsexuals is considerably higher with administration of oral ethinyl estradiol (EE) than with transdermal (td) 17-beta-estradiol (E(2)). To find an explanation for the different thrombotic risks of oral EE and td E(2) use, we compared the effects of treatment of M-->F transsexuals with cyproterone acetate (CPA) only, and with CPA in combination with td E(2), oral EE, or oral E(2) on a number of hemostatic variables [activated protein C (APC) resistance and plasma levels of protein S, protein C, and prothombin], all of which are documented risk factors for venous thrombosis. APC resistance was determined by quantification of the effect of APC on the amount of thrombin generated during tissue factor-initiated coagulation; plasma levels of total and free protein S were determined by standard ELISA; and levels of prothrombin and protein C were determined with functional assays after complete activation of the zymogens with specific snake venom proteases. CPA-only, td-E(2)+CPA, or oral-E(2)+CPA treatment produced rather small effects on hemostatic variables, whereas oral EE treatment resulted in a large increase in APC resistance from 1.2 +/- 0.8 to 4.1 +/- 1 (P < 0.001), a moderate increase in plasma protein C (9%; P = 0.012), and a large decrease in both total and free plasma protein S (30%; P < 0.005). The large differential effect of oral EE and oral E(2) indicates that the prothrombotic effect of EE is due to its molecular structure rather than to a first-pass liver effect (which they share). Moreover, these differences may explain why M-->F transsexuals treated with oral EE are exposed to a higher thrombotic risk than transsexuals treated with td E(2). Testosterone administration to female-to-male transsexuals had an antithrombotic effect.

Activated Protein C Resistance↗
PubMed2004

Thrombin generation in non-cardioembolic stroke subtypes: the Hemostatic System Activation Study.

BACKGROUND: The association between hemostatic activation, stroke mechanism, and outcome is poorly defined. The Hemostatic System Activation Study (HAS) investigators measured serial levels of prothrombin fragment F1.2, a marker of thrombin generation, in patients enrolled in the Warfarin Aspirin Recurrent Stroke Study (WARSS). METHODS: HAS enrolled 631 of the 2,206 patients in WARSS. Strokes were subtyped according to inferred mechanism. Plasma was collected for F1.2 at randomization (within 30 days of stroke), 3 months, 12 months, and 18 months. The 3 to 6 month samples in aspirin-treated patients were used for the primary analysis. RESULTS: The authors analyzed 3 to 6 month samples on 320 patients. Higher F1.2 levels were associated with older age, female sex, and hypertension. There was no difference between mean F1.2 levels in 56 cryptogenic (0.9 +/- 0.32 nmol/L) and 114 non-cryptogenic (1.13 +/- 0.74 nmol/L) patients or across specific stroke subtypes. There was an 8.8%/year (p = 0.006) increase in mean F1.2 levels. There was a trend toward higher risk of recurrent stroke or death as F1.2 levels increased in aspirin (RR: 1.30, 95% CI: 0.57 to 2.94, p = 0.53) and warfarin treated patients (RR: 1.68, 95% CI: 0.48 to 5.94, p = 0.42). F1.2 levels were reduced on average 70% in warfarin-treated patients in a dose-dependent fashion. CONCLUSION: F1.2 levels did not appear to differ by stroke subtype, suggesting that factors other than underlying stroke pathophysiology influence thrombin generation in the post-acute stroke period. F1.2 levels were suppressed by warfarin in a dose-dependent fashion. Additional research is needed to determine the predictive value of F1.2 after stroke.

Aged↗
PubMed2001

Genetic aspects of the hemostatic system in cerebrovascular disease.

Despite considerable research into the pathogenesis of cerebrovascular disease (CVD), acute stroke is the third most common cause of mortality in the Western world. The clinical management of acute stroke is largely supportive, although evidence is emerging for the benefit of early pharmacologic intervention. Even when the benefits of these therapies are accounted for, a significant proportion of patients remain disabled or die. Accordingly, stroke prevention is likely to offer the most effective manner of reducing stroke incidence. However, effective prevention depends on a reliable means of identifying and treating the risk factors associated with stroke and possibly targeting preventive measures at high-risk groups. Atherosclerosis is the process responsible for the development of ischemic CVD, and evidence is accumulating to suggest that these disorders are multifactorial, resulting from a complex series of interactions between genes and the environment. The outward expression of the disease, or the disease phenotype, is in part the product of gene-gene and gene-environment interactions. Research methods harnessing molecular biology techniques, including polymerase chain reaction (PCR) and sequencing have, in contrast to coronary artery disease (CAD), been under-utilized when it comes to furthering our understanding of the molecular epidemiology of CVD. This article reviews the evidence that stroke has a genetic basis and that the hemostatic system is an important risk factor for stroke. The genetic regulation of a number of these hemostatic proteins is evaluated.

Homeostasis↗
PubMed1984

Chitosan: a new topical hemostatic agent for diffuse capillary bleeding in brain tissue.

The effectiveness of chitosan as an intraoperative topical hemostatic agent for brain tissue was tested. Cerebral cortical lesions were made in 10 cats. Chitosan was used to obtain hemostasis. The elapsed time from the application of the hemostatic agent to hemostasis was determined. The animals were killed and the lesions were examined grossly and microscopically to evaluate the biocompatibility of chitosan. Chitosan was easy to apply and required minimal subsequent manipulation. Histopathological examination revealed that chitosan is biocompatible with cerebral cortex.

Animals↗
PubMed1991

Blood coagulation and fibrinolysis in SART-stressed (repeated cold-stressed) rats and drug effects on the altered hemostatic parameters.

Blood coagulation and fibrinolytic activity was studied in SART (specific alternation of rhythm in temperature)-stressed animals found to exhibit thrombocytopenia and prolonged bleeding time, and drug effects on the abnormalities were evaluated. 1) SART-stressed rats revealed prolongation of activated partial thromboplastin and thrombin time, no change in prothrombin time, decreased plasma fibrinogen levels, and shortened euglobulin clot lysis time (ELT). Antithrombin III and alpha 2-plasmin inhibitor activity remained constant following stress exposure. 2) During stress, fibrinogen levels declined from day 5 and remained depressed up to day 14. Reduction in ELT developed in a similar manner to fibrinogen. 3) Decreased fibrinogen levels were prevented by consecutive doses of tranexamic acid, an antifibrinolytic, and Neurotropin, a sedative analgesic. Shortened ELT was counteracted by chronic treatment with Neurotropin and alprazolam, an anxiolytic. Single administrations of the above agents failed to affect either change. These results indicate that SART-stressed animals exhibit suppressed intrinsic coagulability and enhanced fibrinolytic activity, but normal extrinsic coagulability. Considering the previous report together with the above results, the hemostatic system under SART stress tends uniformly toward hemorrhage. Moreover, Neurotropin appears to improve and normalize hemostatic imbalance due to SART stress, a chronic form of stress.

Alprazolam↗
PubMed2001

Hemostatic problems before, during and after delivery.

Normal pregnancy and childbirth are known to be associated with marked changes in the coagulation and fibrinolytic systems. Generally, enhancement of clotting activity persists to prevent the risk of major hemorrhage. Hemostatic problems, either associated with a specific complication of pregnancy and labor or due to a hereditary or acquired bleeding diathesis or thrombophilias, present a significant cause of maternal and neonatal morbidity and mortality. This article reviews hemostatic disorders in pregnancy and the peripartal period from the standpoint of the obstetrician.

Blood Coagulation Disorders↗
PubMed1998

Relationship between flow dynamics in the left atrium and hemostatic abnormalities in patients with nonvalvular atrial fibrillation.

To investigate the relationship between left atrial (LA) flow dynamics and hemostatic markers in nonvalvular atrial fibrillation (AF), 45 patients with nonvalvular AF who had not received anticoagulants were evaluated by transesophageal echocardiography. We determined the LA appendage flow and the presence of LA spontaneous echo contrast (SEC) or thrombus. We measured plasma levels of thrombin-antithrombin III complex (TAT), fibrinopeptide A, D-dimer, beta-thromboglobulin, and platelet factor 4 in peripheral blood as hemostatic markers. The patients were divided into a low-velocity group (n = 19; sum of peak emptying and filling LA appendage flow velocities < 40 cm/s) and a high-velocity group (n = 26; > or = 40 cm/s). The maximum LA diameter was significantly greater and the LA expansion fraction was significantly smaller in the low-velocity group than in the high-velocity group. LA SEC or thrombus was observed in 11 patients (58%) in the low-velocity group, but not in any patients in the high-velocity group (p < 0.001). The plasma levels of TAT, fibrinopeptide A, D-dimer, beta-thromboglobulin, and platelet factor 4 were significantly higher in the low-velocity group than in the high-velocity group. The plasma levels of TAT, fibrinopeptide A, beta-thromboglobulin, and platelet factor 4 were significantly higher in 8 patients without LA SEC or thrombus in the low-velocity group than in 26 patients in the high-velocity group. Patients with nonvalvular AF accompanied by an enlarged and dysfunctioning LA and a decreased LA appendage flow velocity had increased intravascular coagulation-fibrinolysis activity and platelet activation. These abnormalities may be closely related to the thrombogenetic state in patients with nonvalvular AF.

Adult↗
PubMed2004

Recombinant Factor VIIa: clinical applications for an intravenous hemostatic agent with broad-spectrum potential.

Recombinant Factor VIIa (NovoSeven, Novo Nordisk) is a unique hemostatic agent with potential for broad-spectrum applications in bleeding patients with congenital and acquired bleeding abnormalities. At present, recombinant Factor VIIa is only approved for the treatment of hemophilia A and B patients who have acquired antibodies to Factors VIII and IX. However, the literature is rapidly expanding indicating that rFVIIa could benefit patients with bleeding due to a variety of etiologies. Unfortunately, the vast majority of these reports are case studies or small-series summaries, and are neither prospective nor controlled. Controlled trials are currently underway in several potential areas of application. While the possibility of thrombotic complications has been a clinical concern, safety data on patients treated to date have not revealed a significant problem. Expansion of the clinical applications for this interesting and important hemostatic agent are hampered by its expense, the limited scope of the US Food and Drug Administration approval for its use, and the absence of an appropriate laboratory monitoring assay.

Consumer Product Safety↗
PubMed2002

Molecular views and measurements of hemostatic processes using atomic force microscopy.

Hemostasis and thrombosis are highly complex and coordinated interfacial responses to vascular injury. In recent years, atomic force microscopy (AFM) has proven to be a very useful approach for studying hemostatic processes under near physiologic conditions. In this report, we review recent progress in the use of AFM for studying hemostatic processes, including molecular level visualization of plasma proteins, protein aggregation and multimer assembly, and structural and morphological details of vascular cells under aqueous conditions. AFM offers opportunities for visualizing surface-dependent molecular and cellular interactions in three dimensions on a nanoscale and for sensitive, picoNewton level, measurements of intermolecular forces. AFM has been used to obtain molecular and sub-molecular, resolution of many biological molecules and assemblies, including coagulation proteins and cell surfaces. Surface-dependent molecular processes including protein adsorption, conformational changes, and subsequent interactions with cellular components have been described. This review outlines the basic principles and utility of AFM for imaging and force measurements, and offers objective perspectives on both the advantages and disadvantages. We focus primarily on molecular level events related to hemostasis and thrombosis, particularly coagulation proteins, and blood platelets, but also explore the use of AFM in force measurements and surface property mapping.

Adsorption↗
PubMed2004

Normalization of multiple hemostatic abnormalities in uremic type 1 diabetic patients after kidney-pancreas transplantation.

To evaluate the effects of kidney-pancreas transplantation on hemostatic abnormalities in uremic type 1 diabetic patients, we conducted a cross-sectional study involving 12 type 1 diabetic patients, 30 uremic type 1 diabetic patients, 27 uremic type 1 diabetic patients who had a kidney-pancreas transplant, 12 uremic type 1 diabetic patients who had a kidney-alone transplant, and 13 healthy control subjects. We evaluated platelet and clotting system. Platelets in the group of uremic type 1 diabetic patients were significantly larger than platelets in the other groups. Resting calcium levels were significantly higher in the uremic type 1 diabetic patients and uremic type 1 diabetic patients who had a kidney-alone transplant than in the type 1 diabetic patients who had a kidney-pancreas transplant and control subjects. CD41 expression was significantly reduced in platelets from the uremic type 1 diabetic patients compared with the other groups. Levels of hypercoagulability markers in the type 1 diabetic patients who had a kidney-pancreas transplant and, to a lesser extent, the uremic type 1 diabetic patients who had a kidney-alone transplant but not the uremic type 1 diabetic patients were similar to those of the control subjects. A reduction in natural anticoagulants was evident in the uremic type 1 diabetic patients, whereas near-normal values were observed in the type 1 diabetic patients who had a kidney-pancreas transplant and uremic type 1 diabetic patients who had a kidney-alone transplant. Hemostatic abnormalities were not observed in type 1 diabetic patients who had a kidney-pancreas transplant. This finding might explain the lower cardiovascular death rate observed in type 1 diabetic patients who had a kidney-pancreas transplant compared with uremic type 1 diabetic patients who had a kidney-alone transplant or uremic type 1 diabetic patients.

Adult↗
PubMed2002

Tissue factor pathway inhibitor and other endothelium-dependent hemostatic factors in elderly individuals with normal or impaired glucose tolerance and type 2 diabetes.

OBJECTIVE: Impaired glucose tolerance (IGT) is believed to be a prediabetic phase that precedes the development of type 2 diabetes. In elderly subjects, IGT and diabetes are both independently associated with the occurrence of cardiovascular disease. Endothelial damage precedes atherosclerotic changes of the vascular wall. Therefore, several markers of endothelial dysfunction were examined in elderly subjects with IGT and elderly patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor type-1 (PAI-1), and thrombomodulin were studied as markers of endothelial dysfunction in a population-based study of elderly subjects with normal glucose tolerance (NGT) or IGT and type 2 diabetes. In addition to these endothelium-dependent factors, we also investigated tissue factor pathway inhibitor (TFPI) activity in relation to metabolic parameters and cardiovascular risk factors. RESULTS: All data were adjusted for age. Increased levels of vWF antigen, t-PA antigen, and PAI-1 activity were seen in the IGT and diabetic group compared with the NGT group. TFPI activity and thrombomodulin levels were increased in all elderly subjects, and no differences were seen between the groups. There was a positive association between HbA(1c) and TFPI activity and vWF antigen. Fasting blood glucose levels correlated with vWF antigen, t-PA antigen, and PAI-1 activity, whereas urine albumin excretion correlated with TFPI activity, vWF antigen, and PAI-1 activity. Serum insulin levels correlated strongly not only with vWF antigen and t-PA antigen but also with PAI-1 activity. This correlation did not change after further adjustment for serum glucose and HbA(1c), which may suggest that in the elderly subjects, impaired fibrinolysis is probably associated with insulin resistance. There were no associations between the endothelium-dependent hemostatic factors and lipids, except for a negative correlation between HDL cholesterol and thrombomodulin. CONCLUSIONS: In elderly subjects with IGT, several endothelium-dependent hemostatic factors are already consistently increased, indicating endothelial damage in this stage.

Aged↗
PubMed2002

Prevalence of insulin resistance syndrome in southwestern France and its relationship with inflammatory and hemostatic markers.

OBJECTIVE: To assess the prevalence and relationships of insulin resistance syndrome (IRS) with inflammatory and hemostatic markers in a representative sample of the population of Southwestern France aged 35-64 years. RESEARCH DESIGN AND METHODS: In this cross-sectional study, data were collected from 597 men and 556 women and were assessed regarding BMI, blood pressure, total and HDL cholesterol levels, triglyceride level, glucose level, plasma insulin level, white blood cell count, fibrinogen level, factor VII level, von Willebrand factor, C-reactive protein level, soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule-1, and soluble CD(14). Insulin resistance was defined by homeostasis model assessment > or =3.8. RESULTS: Prevalence of IRS was higher in men than in women (23 vs. 12%, respectively; P < 0.001) and increased with age in both sexes (9, 24, and 34% for age groups 35-44, 45-54, and 55-64 years, respectively, for men and 4, 10, and 21% for women). After adjusting for age, alcohol consumption, tobacco smoking, and also for menopause in women, subjects (men and women) with IRS had significantly higher white blood cell count, factor VII levels, coagulating factor VII levels, and C-reactive protein levels than the other subjects. In men, further increases in soluble intercellular adhesion molecule and soluble vascular cell adhesion molecule-1 were noted, whereas in women, the differences were borderline significant. Conversely, no differences were found in fibrinogen, von Willebrand factor, and soluble CD(14) in both sexes. CONCLUSIONS: IRS is relatively common in residents of Southwestern France and is related to a deleterious increase in hemostatic and inflammatory parameters.

Adult↗
PubMedDate not supplied

Hypoglycemia and hemostatic parameters in juvenile-onset diabetes.

Hypoglycemia was induced by intravenous infusion of insulin in six juvenile-onset diabetic subjects. Hemostatic parameters were assessed before insulin infusion and 0, 1, and 2 h after discontinuation of insulin infusion. The onset of hypoglycemia coincided with an enhancement of ADP-induced platelet aggregation in five of the patients; platelet aggregation returned to normal levels during the next 2 h. The recalcification time was significantly shortened at the onset of hypoglycemia and continued to decrease for the next 2 h despite the return of serum glucose to normal levels. Correspondingly, a significant increase in fibrinogen was found. The ethanol gelation test was positive in two patients 2 h after stopping insulin infusion. Platelet counts decreased significantly after stopping insulin infusion. Thus, insulin-induced hypoglycemia markedly affects hemostatic balance and may potentially lead to intravascular coagulation in juvenile-onset diabetic patients.

Adenosine Diphosphate↗
PubMed2003

Regulation of angiogenesis by the hemostatic system.

In recent years it has become apparent that the hemostatic system has a role to play in regulating angiogenesis. This is achieved by components of the coagulation and fibrinolytic systems regulating proteolysis in the milieu and context of extra cellular matrix and the fibrin clot. It is also an emerging paradigm that cryptic fragments, released by proteolysis from components of the coagulation and fibrinolytic systems, have a role to play in regulating angiogenesis. Presented herein is a brief overview of the regulation of angiogenesis by the hemostatic system.

Animals↗
PubMed1993

[Alterations of hemostatic markers in elderly patient with atrial fibrillation without a history of stroke].

To evaluate whether hemostatic abnormalities contribute to the increased risk of stroke, the authors prospectively studied the hemostatic markers (HM) (beta-TG, PF4, FPA, TAT, PIC, D-dimer) in 34 elderly patients with atrial fibrillation (Af) without a history of stroke (mean age 79.2) and 14 age-matched controls. In the Af group FPA was significantly higher than in the control group (p < 0.05). Among them, 8 patients showed a similar abnormal HM pattern as in cardioembolic is chemic stroke and in these, 4/8 patients had valvular disease (VD), 2/8 had hypertension (HT), 2/8 had congestive heart failure (CHF), 1/8 had diabetes mellitus (DM) and 1/8 had hyperlipidemia (HL). Eight patients showed the same abnormal HM pattern as atherothrombotic is chemic stroke and of these, 2/8 had HT as complications. Five patients showed combination of a HM abnormal pattern, that was observed in cardioembolic and atherothromboic ischemic stroke. The other 13 patients showed a normal HM pattern, were in these patients, 4/13 had HT, 1/13 had DM, 1/13 had VD, and 1/13 had CHF. The patients with VD complication tended to have embolic HM abnormality. Contrary to previous reports, nonvalvular Af patients do not necessarily tend to have high risk of cardioembolic stroke. Our data suggest difficulties in clinical diagnosis among Af patients with ischemic stroke whether it is cardio embolic or atherothrombotic.

Aged↗
PubMed1982

A simple hemostatic method using a metal shield for injury of a major cerebral artery.

A new hemostatic method has been devised that uses a metal shield for treating accidentally injured major cerebral arteries. The metal shield is made of stainless steel, and has a small plate on its outer surface that allows it to be held in a regular aneurysm clip holder. Three different sizes of shield are available. The metal shield is applied to an injured artery with Oxycel and Biobond and held for a few minutes. Bleeding stops instantaneously. This is a simple and effective hemostatic method for an injured artery of small size. Experimental results and clinical application of this method are described.

Animals↗
PubMed1977

Hemostatic and platelet kinetic studies in dengue hemorrhagic fever.

In an attempt to reveal certain aspects of the pathogenesis of the bleeding disorder in dengue hemorrhagic fever, hemostatic and platelet kinetic studies were carried out in 61 children with this disease. As has been shown by others, thrombocytopenia and hypofibrinogenemia were the two most prominent hemostatic defects constantly discovered. Increased intravascular clotting seemed to be one responsible factor, though not an outstanding one. This was evidenced by mildly and variably low factors II, V, VII, VIII, IX, X, and XII, and by mild to moderate increase of fibrin degradation products as well as low platelet counts and fibrinogen. In 11 cases platelet kinetic study revealed increased destruction as a main cause for the thrombocytopenia, most probably due to the underlying immunologic mechanism, i.e., via the immune complexes formed. Another factor was platelet dysfunction--the release of adenosine diphosphate.

Adenosine Diphosphate↗
PubMed1981

Hemostatic abnormalities following Echis carinatus (saw-scaled viper) envenomation in the rhesus monkey.

Hemostatic abnormalities following lethal and sublethal doses of Echis carinatus venom were studied in a subhuman primate model. The observations suggest the occurrence of disseminated intravascular coagulation of varying magnitude within a few hours of envenomation. A procoagulant effect of the venom of Echis carinatus is likely to be the major cause of the disturbance in the hemostatic mechanism.

Animals↗