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At least 235 records · Page 13Linked to original sources
PubMed1989

Clinical manifestations and laboratory findings in patients with lupus anticoagulants.

Clinical and laboratory features were evaluated in 48 patients with lupus anticoagulants and the efficiency of three different assays in the detection of lupus anticoagulants was compared. The diagnosis of lupus anticoagulants was based on a prolonged activated partial thromboplastin test not corrected in a mixture of 1:1 with normal plasma and lack of specific inhibitors against coagulation factors. Platelet neutralization procedure was positive for lupus anticoagulants in 98% of the patients, tissue thromboplastin inhibition ratio in 79%, and kaolin clotting time index in 77%. At least one of the assays was positive in 100% of the cases. The largest minority of the patients (31%) suffered from systemic lupus erythematosus. The others had a variety of non-immunological disorders. In the 13 patients who had been operated on, only 1 with renal failure developed hemorrhagic complications after renal biopsy due to thrombocytopathy. The incidence of recurrent spontaneous miscarriage, immune thrombocytopenia and positive direct antiglobulin test, anti-nuclear and anti-DNA antibodies and VDRL was significantly higher in patients with lupus anticoagulants and systemic lupus erythematosus compared to patients with lupus anticoagulants but without systemic lupus erythematosus.

Autoantibodies↗
PubMed1976

Influence of cephalosporin antibiotics on blood coagulation and platelet function.

Administration of cephalothin to normal volunteers in maximal doses of 300 mg/kg per day resulted in a combined defect of platelet function and blood coagulation. No such abnormalities were evident after infusion of cefazolin or cephapirin at a maximal dosage of 200 mg/kg per day. The observed thrombocytopathy was similar to but less severe than that induced by carbenicillin or ticarcillin and was not reflected by a prolonged bleeding time test or impaired prothrombin consumption. Moreover, it was not a consistent finding in those persons receiving cephalothin. A separate defect involving blood coagulation appeared to result from delayed fibrinogen-fibrin polymerization and was evidenced by extended values of the activated partial thromboplastin and thrombin time tests. It remains uncertain whether the abnormalities described may constitute clinically important hemostatic disorders in patients with normal renal function receiving large doses of cephalosporin antibiotics.

Blood Coagulation↗
PubMed1979

Effect of peritoneal dialysis, haemodialysis and kidney transplantation on blood platelet function. I. Platelet aggregation by ADP and epinephrine.

Quantitation of the thrombocytopathy of uraemics may be one useful way of evaluating forms of therapy. 24 patients treated by haemodialysis and peritoneal dialysis at two different times had platelet aggregation studies whose parameters were compared with those of 24 normal persons, 5 successful transplants or 13 untreated uraemics. Renal transplantation and peritoneal dialysis improved platelet function. The haemodialysis procedure itself impaired platelet function: this was not due to heparin.

Adenosine Diphosphate↗
PubMed1989

Platelet dysfunction in acute megakaryoblastic leukemia.

Platelet function profiles were studied in 3 patients with megakaryoblastic leukemia. All patients had a moderate decrease in platelet counts with abnormal platelet retention. One patient who developed hemorrhagic diathesis had prolonged bleeding time. In all patients platelet aggregation was defective after the addition of ADP, collagen, adrenaline, or U46619, a thromboxane A2 agonist. Malondialdehyde was reduced in all patients, as was platelet serotonin. Plasma beta-thromboglobulin levels were normal in all cases whereas PF4 was markedly elevated in one. Platelet dysfunction was not reversed by clinical remission. These studies confirm that megakaryoblastic leukemia is associated with a thrombocytopathy which may play a role in hemorrhagic diathesis and should be taken into account in the management of these patients.

Blood Platelets↗
PubMed1985

Platelet X-ray microanalysis in patients with chronic renal failure.

The platelet element content was determined by semiquantitative X-ray microanalysis in 6 patients with chronic renal failure. The patients showed a different degree of thrombocytopathy expressed by impaired adhesiveness, epinephrine-induced aggregation and platelet factor 3 availability. The microanalysis indicated significantly increased quantities of phosphorus and copper in patients' platelets. Sodium and zinc showed a decrease in about half of the patients, whereas iron was significantly increased in at least 50% of the patients. Magnesium and potassium did not show any difference from the control. The results of sulfur, chlorine and calcium did not reveal a consistent pattern.

Arachidonic Acid↗
PubMed1984

Platelet aggregation defect in megakaryoblastic leukemia.

Platelet aggregation induced in vitro with ADP, adrenalin and ristocetin was tested in 7 patients with megakaryoblastic leukemia (MKL). All patients had normal or high platelet counts and presented with hemorrhagic diathesis including purpura ecchymosis and epistaxis. Platelet morphology was grossly abnormal and electron microscopy revealed few, or absence of, alpha-granules. Platelet aggregation was reduced in all the cases with at least one aggregating agent. Our studies confirm that MKL is often accompanied by a thrombocytopathy which should be taken into account in the management of these patients.

Aged↗
PubMed1977

Inherited platelet abnormalities associated with low factor VIII activity in the same family.

Six of eight examined members belonging to two generations of the same (NEG-TUR) family were shown to have functional changes in platelets and/or a moderate decrease of factor VIII activity (FVIII:C) in plasma, with normal values of factor VIII-related antigen (VIII R:AG). Platelet defects (mainly a reduced PF3 availability, present in five patients) and factor VIII decrease were combined differently in individual members. Only two male members with both the PF 3 and FVIII:C defects had moderate haemorrhagic symptoms following traumatic injuries. One of them had also an absent adhesiveness to glass, the other one an absent adhesiveness to collagen and a reduced platelet aggregation by ADP and by collagen. Bleeding time, platelet function tests (in the other members), and routine coagulation tests were within normal range; ristocetin aggregation was also normal in all members. We think that two inherited defects, a mild haemophilia A and a "sui generis" thrombocytopathy, co-exist in this family.

Adolescent↗
PubMed2001

The peculiar features of changing the hemostasis in children with chronic constipation.

Our purpose was to study the peculiarities of changing the hemostasis in children with chronic constipation. In the course of our investigation of hemostasis in children with chronic constipation, we found chronometric hypocoagulation with impairment of internal (XII, XI, IX, VIII) and external (II, V, VII, X) mechanisms of blood clotting, at the base of which is a deficit of vitamin K-dependent factors (II, VII, IX, X) and a slight impairment of the final stage of coagulation. In thrombocytovascular hemostasis, thrombocytopathy demonstrated increased adenosine-5-diphosphate aggregation and suppression of the internal route of fibrinolysis and endotheliosis. We must point out that all these changes lead to impairment of microcirculation in the form of thromboses, particularly in the submucous and mucous membrane vessels, which is confirmed by the morphologic findings. In the compensated form, chronometric hypocoagulation with a deficit of II, IX, and X factors is noted. In the subcompensated form, hypocoagulation increases, and the deficit of V and VII factors is in part the cause. Endotheliosis and the increase of the thrombogenesis dynamics are noted in the thrombocytovascular section. In the decompensated form, there is marked hypocoagulation. Low activity of antithrombin III leads to high content of fibrinmonomeasured complexes in combination with reduction of the thrombocytes quantity and to hypercoagulation. The present changes are confirmed by the morphologic research methods of studying the vascular channel of the large intestine wall, where organized thrombi and a marked plethora of neutrophil tissue infiltration are often revealed.

Adolescent↗
PubMed1976

[Anti-thrombocyte antibodies].

1. There are two possible ways in which platelets may be involved in immune reactions: a) as target cells for antiplatelet antibodies, and b) as receptor cells for circulating antigen-antibody complexes. Since most of the clinical tests used to detect "antiplatelet antibodies" are incapable of discriminating between the two mechanisms, thrombocytopenia in many autoimmune diseases with "antiplatelet antibodies" may well be caused by immune complexes. 2. Immune reactions involving platelets do not always lead to thrombocytopenia. A moderate acceleration of platelet destruction can easily be compensated by increased production: this situation corresponds to a "compensated thrombocytolytic state". Evidence is also presented for immunologically induced functional platelet defects of "immunologic thrombocytopathy.

Agranulocytosis↗
PubMed1999

Recombinant factor VIIa is effective for bleeding and surgery in patients with Glanzmann thrombasthenia.

Recombinant activated factor VII (rFVIIa) was found to be effective and safe in treating 24 bleeding episodes and to prevent bleeding during one bilateral herniorrhaphy in four children with Glanzmann thrombasthenia. One of the patients had alloantibodies to platelet membrane glycoprotein (GP) IIb/IIIa and was refractory to platelet transfusion. rFVIIa was administered at 89 to 116 microg/kg per injection every 2 hours, in association with antifibrinolytic drugs. Bleeding stopped in all cases, but platelet transfusion was required in one. Two bleeding episodes recurred 36 and 63 hours after discontinuation of rFVIIa, but were successfully treated with additional doses. No adverse effects of rFVIIa were observed. Although the number of patients is small, our study suggests that rFVIIa may be an alternative to platelet transfusions in patients with a severe congenital thrombocytopathy.

Blood Loss, Surgical↗
PubMed2000

Recombinant activated factor VII (NovoSeven) treatment of platelet-related bleeding disorders. International Registry on Recombinant Factor VIIa and Congenital Platelet Disorders Group.

Recombinant activated factor VII (rFVIIa; NovoSeven, Novo Nordisk A/S, Bagsvaerd, Denmark), used extensively for the management of hemophilia patients with inhibitors, has also been shown to be effective in the treatment of severe bleeding episodes and for coverage of surgical procedures in patients with platelet disorders. Cases include seven patients with congenital platelet disorders [Glanzmann thrombasthenia (n = 5), Bernard-Soulier syndrome (n = 1), platelet type (pseudo-) von Willebrand disease (n = 1)] and two patients with acquired thrombocytopathy associated with myelodysplastic syndrome and uremia. The clinical efficacy of rFVIIa in functional platelet disorders has been reported as good or excellent, although some cases of ineffectiveness exist. The agent is well tolerated with a single published case of thromboembolism as a postoperative complication. In addition to these reported cases, there are others that remain unreported and unpublished. An International Registry on Recombinant Factor VIIa and Congenital Platelet Disorders (forms in Appendix 1) has been established to obtain more safety and efficacy data on patients with congenital platelet disorders treated with NovoSeven. Analysis of data from this larger population will allow better comprehension of the role of NovoSeven in these disorders, and assist in the design of formal studies to address issues associated with the treatment of these disorders.

Blood Coagulation Disorders↗
PubMed2000

Capillary microscopic and rheological dimensions for the diagnosis of von Willebrand disease in comparison to other haemorrhagic diatheses.

It is known that angiodysplasia influence macrocirculation as well as microcirculation in patients with vWD. In the present study it was examined if intravital capillary microscopic dimensions (morphologic and dynamic) in skin (nailfold) in combination with rheologic parameters could give indications for the presence of vWD in patients with haemorrhagic diathesis. Patients with vWD (n = 100; 92 type 1: definite type 1:78 and possible type 1:14: 8 type 2A) have in comparison to patients with other haemorrhagic diathesis [thrombocytopathy (n = 122), thrombocytopenia (n = 101). severe haemophilia A (n = 50) and severe haemophilia B (n = 20). congenital dysfibrinogenaemia (n = 22), oral anticoagulation with phenprocoumone (n = 112)] and to apparently healthy subjects (n = 100) a significantly increased capillary torquation (median index: 3.5), a venolar and an arteriolar capillary dilatation (median: 16.5 microm; median: 15.1 microm) and the highest part of microscopic bleedings (extravasates) with 40% in the video capillary microscopy as morphological changes. Only the congenital dysfibrinogenaemia appears with a larger dilatation in venolar capillaries (median: 14.5 microm). Microscopic bleedings are much less common in other haemorrhagic diatheses with a frequency between 4% and 13%. In the vWD a significantly reduced duration of reactive hyperaemia (median: 150 sec). This is the only dynamic change that can be taken as a possible hint for a loss of flexibility within the precapillary vessels. A significantly reduced plasma viscosity (< 1.25 mPas) is typical for the vWD due to the increase of the shear stress in blood plasma because of the reduction of vWF-activities. Changes of the capillary morphology (dilatation, extravasates, capillary torquation) and the hypoplasmaviscosity are most sensitive for the vWD (75%, 65%, 40%, 80%) with a fairly high specifity (up to 93%) and a positive predictive value of 99%. As a conclusion it seems reasonable to discuss the introduction of video capillary microscopy as a screening test for haemostasiological and angiological centers.

Adult↗
PubMedDate not supplied

[Effects of basic therapy of ischemic heart disease on vascular-platelet hemostasis during myocardial revascularization].

Effects of preoperative therapy of coronary diseases with calcium antagonists and aspirin on vascular platelet hemostasis during aortocoronary shunting (ACS) have been studied in order to evaluate the role of hemostasis disorders in the pathogenesis of perioperative hemorrhagic complications. Therapy of coronary disease with these drugs during preparation to ACS can involve changes in platelet functional activity, depending on the individual sensitivity of patients. Drug-induced thrombocytopathy can induce pathological hemorrhages in the perioperative period of ACS.

Adult↗
PubMed1975

[Recurring retinal haemorrhages with tortuosity of the retinal arteriols (author's transl)].

Four young and healthy adults with tortuosity of the retinal arterioles of the posterior pole and recurring superficial retinal haemorrhages are described. Two of them had a suspected mild thrombocytopathy without clinical manifestations in other organs. Inheritance of the syndrome was not demonstrated and the pathogenic mechanism still remains obscure. All the described patients had been at risk of a retinopathy of praematurity. Knowing that familial retinal haemorrhages without retinal tortuosity do occur and retinal tortusity may persist as a minimal change of retinopathy of praematurity, it is suggested that this syndrome might be a combination of two entities.

Adult↗
PubMed2003

[Strokes and their causes in children].

Based on the literature and their own observations of 44 children aged 5-15 years (27 girls, 17 boys) with prior strokes, the authors characterize the types of strokes and principle causes of the disease as follows: (1) intracerebral and subarachnoidal hemorrhages (key etiology--arteriovenous malformations, blood disorders, coagulopathy, thrombocytopenias, thrombocytopathy, etc.) and (2) ischemic strokes i.e. (i) thrombotic (congenital and acquired vascular aplasias, angiitis, antiphospholipoid and viral vasculopathy, blood system coagulate activation, etc.); (ii) embolic (cardiogenic, septic, placental, etc.) and (iii) hemodynamic as a consequence of severe cardiomyopathy and disrupted total hemodynamics. The definitions of metabolic stroke as a complication of mitochondrial encephalopathy, homocystinuria and non-differentiated stroke caused more often by emergence of pathologic weariness of connective tissues were suggested. To elicit the stroke causes and types in children, the authors propose a reliable algorithm for clinico-instrumental diagnostic screening in acute period of stroke.

Adolescent↗
PubMed1992

[The immunodiagnosis of thrombocyte membrane glycoprotein deficiencies: Glanzmann's thrombasthenia, Bernard-Soulier syndrome and GMP-140 protein deficiency].

Immunological methods were developed for the diagnosis of platelet membrane glycoprotein (GP) deficiencies. The number of membrane GP on platelet surface was determined as the binding of 125I-labeled monoclonal antibodies (mAB) directed against individual platelet GP. Total amount of GP in platelet lysate was assessed by immunoblotting with specific polyclonal antibodies. Methods were applied for patients with different thrombocytopathies. Binding of mAB VM16a, directed against GP IIb-IIIa was strongly decreased in patients with Glanzmann's thrombasthenia (0.5-14.5% of normal) and binding of anti-GP Ib mAB VM16d--in patient with Bernard-Soulier syndrome (0.5% of control) indicating the deficiencies of corresponding GP. In patient with gray platelet syndrome binding of both antibodies was not decreased but even increased. It was shown by immunoblotting that platelets from the patient with gray platelet syndrome contained normal amount of GP IIa, but strongly decreased amount of GMP-140 (14.5% of control)--membrane GP of platelet--granules.

Antibodies, Monoclonal↗
PubMed1976

[Complications during and following tonsillectomy].

Not considering the complications due to anesthesia, postoperative hemorrhage is certainly the most frequent complication following tonsillectomy. When injury of a major vessel can be ruled out as the cause of bleeding, a discrete disturbance of hemostasis must be considered. These are mainly thrombocytopathies or a pathologically increased fibrinolysis which were not detected by routine tests and the past history. Preoperatively one should ask for more or less regular use of analgesics containing salicylates which should not be administered postoperatively. The worst attitude is case of a post-tonsillectomy hemorrhage is to do nothing or to rely on non-specific measures hoping that the bleeding will stop anyway.

Aged↗
PubMed2005

[Treatment of patients with chronic adenoiditis and abnormal coagulation].

Chronic adenoiditis (CA) prevails among ENT diseases in children. It often demands surgical intervention. Frequent hemorrhagic complications during adenotomy necessitate assessment of the patient's hemostasis. A preoperative examination of 43 children has detected primarily dysaggregation thrombocytopathies. Streptococcus pneumoniae is a dominating etiological agent. Chronic focal infection is involved in pathogenesis of systemic disorders in CA including those provoking coagulatory disturbances. An algorithm of hemostatic disorders diagnosis in CA children is proposed as well as an effective program of targeted pre- and intraoperative hemostatic therapy.

Adenoidectomy↗