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PubMed1990

Platelet transfusion therapy.

This article reviews appropriate platelet support of those patients who are chronically thrombocytopenic because of decreased platelet production, including those receiving chemotherapy or radiation treatments and those undergoing bone marrow transplants. The platelet products available for transfusion and the indications for platelet transfusions are discussed. Expected responses to platelet transfusions are reviewed as well as the prevention of platelet alloimmunization. Finally, a discussion of the mechanisms and management of platelet refractoriness is included.

Adult↗
PubMed1987

Biochemical and functional changes of platelet stored for transfusional use.

A protocol for the biochemical study of platelet stored for transfusional use at 22 degrees C and under continuous shaking in a plastic bag highly permeable to gases and with a suitable area/volume ratio, is described. Plasmatic dextrose, lactic acid, lactic dehydrogenase activity, cellular ATP and malonyldialdehyde were monitored during the storage, as well as some acid-base indexes namely: pH, pCO2, HCO3-, pO2. The platelet functional status was checked as aggregating power induced by ADP and collagen and by beta-thromboglobulin release. The results obtained are indicative of a discrete maintenance of aerobic metabolism by platelets which are able to give up CO2 and take up O2 so that the plasmatic pH is constant during the storage. However, the malonyldialdehyde increase suggests that platelets become increasingly susceptible to peroxidative attacks. The aggregating response was dramatically reduced even on the third day of storage. The data obtained point out that, under the conditions reported, platelets can be transfused up to the third day of storage.

Blood Preservation↗
PubMed1988

Irreversible platelet fibrinogen interactions occur independently of fibrinogen alpha chain degradation and are not mediated by intact platelet membrane glycoprotein IIb-IIIa complexes.

Interactions between fibrinogen and human platelets leading to irreversible fibrinogen binding are poorly understood. Because fibrinogen possesses platelet recognition sites on both its alpha and gamma chains, the present study examined the hypothesis that irreversible platelet fibrinogen interactions occurred as a result of multivalent fibrinogen binding to platelet membrane glycoprotein IIb-IIIa complexes. Fibrinogen binding to human, gel-filtered platelets was assessed by using intact fibrinogen and a plasmic fibrinogen degradation product (8D-50) lacking intact alpha chains and resembling an intermediate fragment X. Irreversibly bound fibrinogen was defined as fibrinogen that remained associated with thrombin-stimulated platelets in the presence of 10 mmol/L ethylenediaminetetraacetic acid (EDTA) or excess unlabeled fibrinogen. The amount of intact fibrinogen that bound irreversibly to platelets comprised 54% +/- 12% (mean +/- SD, n = 8) of total binding. It was unaffected by fibrinogen receptor saturation and platelet alpha granule release. Similar amounts of 8D-50 (56% +/- 10%) bound irreversibly to platelets. Addition of 50 mumol/L arginine-glycine-asparagine-serine, after the initial binding of either fibrinogen or 8D-50, had no effect on the subsequent stabilization of platelet-fibrinogen or platelet-8D-50 interactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1988

The hemostatic effect of transfusing fresh whole blood versus platelet concentrates after cardiac operations.

The major cause of nonsurgical bleeding after cardiopulmonary bypass is delayed recovery of platelet count and function. Recovery of platelet count and function was compared in 27 patients who were randomized preoperatively to receive after cardiopulmonary bypass either 1 unit of fresh whole blood (15 patients) or 10 units of platelet concentrates (12 patients). Platelet count, bleeding time, platelet aggregation (adenosine diphosphate, collagen, epinephrine, and ristocetin) and platelet thromboxane formation were abnormal after cardiopulmonary bypass in all the patients. The increase of platelet count after 1 unit of fresh whole blood (from 115 +/- 32 X 10(9)/L to 148.5 +/- 36 X 10(9)/L) was similar to that achieved by 4 units of platelets (from 140 +/- 61 X 10(9)/L to 171 +/- 60 X 10(9)/L). The increase was doubled after 10 platelet units (from 140 +/- 61 X 10(9)/L to 209 +/- 55 X 10(9)/L). Bleeding time returned to normal values after fresh whole blood or after 8 platelet units. However, platelet thromboxane formation was higher after 1 unit of fresh whole blood than after 10 platelet units (95 +/- 25 versus 46 +/- 35 ng/ml, p less than 0.05), as was platelet aggregation response to collagen and epinephrine. The 24-hour blood loss was smaller in the fresh whole blood group (560 +/- 420 ml versus 770 +/- 360 ml), although the difference was not statistically significant. The results suggest that the hemostatic effect of 1 unit fresh whole blood after cardiopulmonary bypass is at least equal, if not superior, to the effect of 10 units of platelets.

Blood Transfusion↗
PubMed1988

Seven-day storage of single donor platelets in polyolefin bags: clinical, biochemical, morphological and microbiological evaluation.

We compared the in vitro and in vivo function of fresh and stored platelet concentrates (PCs) collected by an automated continuous-flow blood cell separator (CS 3000 Fenwal) in a closed-system apheresis kit in order to evaluate the possibility of extending the storage time to seven days with the polyolefin container (PL-732). The initial 220 ml platelet volume (5.14 +/- 1.23 x 10(11) was divided into two parts. Half was transfused and the other half was stored for 7 days. All cultured units were negative for bacterial contamination. Mean counts for fresh and stored platelets were respectively 2.34 +/- 0.59 and 2.17 +/- 0.50 X 10(11)/100 ml of PCs (mean recovery 88.7 +/- 11.9%). The pO2 levels were maintained during storage (179.9 +/- 30.5 mmHg) but pCO2, pH, LDH, osmolality, glucose consumption, bicarbonates, ATP, and osmotic stress values changed significantly after 7 days storage. From a clinical point of view, in 14 patients receiving a total of 38 PC transfusions no statistically significant change in corrected post-transfusional levels was observed between fresh and stored PC. Biochemical and morphological data and clinical results suggest that PCs collected with CS-3000 blood cell separator in a closed system and stored for 7 days in polyolefin bags (PL-732) can be satisfactorily employed in clinical practice.

Blood Platelets↗
PubMed1987

Shear stress activation of platelet glycoprotein IIb/IIIa plus von Willebrand factor causes aggregation: filter blockage and the long bleeding time in von Willebrand's disease.

The article explores the finding that high shear alone applied to normal, native blood results in platelet aggregation. A filter with tortuous capillary-sized channels permits a study of the effect of shearing forces at different pressures. Native, heparinized, citrated and EDTA blood and platelet-rich plasma (PRP) were forced through the filter. Normal and von Willebrand's blood were studied, as were the effects of antibodies to platelet glycoproteins (GPr) and to von Willebrand's factor (vWf) and of "membrane-active" drugs. Normally, the filter blocked at 40 mmHg but not at 5 mmHg. Transmission electronmicroscopy of the filter at 40 mmHg showed blockage by platelet aggregates. Initially, the mean transit time through the filter was 8 milliseconds. Platelet retention in the filter occurred in two phases. From 0 to 3 seconds, only high-shear, vWf, and GPrIIb/IIIa were required. From 10 to 20 seconds, retention presumably involved these three attributes, but divalent cations were also essential. Only this phase was inhibited by some membrane-active drugs. ADP- and thrombin-induced aggregation requires GPrIIb/IIIaand fibrinogen. Shear-induced blocking of the filter by blood with a normal concentration of fibrinogen requires GPrIIb/IIIa and vWf. This indicates a different type of exposure of GPrIIb/IIIa. The long bleeding time in vW disease highlights the absolute requirement for vWf and emphasizes the difference in exposure of GPrIIb/IIIa induced by shear stress. Evidently, a process similar to that occurring in the filter is required in normal capillary hemostasis.

Antibodies↗
PubMed1983

Massive hematuria of nontraumatic renal origin in dogs.

Massive hematuria of renal origin was diagnosed in 4 dogs. In all dogs, blood and blood clots were clearly visible in the urine. Serum urea nitrogen and urine concentrating ability were normal. All dogs were anemic, and results of coagulation and platelet function tests were within normal limits. Excretory urography indicated hydroureter and hydronephrosis in all dogs, with filling defects in the bladder attributable to large blood clots in 2 dogs. Cystotomy and catheterization of the ureters enabled identification of one kidney as the source of bleeding in 3 dogs. Unilateral nephrectomy and ureterectomy resolved their hematuria. The results of histologic examination were normal in 2 dogs. The 3rd dog had evidence of pyelitis. Cystoscopy of the 4th dog did not reveal hematuria from either ureter. The dog was not operated on and it continued to have intermittent hematuria.

Animals↗
PubMed1981

Treatment of severe aplastic anemia using antithymocyte globulin with or without an infusion of HLA haploidentical marrow.

Nineteen patients with severe aplastic anemia were treated with a 4-day course of horse-anti-human thymocyte globulin (ATG). Thirteen of these patients also received an infusion of HLA one haplotype-identical bone marrow. Toxicity of ATG included fever, chills, rash, arthralgias and elevated liver function tests. Platelet transfusion requirements increased during therapy. Eleven patients died 0.2-9.4 months after beginning ATG therapy. None of the 11 patients had any improvement in hematologic status prior to death. The eight surviving patients have been followed for at least 24 months. Six had evidence of hematologic improvement within 6-8 weeks after ATG therapy and are transfusion-independent. The other two patients improved more than one year after treatment. Survival after ATG therapy did not correlate with the presumed etiology of aplasia, duration of aplasia, patient age or sex, prior therapy, or admission granulocyte count. Addition of bone marrow infusion to ATG treatment also did not affect survival. This study demonstrated the necessity for a randomized trial of ATG versus supportive care alone for the treatment of severe aplastic anemia.

Adolescent↗
PubMed1995

[Detection of platelet activation].

It is important to detect platelet activation in order to predict prethrombotic states. We investigated the method for detection of in vivo platelet activation. First, we compared the assay of CD62P and Glycocalicin (GC) in plasma with plasma beta-thromboglobulin (beta-TG) measurement. Plasma CD62P and GC assay using enzyme-immunoassay (EIA) was inferior to plasma beta-TG assay in precision. The concentration of CD62P and beta-TG in plasma prepared with anticoagulant mixture was lower than that prepared with Na citrate only. The level of plasma CD62P did not correlate with that of beta-TG and GC and platelet counts, although the level of plasma GC correlated with plasma beta-TG levels positively. These studies suggest that GC may be a useful marker of platelet damage or activation, but CD62P may reflect the activation of endothelial cells rather than platelets. Secondly, we assayed the appearance of activation-dependent granular protein on platelet plasma membrane using flow cytometry. Thrombin stimulated increase in surface expression of CD62P, CD63 and Factor XIII a-chain(XIII-a) on platelet membrane in vitro. The expression of CD63 was more sensitive than that of CD62P. The platelets of patients with chronic hemodialysis showed increased in expression of CD63 and XIII-a compared with control subjects. These data suggest that the surface expression of CD63 and XIII-a on platelets may be useful markers of in vivo platelet activation.

Biomarkers↗
PubMed1975

Mastocytosis: unusual manifestation; clinical and radiologic changes.

Two patients with mast cell disease presented with unusual features. In one the absence of skin lesions made the diagnositic problem a challenging one. Certain of the laboratory findings, especially those related to the serum cholesterol concentration and platelet function tests, were particularyl interesting. Chemotherapy induced partial remission. The second patient had a long, relatively benign course complicated by two episodes of herpes zoster, the last being associated with the Landry-Guillain-Barre syndrome. In both patients the skeletal abnormalities were radiologically similar. When these are present they should be considereed sufficiently characteristic to indicate strongly a diagnosis of mastocytosis.

Aged↗
PubMed1994

Biocompatibility of extracorporeal blood treatment. Selection of haemostatic parameters.

Since thrombogenesis is a multifactorial process, assessment of the thrombogenic property (thrombogenicity) of a material or device in contact with circulating blood requires the consideration of a number of pathways and their extent as well as time course of activation. The processes to be considered are: (a) thrombosis, (b) activation of the blood coagulation system, and (c) activation of blood platelets. The clinical relevance of testing the thrombogenicity on the basis of these three categories largely depends on the experimental conditions of the test model. Only test models that simulate the conditions of a device during use may predict accurately the thrombogenicity of a material or device during clinical application. Regarding the test category of thrombosis a visual inspection of the device (clotting within the device) is highly relevant but difficult to standardize. Microscopic analysis, either by light-microscopy or scanning electron-microscopy, of the surface of the material or device after its removal from the in-use position is of great importance in evaluating the biological response of the material to blood. For the test categories of blood coagulation and platelets, a rather large number of standardized ready-to-use kits are commercially available. In spite of their aforementioned limitations the assays listed in Table 2 are recommended for their use in assessing thrombogenicity. Because an adequate heparin treatment will mask the intrinsic thrombogenicity of a material or device, monitoring heparin treatment is strongly recommended. If heparin levels have to be measured in whole blood, a clotting assay like the Heptest is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)

Biocompatible Materials↗