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PubMed1985

Effect of smoking and dietary saturated fats on platelet functions in Scottish farmers.

Coagulation and platelet aggregation to thrombin and adrenaline, before and 10 min after smoking one high nicotine cigarette, were studied in 40 healthy male farmers (40 to 45 years) from the South-West and North-East of Scotland. These tests were conducted in association with detailed dietary studies. In the West group the intake of dairy fats, saturated fats and P/S ratio as well as most of the platelet function tests estimated were significantly higher than in the East group. Serum cholesterol (total and HDL) was similar in the two regions, while triglycerides were lower in the West. Smoking one cigarette considerably enhanced the platelet functions in both areas but the increases were more marked in the West group. The increase in the response of platelets to smoking was additive to that apparently induced by the intake of saturated fat in such a way the response of platelets to thrombin and epinephrine after smoking one cigarette in the West was approximately four times this obtained before smoking (or in a non-smoker) in the East. These additive effects of cigarette and saturated fat might be relevant to the reported higher incidence of coronary heart disease in the West of Scotland.

Adult↗
PubMed2003

Shear-induced in-vitro haemostasis/thrombosis tests: the benefit of using native blood.

The historical development of in-vitro bleeding time tests, using solely shear forces to initiate haemostatic plug formation, in the absence of the vessel wall or its components, is described. Techniques that have no potential for routine use in clinical practice, such as flow chambers and cone-and-plate viscometers, are excluded. The problems related to the use of citrated blood in platelet function tests are discussed. In light of the pivotal role of thrombin and platelet-dependent thrombin generation in haemostasis/thrombosis, the advantage and clinical benefits of testing unadulterated native blood is discussed.

Bleeding Time↗
PubMed1983

Nafcillin-induced platelet dysfunction and bleeding.

This paper describes two cases of nafcillin-induced platelet dysfunction, with positive rechallenge data for one patient. Nafcillin resulted in abnormal bleeding times in both patients and a clinically apparent bleeding episode in one of the cases. Platelet function tests were performed on one patient during the initial therapy and after rechallenge with nafcillin. Platelet aggregation showed abnormal responses to ADP, collagen, and epinephrine. Platelet count and morphology were normal. Nafcillin should be recognized as another antibiotic which causes platelet function abnormalities and clinical bleeding episodes.

Adolescent↗
PubMed1979

Factor XIII.

1. Activated factor XIII is the enzyme that covalently cross-links fibrin monomers into fibrin polymers and results in increased clot strength and resistance of the clot to fibrinolysis. 2. Small amounts (greater than 1% of normal) of factor XIII are necessary for normal in vitro and in vivo activity. 3. Factor XIII deficiency is a rare autosomal recessive illness in which a hemorrhagic diathesis is caused by the virtual absence of the active a subunit of factor XIII. Approximately 100 cases have been described. 4. The disease in homozygotes is characterized by umbilical stump bleeding, a high incidence of fetal wastage, delayed soft tissue hemorrhage, and a high incidence of intracranial bleeding. The heterozygote is asymptomatic. 5. This paper calls attention to the apparent high incidence of oligospermia and small testes seen in homozygote males. Otherwise secondary sex characterics are normal. 6. Because there is no abnormality in thrombin generation and conversion of fibrinogen to fibrin, route coagulation tests (prothrombin time, partial thromboplastin time, thrombin time, etc.) are normal. Platelet function tests are normal. 7. Clots made from recalcified plasma severely deficient in factor XIII are soluble in 5 M urea or 1% monochloroacetic acid. These screening tests are simple and nearly pathognomonic of the illness. 8. More sophisticated and quantitative tests (e.g., dansylcadaverine incorporation) are available for definitive diagnosis and heterozygote detection. 9. Replacement treatment of the illness is simple, effective, and relatively inexpensive. Due to the long half-life of infused factor XIII and the small amounts necessary for normal hemostasis, prophylaxis is feasible and encouraged.

Adult↗
PubMed1989

[Antiplatelet effects of combination therapy with low-dose aspirin and ticlopidine in cerebral ischemia].

Antiplatelet effects of combination therapy with aspirin and ticlopidine were investigated in comparison with single aspirin or ticlopidine therapy in 62 patients with cerebral thrombosis or transient ischemic attack. The 14, 21 and 27 patients were given orally daily aspirin 300mg, ticlopidine 200mg and aspirin 81mg with ticlopidine 100mg, respectively. Various platelet function tests were performed before and a week after medication. They included platelet aggregation (PA) to adenosine diphosphate (ADP), arachidonic acid (AA) and platelet activating factor (PAF) with turbidimetry, plasma beta-thromboglobulin (beta TG), platelet factor 4(PF4), thromboxane B2(TXB2) and 6keto-prostaglandin-F1 alpha(6keto PGF1 alpha) with radioimmunoassay, bleeding time with Simplate device, and platelet survival and lysis with Indium-111-tropolone-labelled platelets. Aspirin inhibited PA to ADP and AA but not to PAF, while ticlopidine inhibited PA to ADP and PAF but not to AA. In contrast, aspirin with ticlopidine inhibited PA to all of these agonists despite their smaller doses used. Aspirin reduced plasma TXB2 but not beta TG or PF4, while ticlopidine reduced beta TG and PF4 but not TXB2. On the contrary, aspirin with ticlopidine reduced TXB2 as well as beta TG and PF4. 6keto PGF1 alpha tended to be reduced by aspirin 300mg alone but not by ticlopidine with or without aspirin 81mg. Bleeding time was significantly prolonged by aspirin or ticlopidine alone, although most prolongation was produced by combination of aspirin and ticlopidine. Platelet survival and lysis remained unaltered in 4 patients treated with aspirin or ticlopidine alone, whereas platelet survival was prolonged and platelet lysis was reduced in 4 patients treated with both aspirin and ticlopidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

[Obstetrical problems in patients with Glanzmann's thrombasthenia. A casuistic presentation (author's transl)].

Glanzmann's thrombasthenia is a rare, autosomal recessive disorder of bleeding arrest. The differential diagnosis of this platelet defect with respect to recently gained knowledge is presented in the case of a pregnant woman. Because of pelvic presentation a cesarean section was performed after adequate platelet substitution, which did not involve excessive blood loss. A severe puerperal infection necessitated an abdominal hysterectomy after appropriate platelet transfusion. The difficulties in testing platelet function in the newborn are discussed. The effectiveness of a commercially available homologous phospholipide complex (Fibraccel) was tested on the patient in a noncritical phase. The results appear important for general procedure when pregnancy and platelet dysfunction concur.

Adult↗
PubMed1984

Haemostatic mechanisms of the newborn foal: reduced platelet responsiveness.

Whole blood platelet counts, coagulation profiles and in vitro platelet function tests were monitored in newborn foals during the first week of life. Platelet counts, mean platelet volumes and thrombin-induced malondialdehyde production were not different from adult mares. Prothrombin and partial thromboplastin times were slightly, but not significantly, longer for neonatal blood samples than for mare samples. Platelet aggregation responses to serotonin, arachidonic acid or adrenaline did not change during the study. On the other hand, adenosine diphosphate-induced aggregation and collagen-induced aggregation increased progressively over the first week of life. Adrenaline exposure diminished adenosine diphosphate-induced aggregation only during the first 12 h of life. The results of this study indicate that the haemostatic mechanisms of equine neonates are immature at birth and that, during the maturation period, the equine neonate may be at risk of platelet-associated haemorrhagic disorders.

Adenosine Diphosphate↗
PubMed1998

Laboratory investigation of hypercoagulability.

For many years, the laboratory investigation of patients with thrombophilia has lagged behind that of patients with bleeding diathesis. Improved understanding of the mechanisms that control and regulate coagulation, and the resultant recognition of new defects, have greatly stimulated clinical laboratory interest in this area. Assays to detect resistance to activated protein C; deficiencies of antithrombin, protein C, and protein S; and the presence of antiphospholipid antibodies are widely available and should form part of the investigation of patients that present with idiopathic thrombosis. Such a work-up will likely provide an explanation for thrombosis in 40 to 60% of patients. Abnormalities of fibrinogen and fibrinolysis may explain still more, although such defects are currently considered rare. In addition, presently unrecognized defects almost certainly exist, and the identification of such individuals will undoubtedly improve our understanding of the hemostatic mechanism. Laboratory tests to define the hypercoagulable state are continually being developed. They include whole blood coagulation and platelet function tests and novel activation markers. However, acceptance of these approaches by clinical laboratories has been slow.

Afibrinogenemia↗
PubMed1980

Platelet proteins (beta-TG and PF4) in atherosclerosis and related diseases.

The mean plasma concentrations of beta-TG and PF4 were significantly elevated in patients with diabetes mellitus, peripheral vascular disease and coronary artery disease reflecting enhanced in vivo platelet activity in some of these patients. No correlations could be observed between state of metabolic control and concentrations of platelet specific proteins in diabetic subjects. High mean beta-TG levels were noticed in diabetic patients with increasing severity of retinopathy. Raised beta-TG values decreased significantly after two weeks of treatment with dipyridamole in 10 type-I diabetics. In patients with peripheral vascular disease the WU-test, but not the ADP- or collagen induced platelet aggregation was significantly different between patients and controls, but there were no correlations between the mentioned platelet function tests.

Arteriosclerosis↗
PubMed1979

Blood coagulation abnormalities in the Schönlein-Henoch syndrome in adults.

23 adult patients with Schönlein-Henoch's syndrome were observed between 1965 and 1976. Nephropathy was noted in 18, gastrointestinal bleedings in 13, thrombosis of legs in 4, cases. Haemostasis was studied in the successive phases of the process on 185 occasions altogether. The studies included four different capillary tests, thromboelastography, the Gerendás coagulogram, determination of partial thromboplastin time and two platelet-function tests. Additional renal biopsy was performed in 10 cases, mesocolon and skin biopsy in one case each. The results of at least one of the capillary tests were found positive in each of the patients in some stage of the process. The coagulation status was marked by hyperocagulability either in itself or combined with laboratory signs of hypocoagulability. Immunohistological study of the biopsy specimens revealed glomerular fibrin deposits in 7 cases. On the evidence of the follow-up studies the laboratory tests may be used for the assessment of the activity of the process. The alternatives of local intravascular coagulation (LIC) or of compensated diffuse intravascular coagulation (DIC) are offered for the interpretation of hypercoagulability.

Adolescent↗
PubMed1992

A rapid method to isolate platelets from human blood by density gradient centrifugation.

Platelets can be damaged easily or activated during isolation, making them unsuitable for functional studies. The most common technique for isolating platelets involves centrifugation. Although gentler methods have been devised to isolate platelets by density gradient centrifugation or electrophoresis, these techniques either result in a relatively dilute platelet preparation or are time-consuming. A simple, gentle technique for isolating concentrated platelet preparations for experimental or clinical use is reported. Freshly drawn whole blood was spun over a commercially available density gradient medium for 30 minutes. The mononuclear cell layer (which also contains most of the platelets) was collected and nucleated cells were pelleted by centrifugation. The recovery of platelets was about 60%. Contamination with leukocytes was less than 1%, and the platelet concentration was about 130% of blood concentration. Higher concentrations can be obtained if more whole blood is layered onto the Mono-Poly Resolving Medium (MPRM; Flow Laboratories, McLean, VA). About 10% of the platelets expressed the activation marker GMP-140 by flow cytometric analysis. They could be activated by thrombin so that 70% to 90% of the platelets expressed GMP-140. Thus, this technique can rapidly and easily yield a functionally intact platelet preparation. This preparation can be purified again if needed. No specialized skills or equipment are needed. A significant advantage of the method is that platelets can be obtained from thrombocytopenic patients in final concentrations that are high enough to use for platelet function testing.

Blood Platelets↗
PubMed2006

The gray platelet syndrome: clinical spectrum of the disease.

The gray platelet syndrome (GPS) is a rare inherited disorder of the megakaryocyte (MK) lineage. Thrombocytopenia and enlarged platelets are associated with a specific absence of alpha-granules and their contents. GPS patients exhibit much heterogeneity both in bleeding severity and in their response to platelet function testing. A unique feature is that proteins endogenously synthesised by megakaryocytes (MK) or endocytosed by MK or platelets fail to enter into the secretable storage pools that characterise alpha-granules of normal platelets. Although the molecular basis of the disease is unknown, evidence suggests that alpha-granules simply fail to mature during MK differentiation. One result is a continued leakage of growth factors and cytokines into the marrow causing myelofibrosis. While for some patients platelet function may be only moderately affected, for others thrombin and/or collagen-induced platelet aggregation is markedly modified and an acquired lack of the GPVI collagen receptor has been reported. In this review, we document the clinical and molecular heterogeneity in GPS, a unique disease of the biogenesis of platelet alpha-granules and of the storage of growth factors and secretable proteins.

Blood Platelets↗
PubMedDate not supplied

Platelet function in leprosy.

In a group of 50 leprosy patients, platelet function tests were found to be abnormal in 44. More than half the patients showed significant impairment in platelet adhesiveness and aggregation to collagen which correlated best with increase in serum IgM levels. ADP-induced aggregation of platelets was not a major defect and Pf-3 availability was reduced only in a fourth of the patients. In vitro incubation of collagen with plasma from leprosy patients significantly reduced its ability to clump normal platelets. This appears to be the first report of defective platelet function in leprosy, and it is thought that such changes may in part be due to increased IgM globulins in the blood and/or to alterations in the collagen brought about thereby.

Adenosine Diphosphate↗
PubMed1975

[Inhibitory activity of bencyclan on platelet aggregation in vitro and in vivo (author's transl)].

N-[3-(Benzyl-cycloheptyloxy)-propyl]-N,N-dimethyl-amine (bencyclan-hydrogenfumarate, Fludilat¿) inhibits spontaneously enhanced aggregation in the tests which detect a spontaneous aggregating activity (PAT I--III) in 10(-5) molar concentration. Bencyclan also inhibits platelet adhesiveness and ADP or collagen induced platelet aggregation. 10(-5) M of bencyclan induced a slight swelling of platelets 5 times 10(-4) Mol inhibited the formation of tentacles completely and transformed the platelets into small spheres if investigated with interference-phase contrast microscopy. It is likely that the morphologic changes induced by bencyclan are responsible for the inhibitory effect on the different platelet function tests in vitro. In vivo oral application of 300-600 mg of bencyclan per day did not inhibit platelet aggregation. In patients with enhanced aggregating tendency i.v. injection of 200-400 mg bencyclan led to a short-time inhibition of platelet aggregation which usually did not last for more than 1 h. No binding of 14C-labelled bencyclan to platelets was found. In vitro and in vivo some 14C-labelled bencyclan was bound to albumins.

Adenosine Diphosphate↗
PubMed1990

Platelet abnormalities in myeloproliferative disorders.

A large number of various platelet abnormalities are described in patients with MPD. These abnormalities serve diagnostic purposes only. They appear to have little or no predictive value regarding the clinical manifestations of the patients or the progress of the disease. Those platelet characteristics most consistently reported to be defective include a decrease in the platelet content of serotonin and adenine nucleotides, decreased platelet density, an abnormal ultrastructure characterized by paucity of granules and hypertrophy of the surface connecting canicular system, an altered membrane glycoprotein profile that includes reduced levels of GPIb, and reduced lipoxygenase activity and aggregation response with epinephrine. These abnormalities may originate at the megakaryocyte level. Furthermore, the released abnormal platelets may undergo modification of their functional and biochemical characteristics as a result of episodes of intravascular thrombosis or aging in circulation or as a result of the progression and treatment of the disease, thus creating the paradoxic and often conflicting relationship between the thrombotic and hemorrhagic events and the results of platelet functional tests as observed in this disorder.

Blood Platelets↗
PubMed1991

Acquired disorder of platelet function associated with autoantibodies against membrane glycoprotein IIb-IIIa complex--1. Glycoprotein analysis.

A patient with idiopathic thrombocytopenic purpura developed after splenectomy a thrombasthenia-like severe haemorrhagic diathesis characterized by a normal or subnormal platelet count, prolonged bleeding time, strongly reduced platelet adhesion to glass and defective platelet aggregation in response to ADP and collagen. In contrast to hereditary thrombasthenia membrane glycoproteins (GP) IIb and IIIa were normally present in the patient's platelets. Immunoelectrophoretic analysis revealed an abnormal behaviour of the patient's GP IIb-IIIa complex. Autoantibodies against GP IIb-IIIa were detected in Triton-extracted washed platelets. Incubation of normal platelets with plasma from the patient resulted in a similar immunoelectrophoretic abnormality of the GP IIb-IIIa complex indicating that bound autoantibodies (IgG) are responsible for the abnormal immunoelectrophoretic behaviour of the patient's GP IIb-IIIa complex. Platelet fibrinogen was severely reduced similar to classical thrombasthenia suggesting that the GP IIb-IIIa complex is involved in platelet fibrinogen storage.

Autoantibodies↗
PubMed2000

Testing of platelet deposition on polystyrene surface under flow conditions by the cone and plate(let) analyzer: role of platelet activation, fibrinogen and von Willebrand factor.

Recently, we described a method of testing platelet deposition on extracellular matrix under flow conditions. The method was used for assessment of platelet function in various platelet disorders, for monitoring of replacement and anti-platelet therapy. In the present study, we investigated platelet deposition on a polystyrene surface compared with that on extracellular matrix, under defined shear rates, using the original Cone and Plate(let) Analyzer. A correlation of adhesion rate (surface coverage) and aggregate formation (average size) of platelets from normal citrated blood between polystyrene and extracellular matrix was observed. Blocking of von Willebrand factor binding to glycoprotein Ib by a recombinant von Willebrand factor fragment substantially decreased platelet adhesion to both surfaces. Blocking of GPIIb-IIIa by Arg-Gly-Asp-Ser peptide prevented platelet adhesion to the polystyrene while an extensive adhesion of single platelets to extracellular matrix was observed. Furthermore, platelet adhesion to polystyrene but not to extracellular matrix was completely inhibited by platelet inactivation with prostaglandin E(1). Platelets from patients with severe von Willebrand disease yielded very low adhesion to both polystyrene and extracellular matrix. The addition of von Willebrand factor to the blood of these patients or pre-coating of polystyrene surface with von Willebrand factor restored the ability of platelets to adhere and aggregate on the surface. Platelets from patients with Glanzmann's thrombasthenia and afibrinogenemia adhered to extracellular matrix (with defective aggregate formation), while they failed to adhere to the polystyrene. Fibrinogen added to afibrinogenemia blood or pre-coating of the polystyrene with fibrinogen restored the ability of platelets to adhere and aggregate on the surface. In conclusion, the polystyrene surface, like extracellular matrix, can be used to assess platelet function disorders taking in account that platelet deposition on polystyrene under flow is absolutely dependent on platelet activation and on the presence of fibrinogen, von Willebrand factor, and their receptors.

Afibrinogenemia↗