Platelet Function in Hemostasis and Inherited Disorders of Platelet Number and Function

SummaryThe tail bleeding time (BT) in rats definitely varies according to the method applied. Of the various variables that may influence BT, we have evaluated the position (horizontal or vertical) of the tail, the environment (air or saline), the temperature (4°, 23° or 37° C) and the type of anaesthesia. Transection of the tail tip cannot be used to screen drugs active on platelet function since it is sensitive to coagulation defects. Template BT in contrast is not modified by heparin and is sensitive to defects of platelet number and function (“storage pool disease”, dipyridamole-like drugs, exogenous prostacyclin). In contrast the test fails to detect aspirin-induced platelet dysfunction. The evidence reported indicates that thromboxane A2-prostacyclin balance is not a factor regulating BT. Aspirin treatment however may be a precipitating factor when associated with other abnormalities of platelet function.Template BT is a valid screening test for platelet disorders and for antiplatelet drugs.

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Genetic Techniques Used in the Diagnosis of Inherited Platelet Disorders

Seminars in Thrombosis and Hemostasis ◽

10.1055/s-0039-1687888 ◽

2019 ◽

Vol 45 (07) ◽

pp. 685-694 ◽

Cited By ~ 2

Author(s):

Andrew D. Mumford ◽

Sarah K. Westbury

Keyword(s):

Genetic Analysis ◽

Genetic Disorders ◽

Genetic Diagnosis ◽

Inherited Disorders ◽

Recent Advances ◽

Platelet Number ◽

Genetic Techniques ◽

Platelet Disorders ◽

And Function

AbstractRecent advances in genetic analysis are bringing huge benefits to patients with rare genetic disorders, including those with inherited disorders of platelet number and function. Modern clinical hematological practice now has a range of genetic techniques available to enable the precision diagnosis of inherited platelet disorders (IPDs). There are some features of this disparate group of inherited disorders that present specific challenges to establishing an accurate genetic diagnosis. This review aims to introduce the techniques that are relevant for the genetic diagnosis of IPDs and will discuss the key considerations necessary for their application to the clinic.

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Platelet Number and Function in Diamond-Blackfan Anemia

PEDIATRICS ◽

10.1542/peds.68.2.238 ◽

1981 ◽

Vol 68 (2) ◽

pp. 238-241

Author(s):

George R. Buchanan ◽

Blanche P. Alter ◽

Christine A. Holtkamp ◽

Elaine G. Walsh

Keyword(s):

Platelet Count ◽

Platelet Aggregation ◽

Platelet Function ◽

Signs And Symptoms ◽

Red Cell ◽

Normal Range ◽

Platelet Counts ◽

Diamond Blackfan Anemia ◽

Platelet Number ◽

And Function

Congenital red cell aplasia (Diamond-Blackfan anemia) is occasionally associated with hematologic defects other than a deficiency of red blood cell progenitors, but such alterations have not been well studied. The frequency and magnitude of abnormalities in platelet count and platelet function were therefore examined in 38 patients. Thrombocytosis was seen in 21 patients, and 12 had mild thrombocytopenia on at least one occasion. Elevated platelet counts were demonstrated repeatedly in nine children. The three patients with the lowest platelet counts also had leukopenia. Platelet aggregation was normal in all 16 patients in whom it was studied, and bleeding times were within the normal range in 14 of them. Bleeding signs and symptoms were not observed. It is concluded that thrombocytosis or thrombocytopenia often occurs but that platelet function is normal in patients with Diamond-Blackfan anemia.

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Evaluation of platelet number and function and fibrinogen level in patients bitten by snakes of the Bothrops genus

Revista da Sociedade Brasileira de Medicina Tropical ◽

10.1590/s0037-86821995000100004 ◽

1995 ◽

Vol 28 (1) ◽

pp. 19-24 ◽

Cited By ~ 2

Author(s):

Fábio Cardoso Luan ◽

Izolete Aparecida Thomazini ◽

Iracema Carvalho ◽

Delane Mercedes Gonçalves Carreira ◽

Valter José Cassinelli ◽

...

Keyword(s):

Platelet Function ◽

Degradation Product ◽

Statistical Difference ◽

Fibrinogen Level ◽

Plasma Fibrinogen ◽

Fibrin Degradation Product ◽

Platelet Number ◽

And Function

Platelet function and plasma fibrinogen levels were evaluated in 14 patients, 10 males and 4females, aged 13-59years bitten by Bothrops genus snakes. There was a statistical difference (p < 0.05) among plasma fibrinogen levels evaluated 24 and 48 hours after envenomation. There was a tendency towards normalization after 48 hours of treatment. The low platelet number was clear in 24-48 hour evaluations with a tendency towards normalization after 48 hours of treatment (p<0.05). Fibrinogen levels and fibrin degradation product (FDP) levels appeared to be altered in 83.33% of patients evaluated. The authors suggest that platelet hypoaggregation is related to decreased fibrinogen and increased FDP levels.</

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Platelet Suruival and Function in Rats with Enhanced Thrombotic Tendency

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660122 ◽

1985 ◽

Vol 54 (04) ◽

pp. 739-743 ◽

Cited By ~ 2

Author(s):

Federica Delaini ◽

Elisabetta Dejana ◽

Ine Reyers ◽

Elisa Vicenzi ◽

Germana De Bellis Vitti ◽

...

Keyword(s):

Arachidonic Acid ◽

Nephrotic Syndrome ◽

Platelet Function ◽

Laboratory Tests ◽

Thrombus Formation ◽

The Other ◽

Mean Survival Time ◽

The Mean ◽

And Function ◽

Thrombotic Tendency

SummaryWe have investigated the relevance of some laboratory tests of platelet function in predicting conditions of thrombotic tendency. For this purpose, we studied platelet survival, platelet aggregation in response to different stimuli, TxB2 and 6-keto-PGFlα production in serum of rats bearing a nephrotic syndrome induced by adriamycin. These animals show a heavy predisposition to the development of both arterial and venous thrombosis. The mean survival time was normal in nephrotic rats in comparison to controls. As to aggregation tests, a lower aggregating response was found in ADR-treated rats using ADP or collagen as stimulating agents. With arachidonic acid (AA) we observed similar aggregating responses at lower A A concentrations, whereas at higher AA concentrations a significantly lower response was found in nephrotic rats, despite their higher TxB2 production. Also TxB2 and 6-keto-PGFlα levels in serum of nephrotic rats were significantly higher than in controls. No consistent differences were found in PGI2-activity generated by vessels of control or nephrotic rats.These data show that platelet function may appear normal or even impaired in rats with a markedly increased thrombotic tendency. On the other hand, the significance of high TxB2 levels in connection with mechanisms leading to thrombus formation remains a controversial issue.

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Platelet Function in Experimentally Induced Pancreatitis in the Dog

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661521 ◽

1986 ◽

Vol 55 (02) ◽

pp. 197-200 ◽

Cited By ~ 6

Author(s):

R M Jacobs ◽

R J Murtaugh ◽

R H Fertel

Keyword(s):

Platelet Function ◽

Disseminated Intravascular Coagulation ◽

Degradation Products ◽

Plasma Concentrations ◽

Adenosine Diphosphate ◽

Intravascular Coagulation ◽

Fibrin Degradation Products ◽

Functional Defect ◽

And Function ◽

Experimentally Induced

SummaryEvidence suggests that changes in prostaglandins and disseminated intravascular coagulation accompany pancreatitis. Both may induce changes in platelet function. We wished to determine if experimentally induced pancreatitis in the dog was associated with altered platelet number and function, and whether there were concomitant changes in prostaglandins. Evidence for disseminated intravascular coagulation in the dogs with pancreatitis were red blood cell fragmentation, increased platelet turnover indicated by macro-platelets and the transient presence of fibrin degradation products in urine. There were no significant changes in platelet count. The platelets from dogs with pancreatitis showed a functional defect characterized by significantly decreased aggregation in response to adenosine diphosphate, arachidonic acid, and collagen. Release of adenosine triphosphate from platelets was reduced in collagen-stimulated aggregation. There were no changes in the plasma concentrations of thromboxane B2, 6-Keto-PGF1a, and PGE2. This defect may have been due to the generation of fibrin degradation products and platelet “exhaustion”.

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