Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOCYTOPATHY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1996

Hemostatic alterations during continuous venovenous hemofiltration in acute renal failure.

In order to determine changes in hemostasis occurring during continuous venovenous hemofiltration (CVVH), we made a prospective study of 14 patients with acute renal failure. Fibrinopeptide A, thrombin-antithrombin III complex, beta-thromboglobulin and platelet retention were determined serially. Fibrinopeptide A (x +/- SD: 33 +/- 20 ng/ml, ref. < 3.0) and thrombin-antithrombin III complex (11 +/- 5 ng/ml, ref. 1.0-4.0) were enhanced prior to commencement of treatment but showed no further increase during therapy. Platelet retention (Hellem II, ref. 60-99%) fell from 39 +/- 32% before treatment to 16 +/- 15% after treatment, while the beta-thromboglobulin/creatinine ratio (ref. 0.23-0.41) rose from 0.39 +/- 0.20 to 0.64 +/- 0.44. Via platelet activation, CVVH leads to a reinforcement of the existing platelet dysfunction (thrombocytopathy), without influencing plasmatic coagulation. In order to analyze the influence of pre-existing hemostatic alterations on filter running time during CVVH, 60 patients were examined retrospectively in a second study. Filter running time, global coagulation tests, fibrinogen, antithrombin III, platelet count and hematocrit were registered daily. There was no significant correlation between filter running time and fibrinogen concentration, thrombin time, platelet count or hematocrit. Apart from filter occlusion, no thrombotic complications were observed. The frequency of filter occlusion increased with falling activated clotting time (ACT) (p < 0.05). Rising platelet count led to an increase in heparin dose (p < 0.05), primarily due to the anti-heparin effect of platelet factor 4.

Acute Kidney Injury↗
PubMed1996

[Use and preparation of thrombocyte concentrates].

Blood component transfusion therapy is an achievement of up-to-date transfusiology and is possible due to plastic equipment, centrifuge with air conditioning and modern technology which enables splitting blood into its components. Platelet concentration is a preparation of platelets gained from one unit of the whole blood and is used in therapy of patients with thrombocytopenias and thrombocytopathies. It can be preserved, depending on plastic bags, from 1 to 5 days with rotation on 22 degrees Celsius. This paper presents two methods of platelet concentration preparation (out of thrombocytes rich plasma and buffy coat) contribution of thrombocytes in concentrations and contamination of concentration with leucocytes, as well as changes during 72 hours of concentration preservation. One hundred units of thrombocytes had an average volume 51.42 ml. Platelet concentration gained out of thrombocyte rich plasma was 0.98 x 1011/l, and 0.80 x 109/l leucocytes. The number of thrombocytes in concentrations from buffy coat was 0.82 x 101/l, and 0.10 x 109/l leucocytes. Plasma pH after preparation was 7.21, and three days of conservation later it was 6.68. During these 72 hours of preserving the concentration there has not been a significant decrease in regard to the number of thrombocytes.

Humans↗
PubMed1977

[Septic shock in the urologic patient. II. Pathomechanisms of hemostatic disorders (author's transl)].

In urosepsis endotoxins usually deriving from gram-negative bacteria can initiate primary disturbances of hemostasis by activation of coagulation up to clinically manifest consumption coagulopathy. The reaction is triggered by an endotoxin induced alteration of granulocytes, endothelial cells, and platelets, thereby releasing procoagulant activities that possibly cause diffuse intravascular coagulation with impairment of vital organs. Additional negative effects on hemostasis can be caused by secondary hyperfibrino(geno)lysis. Secondary disturbances of hemostasis occur in urosepsis as a consequence of an impairment of liver (hypoproduction of coagulation factors, decrease of the clearance of activated coagulation factors) and kidney function (thrombocytopathy by uremic toxins). Disturbances of hemostasis induced by the treatment of urosepsis are the K-hypovitaminosis in parenteral feeding accompanied by antibiotics affecting the intestinal bacterial growth and the alteration of platelet function and fibrin formation by carbenicillin.

Carbenicillin↗
PubMed1997

[Hematological emergencies].

In this short review some important hematologic emergencies, that have been discussed at a round table on the occasion of the 22, meeting of internal medicine in central Switzerland are outlined without intention to be complete. The following emergencies are featured: Anemia, increased hematocrit (polyglobulia), severe (unexpected) neutropenia, marked hyperleukocytosis and leukemias, severe thrombocytopenia; thrombocytopathies (hereditary or acquired), von Willebrand-disease, acquired or hereditary coagulation disorders (coagulopathies), acute venous thrombosis; acute hemolytic transfusion reaction, posttransfusion purpura, severe autoimmune hemolysis.

Anemia↗
PubMed1977

[Anti-phospholipid antibodies as a cause of immunologic thrombopenia and thrombopathies].

The simultaneous occurrence of platelet antibodies (ab) and a circulating "antithromboplastic" anticoagulant in a patient with thrombocytopenia led to the hypothesis that antiphospholipid ab may be causing both phenomena. Of 55 sera obtained from thrombocytopenic patients exhibiting a positive microtest for complement fixation (CFT) with platelets, 37 also gave positive results with highly purified phospholipids (Phl) used as antigen. In order to further evaluate the role of Phl, 40 different liposome suspensions obtained by sonication of various mixtures of Phl (with/without addition of cholesterol) were tested as antigen in the CFT with 11 selected sera, and as platelet factor 3 (PF3) reagent in the partial thromboplastin time test with normal plasma. Eight liposome preparations with PF3 activity (all containing phosphatidyl-serine) were equally active as antigen (ag) in the CFT. Liposomes composed of phosphatidyl-ethanolamine and sphingomyeline delivered ag-activity only. Since the two substances are accessible components of the outer membrane surface of thrombocytes, anti-Phl-ab may well bind to platelets in vivo, causing thrombocytopenia. Coagulation-inhibiting activity of these ab could be directly demonstrated in a PF3-test system (thrombocytopathy caused by PF3 inhibition). The identity of antithromboplastic anticoagulant and anti-Phl-ab was further substantiated by immunoabsorption, since both activities were simultaneously eliminated from the sera with a Phl-charcoal adsorbent.

Antibodies↗
PubMed1998

[New possibilities in the management of hemorrhagic diathesis caused by factor deficiency and thrombocytopenia: recombinant active factor VII concentrate].

Recombinant Factor VIIa, a new therapeutic tool to treat severe bleeding caused by inhibitory haemophilia cases, some cases of thrombocytopenia and thrombocytopathy (e.g. severe type III von Willebrand disease) receives growing attention in clinical practice. Exogeneous FVIIa-in a supraphysiological concentration (clearly over 6 U/ml) seems to be able to generate quickly and safely (without thrombotic side effects) thrombin--the final enzyme of clotting--in physiological, or pathological conditions. A concise review about the possible mechanisms of action, indications, monitoring and clinical experience gained sofar with FVIIa is given in this report.

Factor VII↗
PubMed1998

[Constitutional thrombopathies: from the clinical description of rare diseases (Glanzmann thrombasthenia and Bernard-Soulier syndrome) to the development of new antithrombotic agents].

The study of exceptional thrombocytopathies has led to considerable progress in the understanding of normal and pathologic haemostasis. Thus, precise structure/function relationships were able to be established. The lack or the abnormalities of the glycoprotein IIb/IIIa complex is responsible for the complete defect in platelet aggregation characterizing Glanzmann's Thrombasthenia, while the lack or the abnormalities of the glycoprotein Ib/IX/V complex is responsible for the defect in platelet adhesion to the subendothelium noted in the Bernard-Soulier syndrome. The bases for these abnormalities are now known at the molecular level. Recent data also underline the role of these glycoproteinic complexes as receptors for platelet activation; besides an involvement of the GPIIb/IIIa complex in adhesion and of the GPIb/IX/V complex in platelet aggregation, von Willebrand factor dependent, were newly evidenced. New antithrombotic agents directed against the GPIIb/IIIa complex are currently being tested in large clinical trials, especially in cardiovascular diseases. In the future, the inhibition of the GPIb-IX-V/von Willebrand factor axis should permit the development of a new class of antithrombotics, perhaps even more promising since they will act at the very early phases of primary hemostasis.

Bernard-Soulier Syndrome↗