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At least 253 records · Page 14Linked to original sources
PubMed1991

[Thrombocytic component of hemostasis in patients operated on for acute inflammatory diseases of the abdominal organs].

Thrombocytopathy in the form of dissociation of functional properties of the thrombocytes was revealed in patients with purulent appendicitis. Patients with restricted peritonitis had an increased amount of thrombocytes, activation of their functions, changes in the thrombocyte formula, different correlative interrelations between the size of thrombocytes and their properties.

Acute Disease↗
PubMedDate not supplied

[Pre-hospital diagnosis of nosebleed in children].

Early signs of haemorrhages develop in the childhood, nose bleeding being predominant. Recurrent nose bleeding was observed in 130 (89.0%) patients with thrombocytopathies, 37 patients with nasal pathologies, 13 out of 14 children having willebrand's disease, 3 patients suffering from Rendu-Osler disease, in a boy with a factor XIII deficiency, and in a girl with psoriasis. In the case of haemorrhagic diathesis, nose bleeding was, as a rule, combined with haemorrhages of other types (skin, gum, uterine, etc.) whereas in the case of ENT pathology, nose bleeding was the only haemorrhagic symptom. Medical examinations of patients suffering from recurrent nasal haemorrhages at the prehospital stage should include: study of the history case, ENT-doctor examination, and blood analysis using standard tests (micro-coagulation, prothrombin, hemolysate-aggregation). The battery of blood tests can be performed without costly equipment or reagents. It became routine in the work of a regular polyclinical laboratory and helped identify the causes of nose hemorrhages in 94.6% children.

Blood Coagulation Disorders↗
PubMedDate not supplied

Platelet abnormalities in hepatobiliary diseases.

Platelet abnormalities associated with hepatobiliary diseases include increased (thrombocytosis) and decreased (thrombocytopenia) numbers of platelets as well as abnormalities in function (thrombocytopathy or thrombasthenia). Hepatic diseases that are accompanied by platelet abnormalities include hepatitis, cirrhosis, portal hypertension, and neoplastic disorders both benign and malignant. The objective of this work is to examine the platelet abnormalities that occur with a variety of hepatobiliary disorders. Thrombocytosis is seen as a reactive entity following splenectomy. Thrombocytopenia is associated with hypersplenism, dysproteinemias and liver disease related disseminated intravascular coagulation (DIC). Qualitative platelet abnormalities are found in hepatic failure, liver diseases associated with high or low levels of lipid, and with medications given for a variety of hepatocellular diseases. Clinically common and significant platelet abnormalities associated with liver disease are thrombocytopenia secondary to portal hypertension and the thrombasthenias following metabolic changes and/or therapeutic interventions of liver disease.

Biliary Tract Diseases↗
PubMed1990

[Psychodiagnosis and psychotherapy in medico-social adaptation of patients with hemorrhagic diseases].

The investigations were conducted in 264 patients with hemorrhagic diseases. Based on the clinical and psychological analysis most of the patients were found to have borderline psychic disorders. Psychotherapy has promoted diminution of psychic disorders, and in patients with hemorrhagic thrombocytopathy it has resulted in decreased hemorrhage and improved platelet function.

Adaptation, Psychological↗
PubMedDate not supplied

[Characteristics of hemostatic disorders in septic shock in children].

Changes at different stages of coagulation cascade have been assessed during intensive therapy of septic shock in 40 children aged 1 to 14 years. Progressing septic shock is accompanied by chronometric and structural hypocoagulation with potential hypercoagulation in transfer samples, thrombocytopenia and thrombocytopathy. Terminal stages of septic shock are characterized by profound hypocoagulation without potential hypercoagulation, predominance of antithrombin and antiaggregant blood activity with persistent depletion of antithrombin III and plasminogen. The decrement of arterio-venous difference in hemostasis parameters is typical of marked stages of the shock lung. Dynamic control over hemostasis shifts makes it possible to predict the outcome of septic shock.

Adolescent↗
PubMed1989

Functional and morphological studies on blood platelets in a thrombasthenic horse.

A four-year-old Standardbred gelding presented with a 3.5 year history of intermittent epistaxis and spontaneous submucosal petechiae and ecchymoses in the nares and the mouth. Routine haematological and biochemical examinations were unremarkable. A thrombocytopathy was suspected when activated partial thromboplastin time, one stage prothrombin time, plasma fibrinogen and the platelet count were all normal. The patient's platelets failed to aggregate with serotonin, adenosine diphosphate, collagen (at 20 micrograms/ml) or the endoperoxide analogue U46619. Very high levels of collagen (100 micrograms/ml) did cause aggregation. The response to the calcium ionophore A23187 was reduced and although complete degranulation occurred the resulting aggregates were unstable. Thromboxane generation in response to collagen and ADP was inferred from the concentration of its stable metabolite thromboxane B2 and was reduced. A diagnosis of a thrombasthenia-like syndrome possibly equivalent to Type II Glanzmann's thrombasthenia in people was made.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

The effect of alkaline phosphatase on platelet aggregation.

Elevated concentrations of alkaline phosphatase occur in a variety of diseases. The effect of alkaline phosphatase on platelet aggregation was tested. Adenosine diphosphate-induced aggregation was inhibited at the highest concentrations of alkaline phosphatase employed. Similar results were observed when epinephrine, collagen and arachidonic acid were used as aggregating agents. A dose-dependent inhibition of ristocetin-induced aggregation by alkaline phosphatase was observed. These results were confirmed using plasma from patients with cholestatic disease and elevated concentrations of alkaline phosphatase similar to those used in the in vitro studies. These data indicate that patients with significantly elevated levels of alkaline phosphatase may be predisposed to a thrombocytopathy.

Adenosine Diphosphate↗
PubMed1988

[Measurement of bleeding time and study of thrombocyte aggregation. Standardization of methods, normal values and results in patients with suspected hemorrhagic diathesis].

Bleeding time measurement and investigation of platelet aggregation in platelet rich plasma (PRP) are routine procedures for the diagnosis of defects in primary hemostasis. These tests are subject to methodological difficulties and should be well standardized in each individual laboratory. - In the present study, bleeding time was measured using the Simplate II device in 40 normal subjects. Furthermore, platelet aggregation in PRP induced by ADP, collagen, arachidonate, and ristocetin was examined. 26 patients referred for investigation of a suspected mild bleeding disorder, who had a normal plasmatic coagulation profile, a normal von Willebrand factor activity, and a normal platelet count, were similarly studied. - Based on the reference values established in the 40 normal subjects, platelet aggregation was found to be pathologic in 7 patients and normal in 12. In 7 patients platelet aggregation was considered to be borderline-pathologic as defined by the range of platelet aggregability found in the 10% of our normal subjects showing the weakest aggregation responses. Bleeding time was prolonged in only 3 patients whereas it was normal in the remaining 23. There was strong evidence of a hemostatic defect as assessed by systematic patient history in 6 out of 7 patients with pathologic platelet aggregation, but in only 3 out of 19 showing normal or borderline-pathologic aggregation. - Pathologic platelet aggregation, therefore, represents not only an abnormal laboratory finding but is likely to be associated with a hemorrhagic diathesis. Platelet aggregation studies do not permit etiologic diagnosis of the thrombocytopathy except for the well-defined membrane glycoprotein deficiencies. The bleeding time appeared to be of low sensitivity for the diagnosis of mild platelet dysfunction.

Adolescent↗
PubMed1986

[Leukocyte-thrombocyte interactions in chronic myeloleukemia and erythremia].

An effect of the leucocytes of patients with chronic myeloproliferative diseases on the formation of cellular microthrombi in vitro was studied. A high degree of correlation between the amount of leucocytes and the rate of mixed cell leucocyte-thrombocyte aggregation was shown. The clinical signs of enhanced leucocyte-thrombocyte interactions in patients were disorders of microcirculation and intravascular microthrombus formation. It was shown that leucocytes could compensate the manifestations of thrombocytopenia and thrombocytopathy in chronic myeloproliferative diseases. The main types of leucocyte-thrombocyte interactions were singled out. An important role of erythrocyte hemolysis in the initiation of leucocyte-thrombocyte contacts was established. It was proposed that an increased amount of leucocytes especially in noticeable "rejuvenation" of their structure, should be regarded as one of the humoral factors of thrombogenicity in chronic myeloproliferative diseases.

Adult↗
PubMed1987

Effect of lomustin on some platelet functions in vitro.

The effect of lomustin on platelet functions was investigated in vitro using a wide battery of tests. Lomustin was found to act as a specific inhibitor of platelet aggregation, release reaction and clot retraction and to induce acquired thrombocytopathy. Thus, impairment of platelet functions might play a role in hemorrhagic complications accompanying lomustin therapy in some cases.

Adenosine Diphosphate↗
PubMed1986

[Sepsis and blood coagulation].

Septicemia is frequently accompanied by changes in the plasmatic as well as cellular coagulation systems and by microclot formation. The occurrence of a hemorrhagic diathesis and microthrombosis is best explained by the syndrome disseminated intravascular coagulation (= consumption coagulopathy). Disseminated intravascular coagulation can be initiated by different agents and by different pathways. The activation of coagulation by endotoxin is well studied; it is mediated by synthesis of tissue factor by monocytes and endothelial cells. The formation of microthrombi is caused by the precipitation of circulating soluble fibrin under the influence of localizing factors, and it is observed under conditions of reduced fibrinolysis activation. Furthermore, thrombocytopenia, thrombocytopathy and endothelial cell damage caused by a direct effect of the toxic agent contribute to the bleeding diathesis.

Blood Coagulation↗
PubMedDate not supplied

[Thrombosis in disseminated lupus erythematosus].

In the course of disseminated lupus erythematosus (DLE), the development of arterial or venous thrombosis is sometimes observed. They are rare in the course of hematological forms of DLE, in which the more or less constant leucopenia is accompanied to variable extent by the affection of the other blood-lines: thrombocytopenia and/or thrombocytopathy and/or hemolytic anemia. The discovery of a circulating anticoagulant seems to be correlated with the existence of thrombosis. In fact it involves antiphospholipid antibodies, responsible for the protraction of certain coagulation tests, which shows up their existence. Recent studies have shown recognition of the membrane phospholipids of the vascular endothelial cell. A functional imbalance in this would be observed to encourage the synthesis of factors favorable to thrombosis.

Abortion, Spontaneous↗
PubMed1986

[Tendency toward bleeding in Noonan syndrome].

Bleeding tendency in Noonan-patients is only sporadically mentioned in literature. There is no equivocal opinion about its cause. By means of a questionnaire data were collected from 29 Noonan-patients, registered in our hospital. In about half of these patients these data indicated the existence of a bleeding tendency. Some of these patients revealed a marked thrombocytopathy characterised as a disturbance in secondary aggregation. Further research into the cause is desirable.

Adolescent↗
PubMed1975

A new abnormality of platelet functions. Association of storage pool disease (thrombocytopathia A) with impaired reactivity of platelets to collagen.

Multiple platelet abnormalities were found in a patient with bleeding symptoms. The platelet content of ADP and PF 4 was decreased and the uptake of 14C-serotonin was impaired. The content of acid phosphatase, beta-glucuronidase and beta-N-acetylglucosaminidase was, however, normal and these enzymes were normally released or made available by bovine fibrinogen or ADP. There was no adhesion of platelet to collagen, which also failed to induce reptilase clot retraction, platelet aggregation and release of any of the platelet constituents. The platelets therefore exhibited signs of thrombocytopathy of a combined type with a decreased storage pool as well as a qualitative dysfunction with impaired reactivity to collagen.

Adenosine Diphosphate↗
PubMed1977

Influence of cytotoxic drugs on platelet functions and coagulation in vitro. IV. Melphalan.

Influence of melphalan on some platelet functions, plasmatic coagulation and fibrinolysis "in vitro" was investigated, using different concentrations of the drug (25, 50 and 250 mug/ml). The lowest concentration slightly inhibited adrenaline and/or collagen-induced platelet aggregation. Following the highest concentration of the drug, strong inhibition of aggregation was recorded, regardless of the inducer used. Melphalan was also shown to inhibit release of aggregating activity and release of platelet factor 4, as well as availability of platelet factor 3 and platelet acid phosphatase. The intensity of inhibition depended on both, melphalan concentration and the time of preincubation. In contrast to this, adhesion of platelets to glass slide was not found to be influenced by melphalan. Similarly, melphalan did not induce (in any concentration) loss of LDH from platelet cytoplasma, while triton X-100 or freezing and thawing of platelets caused significant increase of LDH activity. From coagulation tests studied, only thrombin time and reptilase time was found to be moderately prolonged in the presence of melphalan. Authors assumed that melphalan acts as a specific inhibitor of release reaction and can induce an acquired thrombocytopathy. The platelet membrane is not damaged by the drug, as was confirmed by the investigation of LDH activity. Influence on coagulation indicates some antithrombin effect of the drug. Although presented results were obtained in vitro, analogous changes in vivo could be suspected. Thus, impairement of platelet functions might play a part in haemorrhagic complications accompanying, in some cases, melphalan therapy.

Acid Phosphatase↗
PubMed1978

[Thrombocyte function in acute leukemia].

The literature data on the condition of the platelet part of the homeostasis in patients with acute leukemia are summarized. The importance of functional changes in blood plates in the development of hemorrhagic complications is demonstrated. In acute leukemia, the development of various platelet syndromes such as thrombasthenia, thrombocytopathy, including a deficiency of the pool of storage of athrombia is possible.

Acute Disease↗
PubMed1981

Daunorubicin and platelet function.

The influence of Daunorubicin on some platelet functions in vitro was investigated, using different concentrations of the drug (0.01-0.02-0.04 microgram/ml). Daunorubicin was shown to inhibit Collagen and Thrombin induced platelet aggregation and the intensity of inhibition on both drug concentration and the time of preincubation. Daunorubicin was also shown to inhibit the release reaction, the platelet prostaglandin pathway and the availability platelet factor 3; the drug at concentrations for clinical use does not damage the platelet membrane, as is the case with the freezing and thawing test, in platelet uptake of 14C-serotonin and as confirmed by the electron microscope. When very high doses (0.16 mg) of Daunorubicin are used, lysis of the platelets can be observed and this is confirmed under the electron microscope by the presence of empty platelets with fractures at the level of the cytoplasmid membrane. Finally, Daunorubicin causes irreversible inhibition of reptilase clot-retraction, even if this is less severe than with Vincristine. Working with gel-filtered platelets, it would appear that the inhibition exercised by the drug on platelet reactions is not caused through modifications in Ca++ metabolism. The authors suggest that Daunorubicin, at the dosages used clinically, induces in vitro thrombocytopathy without damaging the cellular membrane as confirmed by the electron microscope. This impairment of platelet functions could play a part in hemorrhagic diathesis observed during Daunorubicin therapy.

Blood Platelets↗
PubMed1994

Coagulopathies of liver disease.

Disturbed liver parenchymal cell function adversely impacts on the hemostasis system, the extent of which correlates with the degree of liver disease. Because liver parenchymal cells synthesize most factors of the clotting and the fibrinolytic systems, levels of these procoagulant and anticoagulant as well as profibrinolytic and antifibrinolytic factors will decrease in plasma. These changes may be minor in patients with mild liver disease but are severe in patients with cirrhosis. Thrombocytopenia and thrombocytopathy usually complicate the clinical presentation, and systemic activation of the fibrinolytic system is always seen in cirrhotic individuals. Whether this fibrinolytic activation is primary or secondary in response to DIC is controversial. Some of the laboratory findings in DIC may be a reflection of decreased hepatic clearance of activation products by the reticuloendothelial system of the diseased liver. In patients with vitamin K deficiency or in those receiving oral anticoagulants, only the vitamin K-dependent procoagulants and anticoagulants are altered; all other parameters remain in the normal range. Laboratory changes associated with various surgical interventions involving the liver depend on the underlying pathology. Severe hemorrhages are encountered during orthotopic liver transplantation. During the anhepatic phase and during the reperfusion phase, there is a major activation of the fibrinolytic system. It is unclear whether this fibrinolytic response is primary or secondary. The use of antifibrinolytic agents has markedly reduced the clinical bleeding and, thus, the requirement for blood and blood products. Bleeding associated with partial liver resection is usually mechanical in nature, but peritoneovenous shunt operations can result in DIC. Ascites fluid is the trigger. The injection of thrombin containing sclerosants can also activate the hemostasis system in vivo, although, generally, no clinically detectable adverse reactions are noted.

Acute Disease↗