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PubMed1984

Hemostatic disorders in 25 patients with limited and uncomplicated thyroid and breast cancer: prophylactic and therapeutic considerations.

In order to evaluate the efficacy of an anticoagulant treatment in neoplasia, we have looked for the existence and the possible role of hemostatic unbalance in patients affected by limited and uncomplicated thyroid and breast cancer by examining hemostasis in 25 patients. Our data allowed us to evidentiate an accelerated and increased fibrinoformation associated with the presence of plasminogen's activation inhibitor which overlaps the increased plasminogen's activators. We evidentiated also an increase of platelet functions in vitro and of their activation in vivo. These findings support the hypothesis of a possible role played by hemostasis alterations in the pathogenesis of thromboembolic complications, cancer growth and/or metastatization, and justify prophylactic and therapeutic anticoagulation.

Adult↗
PubMed1990

[Clinico-genetic and hemostatic disorders in viral hepatitis B].

Viral hepatitis B is characterized by pronounced chromatid and chromosome structural defects of peripheral blood T lymphocytes. The chromosome aberrations are longer in hepatitis B than in hepatitis A, in protracted and chronic forms in particular. Excessive circulating immune complexes occur in acute hepatitis. Their concentration is higher in protracted viral hepatitis B. Hemostasis is affected too: the more severe hemostatic abnormality, the more grave the disease. Hemocoagulation alterations are linked with the level of circulating immune complexes.

Adolescent↗
PubMed1983

Molecular markers of hemostatic disorders: implications in the diagnosis and therapeutic management of thrombotic and bleeding disorders.

With current technological advances, it is now possible to measure in less than 50 microL of plasma picomolar amounts of circulating products of platelet activation, products of protease activation related to coagulation and fibrinolytic pathways, and prostaglandin metabolites formed during a physiologic or pathologic process. Most of these markers, which circulate in blood in nanogram or picogram amounts per milliliter during or after pathologic activation, provide pertinent information on the status of a patient in terms of specificity and early detection, and will be of crucial value in the diagnosis of hemostatic defects and the management of newer antithrombotic drugs that cannot be monitored by currently available assays. Currently, 125I- and 3H-based simple radioimmunoassays are available for platelet factor 4, beta-thromboglobulin, fibrinopeptide A, B beta 15-42 related peptides, thromboxane B2, and the prostaglandins 6-keto-PGF1 alpha and PGE2. Nonisotopic methods such as enzyme-linked immunosorbent assays and fluoroimmunoassays are being developed. Serotonin and ADP, products of platelet activation, are measurable by liquid-chromatographic, immunoenzymatic, and spectrophotofluorometric methods. Analytical methods for fibrin split products (fragments D and E) and serine protease inhibitor complexes such as thrombin-antithrombin-III, factor Xa-antithrombin-III, and kallikrein-C1-esterase are also being developed. We have evaluated all of these methods and found them to be very sensitive to those components of endogenous activation of the hemostatic system listed above.

Blood Coagulation Disorders↗
PubMed2002

[An inherited hemostatic disorder as the cause of menorrhagia].

Two women aged 39 and 30 years were investigated for possible coagulation disorders because of menorrhagia, anaemia and postoperative haemorrhages. These investigations revealed that they had type 1 Von Willebrand's disease. During the treatment with desmopressin, factor VIII and Von Willebrand factor (VWF) activity normalised. About one third of the patients referred to a gynaecologist for menorrhagia have an inherited bleeding disorder, of which type 1 Von Willebrand's disease is the most prevalent. Once a gynaecological cause of the menorrhagia has been excluded, or in the case of an increased risk on the basis of the medical history, a limited haemostatic investigation can establish or exclude an inherited coagulation disorder. For women with a coagulation disorder the menorrhagia can be treated. Surgical interventions can be carried out safely following treatment with desmopressin or factor VIII/VWF concentrates.

Adult↗
PubMed1982

[Controlled substitution with blood products in hemostatic disorders].

It is essential for an efficient substitution to define the nature of the defect as good as possible. Simple screening tests allow a rapid classification. Prophylactic substitution is recommended in potentially reversible defects (bone marrow aplasia in connection with leukaemia treatment) and/or imminent bleeding (eventually complicated by additional risk factors). If bleeding cannot be stopped surgically therapeutic substitution is indicated. In case of bone marrow failure, a substitution may be particularly promising. In presence of an increased peripheral platelet destruction (disseminated intravascular coagulation, antithrombocytic antibodies) treatment of the basic disease is mandatory. Combined hemostatic defects can be influenced by fresh frozen plasma (FFP). Fresh whole blood (not older than 48 hours) may be considered in cases of thrombocytopenia and concomitant anemia. For isolated defects (e.g. hemophilias with or without antibodies, congenital afibrinogenemia, lack of factor XIII) special preparations are at hand. The clinical effect of substitution depends on the specific activity of the preparation, on the volume of expansion in the recipient and on other pharmacokinetic factors. Hepatitis and antibody-production may be considered as particularly grave side-effects.

Blood Coagulation Factors↗
PubMed2005

Management of excessive menstrual bleeding in women with hemostatic disorders.

Because there are many important considerations for managing excessive menstrual bleeding in women who have systemic disorders of hemostasis, a multidisciplinary approach is the best model for care. Specific attention to effective treatments is highlighted, but few studies have been performed in this population.

Blood Coagulation Disorders↗
PubMed2005

Requirements for research investigations to clarify the relationships and management of menstrual abnormalities in women with hemostatic disorders.

This article highlights a comprehensive range of research investigations which are required to clarify the relationships between the symptom of excessively heavy menstrual bleeding and different disorders of systemic hemostasis and their management. The need for these investigations was stimulated by an international workshop involving hematologists and gynecologists with expertise and interests in these fields. The field was reviewed by a group of experts who systematically considered nomenclature, definitions, investigations, and management and identified areas of uncertainty, controversy, or absence of information. This article is an extension of those preliminary research discussions. Recommendations are made for a range of important research studies to define the nomenclature, definitions, mechanisms, clinical investigations and management of heavy menstrual bleeding in women with disorders of systemic hemostasis.

Blood Coagulation Disorders↗
PubMed1994

Evaluation of desmopressin for dental extractions in patients with hemostatic disorders.

We evaluated the effectiveness of desmopressin to control bleeding of patients with coagulation defects during dental surgery. Thirty-five patients, mainly with moderate and mild hemophilia and Willebrand disease, were undergoing dental extractions (over 80 extractions in total). Bleeding was successfully prevented in 28 patients with the use of a combined treatment incorporating IV desmopressin, an antifibrinolytic agent (tranexamic acid), and local methods (surgical glue and compression techniques). Seven patients had a bleeding episode after dental extraction, which was controlled in two cases by repeated injection of desmopressin and in another two by local methods; Factor VIII substitutive treatment was needed in only three patients. Desmopressin offers an alternative to blood products to control bleeding risk in patients with moderate and mild coagulation defects. Our experience tends to specify the mode of administration of both desmopressin and the associated treatments. Our findings suggest that desmopressin can be used in conjunction with other treatments to prevent bleeding in patients with coagulation defects who undergo dental surgery. This work highlights the concept of multifactorial medical care of these patients in which desmopressin plays a major role.

Adolescent↗
PubMed2003

Homocysteine and hemostatic disorder as a risk factor for myocardial infarction at a young age.

INTRODUCTION: Hyperhomocysteinemia is a coronary risk factor, but its pathophysiologic mechanism remains unclear. MATERIALS AND METHODS: The importance of hyperhomocysteinemia in the pathogenesis of early myocardial infarction, was determined in case-control study of 127 men with a first early myocardial infarction <or=45 years and 150 age-matched male controls. We measured plasma concentrations of homocysteine, fibrinogen, antithrombin, tissue factor, tissue factor pathway inhibitor, tissue plasminogen activator, plasminogen activator inhibitor-I, plasminogen, alpha(2)-antiplasmin, lipoprotein(a), protein C, protein S, factor VII, and activated factor VII. RESULTS: Homocysteine concentrations were higher in patients with early myocardial infarction than in controls (11.2+/-5.3 and 8.3+/-5.0 micromol/l, respectively, P<0.001). Hyperhomocysteinemia was associated with early myocardial infarction (odds ratio=2.22, P<0.001) by multivariate logistic regression analysis. Tissue factor, antithrombin, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor-I, lipoprotein(a), diabetes, and smoking also had associations. In a stepwise logistic regression analysis, hyperhomocysteinemia was the strongest predictor of early myocardial infarction (R(2)=0.19, P<0.001). Hyperhomocysteinemia also had positive correlations with tissue factor (rho=0.26, P=0.009), tissue factor pathway inhibitor (rho=0.23, P=0.020), and tissue plasminogen activator (rho=0.25, P=0.011) in patients with early myocardial infarction, but not in controls. CONCLUSIONS: Hyperhomocysteinemia is an independent risk factor for early myocardial infarction, and is associated with a hypercoagulable state mediated by the extrinsic coagulation cascade.

Adult↗
PubMed1989

[A rare hemostatic disorder: pseudo von Willebrand's disease].

A case of pseudo von Willebrand's disease occurring in a 26 year old pregnant woman is reported. The diagnosis was made during the 33rd week of pregnancy. The patient had excessive bleeding of minor wounds, and biological tests revealed a bleeding time exceeding 20 min, a greatly reduced level of Rco fraction of von Willebrand's factor (27%), the absence of high molecular weight von Willebrand's factor multimers, and a greatly increased platelet aggregation in small doses of ristocetin. The patient was allowed to give birth by the vaginal route, receiving 30 IU.kg-1 highly purified concentrated factor VIII, once cervical dilatation was complete. Uterine revision was carried out for safety's sake because of prolonged post-partum bleeding. Two red cell packs were transfused as haemoglobin concentration decreased from 106 g.l-1 to 80 g.l-1. The newborn also presented with biological signs of pseudo von Willebrand's disease, with a bleeding time exceeding 15 min, hypothrombocytopaenia, and a level of Rco fraction of von Willebrand's factor of 9%. Preoperative assessment should always include an investigation of primary haemostatic mechanisms. In case of pseudo von Willebrand's disease, platelet transfusion combined or not with the transfusion of highly purified factor VIII seems to be useful. Investigation of other family members for a pseudo von Willebrand's disease trait is essential.

Adult↗
PubMed1992

[Hemostatic disorders following polytrauma--the role of physiologic coagulation inhibitors during the preclinical phase].

Coagulation changes due to polytrauma are considered to be an important determinant for the outcome. In this context, physiological inhibitors of activated coagulation are highlighted with special reference to antithrombin-III (AT-III). Blood samples of 20 randomly selected adults with polytrauma (Injury Severity Score mean = 36.7 +/- 8.6) were investigated. To investigate the very early onset of coagulation changes, samples were taken as early as possible at the site of emergency (mean = 18.3 +/- 5.5 min. after trauma) as well as at hospital admission (mean = 78.0 +/- 10.4 min.). By means of a specially designed "mini-lab", basic processing of the samples harvested (centrifugation, pipetting, freezing) was done on the spot to obtain haemostaseological results that agree as closely as possible with the subsequent analyses. Due to the activation of intravascular coagulation as well as the consumption of physiological inhibitors, comprehensive coagulation disturbances become obvious at the time of hospital admission. These are intensified by haemodilution as a consequence of high-dose fluid replacement. However, significantly elevated levels of specific coagulation reaction products (thrombin-antithrombin-III-complex) give evidence of the consumption of inhibitory potential exceeding haemodilution.

Adult↗