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Journal articles on the topic 'Platelet disorder'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Gothwal, M., K. Sandrock-Lang, and B. Zieger. "Genetics of inherited platelet disorders." Hämostaseologie 34, no. 02 (2014): 133–41. http://dx.doi.org/10.5482/hamo-13-09-0049.

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SummaryThe current review describes inherited platelet disorders, illustrates their clinical phenotype and molecular genetic defects. Platelets are the key molecules mediating haemostasis via adhesion, activation and clot formation at the site of injury. The inherited platelet disorders can be classified according to their platelet defects: receptor/cytoskeleton defects, secretion disorder, and signal transduction defect.Patients with inherited thrombocytopathia present with mucous membrane bleedings (epistaxis, gingival bleeding) and may present with serious life threatening bleedings followi

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Zhaoyue Wang, Jumei Shi, Yue Han, Yingchun Wang, and Changgeng Ruan. "Spontaneous Platelet Aggregation With Congenital Giant Platelet Containing Large Granules and Thick Membrane." Clinical and Applied Thrombosis/Hemostasis 7, no. 4 (2001): 305–10. http://dx.doi.org/10.1177/107602960100700410.

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Inherited giant platelet disorders are a heterogeneous group of disorders. In the current study, a patient was reported with moderate bleeding tendency, giant platelets, and spontaneous platelet aggregation, which were not affected by the administration of aspirin or ticlopidine. The electron microscopy of platelets showed a black and thick plasma membrane with crystal-like fine hairs in the exterior coat and more large and variously shaped granules in the cytoplasm. The expression of glycoprotein (GP) Ib, GP IIb, and GP IIIa on platelet surface was normal, and no mutations in genes for GP Ibα

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Naina, Harris V. K., and Samar Harris. "Platelet and Red Blood Cell Indices in Harris Platelet Syndrome." Blood 108, no. 11 (2006): 3988. http://dx.doi.org/10.1182/blood.v108.11.3988.3988.

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Abstract Inherited giant platelet disorders are a group of rare disorders characterized by thrombocytopenia, giant platelets and variable bleeding symptoms. Naina et al., described a new giant platelet disorder called Harris Platelet Syndrome (HPS), the most common inherited giant platelet disorder occurring in up to one third of blood donors from north eastern part of Indian subcontinent. HPS is characterized by an autosomal dominant mode of inheritance with normal to severe thrombocytopenia (less than 50x109/L), giant platelets (mean platelet volume more than 10fL) and absent bleeding sympto

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Pham, Angie, and Jun Wang. "Bernard-Soulier Syndrome: An Inherited Platelet Disorder." Archives of Pathology & Laboratory Medicine 131, no. 12 (2007): 1834–36. http://dx.doi.org/10.5858/2007-131-1834-bsaipd.

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Abstract Bernard-Soulier syndrome is an inherited platelet disorder, which is transmitted in an autosomal recessive manner. This syndrome is characterized by variable thrombocytopenia and large defective platelets. Bernard-Soulier syndrome often presents early with bleeding symptoms, such as epistaxis, ecchymosis, menometrorrhagia, and gingival or gastrointestinal bleeding. Diagnosis can be confirmed by platelet aggregation studies and flow cytometry. The differential diagnosis includes the other inherited giant platelet disorders, as well as von Willebrand disease and immune thrombocytopenia

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Ranalli, Paola, Stefano Baldoni, Daniela Bruno, and Mauro Di Ianni. "MPN/MDS overlap syndrome anticipated by a severe bleeding diathesis: hypothesis of a pre-existing platelet disorder." Mediterranean Journal of Hematology and Infectious Diseases 16, no. 1 (2024): e2024067. http://dx.doi.org/10.4084/mjhid.2024.067.

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We report the case of a patient with a conclusive diagnosis of “MDS/MPN” Overlap Syndrome preceded by platelet disorder and hemorrhagic phenotype. We want to induce a reflection about diagnosis of oncohematological disorders in patient with a documented personal history of bleeding and/or platelet disorder, considering all the possible differential diagnosis: 1) Bleeding as the epiphenomenon of a still undiagnosed Myeloid Neoplasm or 2) Myeloid Neoplasm with germline predisposition and pre-existing platelet disorder; 3) Inherited platelet disorder successively developing MPN/MDS Overlap Syndro

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Antony-Debré, Iléana, Dominique Bluteau, Raphael Itzykson, et al. "MYH10 protein expression in platelets as a biomarker of RUNX1 and FLI1 alterations." Blood 120, no. 13 (2012): 2719–22. http://dx.doi.org/10.1182/blood-2012-04-422352.

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Abstract RUNX1 gene alterations are associated with acquired and inherited hematologic malignancies that include familial platelet disorder/acute myeloid leukemia, primary or secondary acute myeloid leukemia, and chronic myelomonocytic leukemia. Recently, we reported that RUNX1-mediated silencing of nonmuscle myosin heavy chain IIB (MYH10) was required for megakaryocyte ploidization and maturation. Here we demonstrate that runx1 deletion in mice induces the persistence of MYH10 in platelets, and a similar persistence was observed in platelets of patients with constitutional (familial platelet

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7

Handa, Makoto, Yohko Kawai, Tetuji Kamata та ін. "Platelet Unresponsiveness to Collagen: Involvement of Glycoprotein Ia-IIa (α2β1 Integrin) Deficiency Associated with a Myeloproliferative Disorder". Thrombosis and Haemostasis 73, № 03 (1995): 521–28. http://dx.doi.org/10.1055/s-0038-1653807.

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SummaryWe studied a 66-year-old man with a myeloproliferative disorder who presented with a prolonged bleeding time and marked thrombocytosis (platelet count, 3,890 × 109/1). There was no past history of a bleeding disorder. The patient had normal coagulation data. His platelets completely lacked collagen-induced platelet aggregation and adhesion, but showed normal responses to other agonists. All family members tested showed normal platelet aggregation with collagen.Analysis of 125I surface-labeled platelets by two-dimensional SDS gel electrophoresis disclosed absence of the spot correspondin

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Castilloux, Jean, Karen Moffat, Yang Liu, Jodi Seecharan, Menaka Pai, and Catherine Hayward. "A prospective cohort study of light transmission platelet aggregometry for bleeding disorders: Is testing native platelet-rich plasma non-inferior to testing platelet count adjusted samples?" Thrombosis and Haemostasis 106, no. 10 (2011): 675–82. http://dx.doi.org/10.1160/th11-06-0378.

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SummaryLight transmission platelet aggregometry (LTA) is important to diagnose bleeding disorders. Experts recommend testing LTA with native (N) rather than platelet count adjusted (A) platelet-rich plasma (PRP), although it is unclear if this provides non-inferior, or superior, detection of bleeding disorders. Our goal was to determine if LTA with NPRP is noninferior to LTA with APRP for bleeding disorder assessments. A prospective cohort of patients, referred for bleeding disorder testing, and healthy controls, were evaluated by LTA using common agonists, NPRP and APRP (adjusted to 250 x 109

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9

Massey, Gita, Laura Tyrrell, Yaser Diab, and William T. Gunning. "Medich Giant Platelet Syndrome: An Evolving Qualitative and Quantitative Platelet Disorder." Hematology Reports 14, no. 4 (2022): 349–57. http://dx.doi.org/10.3390/hematolrep14040049.

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Qualitative platelet disorders remain rare and varied. We describe here 2 additional patients with giant platelets, thrombocytopenia, deficiency in alpha granules and the presence of membranous inclusions within the cytoplasm. Collectively known as Medich syndrome, we further elucidated structural and clinical features of this rare syndrome. Platelets obtained from 2 patients with macro-thrombocytopenia were evaluated by electron microscopy. Structural findings were correlated with clinical characteristics. The defining morphologic feature found in the platelets of these patients is the presen

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Pujol-Moix, Nuria, Mariana Corrochano, Isabel Badell, Joan Carles Souto, and Josep F. Nomdedeu. "Platelet Ultrastructure in Familial Platelet Disorder with Associated Myeloid Malignancy (FPDMM)." Blood 136, Supplement 1 (2020): 37–38. http://dx.doi.org/10.1182/blood-2020-142248.

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The familial platelet disorder with associated myeloid malignancy (FPDMM) is an autosomal dominant platelet disorder, caused by germline RUNX1 mutations, with predisposition to develop hematologic malignancies, especially acute myeloid leukemia. In many of the FPDMM families reported, the platelet defect was a delta-storage-pool disease (d-SPD) which can also be found without leukemia propensity. However, it has not been studied whether the two types of d-SPD have a common nature. Platelet ultrastructure, previously very little studied, may be one of the aspects to be analyzed to solve this qu

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Starovoitov, A. G., A. L. Lipnitski, and А. V. Marochkov. "ANALYSIS OF PLATELET AGGREGATION IN DONORS OF BLOOD COMPONENTS." Journal of the Grodno State Medical University 19, no. 6 (2021): 646–51. http://dx.doi.org/10.25298/2221-8785-2021-19-6-646-651.

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The functional state of platelets can be determined using the method of platelet aggregation. The aim of our study was to investigate platelet aggregation in donors of blood components and to identify the features of the reactions of these platelets with the most common inducers of aggregation. Material and methods. 31 donors of fresh frozen plasma and platelet concentrate were included in the study. The study of platelet aggregation was carried out by the turbidimetric method with AP2110 analyzer (SOLAR, Minsk, Republic of Belarus). Results. A total of 33 studies of platelet aggregation in do

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Weitz, Ilene Ceil, and Howard Allen Liebman. "Complement in immune thrombocytopenia (ITP): The role of complement in refractory ITP." British Journal of Haematology 203, no. 1 (2023): 96–100. http://dx.doi.org/10.1111/bjh.19070.

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SummaryImmune thrombocytopenia (ITP) is a disorder characterized by low platelets due to increased clearance and decreased platelet production. While ITP has been characterized as an acquired disorder of the adaptive immune system, the resulting platelet autoantibodies provide ancillary links to the innate immune system via antibody interaction with the complement system. Most autoantibodies in patients with ITP are of the IgG1 subclass, which can be potent activators of the classical complement pathway. Antibody‐coated platelets can initiate complement activation via the classical pathway lea

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13

Hayward, CP, GE Rivard, WH Kane, et al. "An autosomal dominant, qualitative platelet disorder associated with multimerin deficiency, abnormalities in platelet factor V, thrombospondin, von Willebrand factor, and fibrinogen and an epinephrine aggregation defect." Blood 87, no. 12 (1996): 4967–78. http://dx.doi.org/10.1182/blood.v87.12.4967.bloodjournal87124967.

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Multimerin is a massive soluble, multimeric protein found in platelets and endothelial cells. Recent studies identified multimerin as a specific coagulation factor V binding protein, complexed with platelet, but not plasma, factor V. These findings led us to investigate individuals with inherited factor V deficiencies for possible multimerin abnormalities. Platelet proteins were evaluated using immunoassays, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, immunoblotting, immunoprecipitation, and direct binding studies. Patients with factor V Quebec, a disorder with abnormal platelet

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Callan, Mary Beth, Joel S. Bennett, Deborah K. Phillips та ін. "Inherited Platelet δ-Storage Pool Disease in Dogs Causing Severe Bleeding: An Animal Model for a Specific ADP Deficiency". Thrombosis and Haemostasis 74, № 03 (1995): 949–53. http://dx.doi.org/10.1055/s-0038-1649853.

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SummaryThe nature of a disorder producing moderate to severe bleeding after minor trauma, venipuncture, and surgery was studied in 3 families of American cocker spaniel dogs. In the 5 affected dogs tested, platelet counts and measurements of plasma coagulant function and von Willcbrand factor were normal. However, bleeding times were prolonged in 4 of the 5 affected dogs tested, and platelet aggregation in response to ADP and collagen was consistently abnormal in 3, suggesting that the bleeding disorder was due to abnormal platelet function. Measurements of 14C-serotonin uptake and retention b

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15

Ranelletti, Franco, Nicola Maggiano, Giovanni Ciabattoni, Raimondo De Cristofaro, Raffaele Landolfi, and Bianca Rocca. "Inherited Macrothrombocytopenia with Distinctive Platelet Ultrastructural and Functional Features." Thrombosis and Haemostasis 83, no. 01 (2000): 35–41. http://dx.doi.org/10.1055/s-0037-1613753.

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SummaryWe report a family with inherited macrothrombocytopenia and characteristic large membrane complexes in the platelets. Two affected subjects had platelet counts of 40 and 65X109/L respectively as assessed by contrast phase microscopy. Ultrastructural studies revealed giant spheroid platelets with characteristic large membrane complexes and/or giant vacuoles containing platelet organelles. Immunohistochemical studies of actin and tubulin showed a disorganization of the microtubule and actin systems. These abnormalities were absent in leukocytes, indicating a platelet-specific cytoskeleton

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Sheth, Prameet, Walter Kahr, Anwar Haq, Dragoslava Veljkovic, Georges Rivard, and Catherine Hayward. "Intracellular activation of the fibrinolytic cascade in the Quebec Platelet Disorder." Thrombosis and Haemostasis 90, no. 08 (2003): 293–98. http://dx.doi.org/10.1160/th02-12-0323.

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SummaryThe Quebec Platelet Disorder (QPD) is an unusual bleeding disorder associated with increased platelet stores of urokinase-type plasminogen activator (u-PA) and proteolysis of platelet α–granule proteins. The increased u-PA and proteolyzed plasmino-gen in QPD platelets led us to investigate possible contributions of intracellular plasmin generation to QPD α-granule proteolysis. ELISA indicated there were normal amounts of plasminogen and plasmin-α2-antiplasmin (PAP) complexes in QPD plasmas. Like normal platelets, QPD platelets contained only a small proportion of the blood plasminogen,

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Hayward, Catherine PM, and Georges E. Rivard. "Quebec platelet disorder." Expert Review of Hematology 4, no. 2 (2011): 137–41. http://dx.doi.org/10.1586/ehm.11.5.

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18

Ninkovic, Ivana, James G. White, Kenyatta W. Stephens, Artur Rangel-Fihlo, Francsisca C. Wu, and Yvonne H. Datta. "Rab38 Expression in Platelet Dense Granule Storage Pool Disease." Blood 110, no. 11 (2007): 2112. http://dx.doi.org/10.1182/blood.v110.11.2112.2112.

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Abstract Platelet dense granule storage pool disease (SPD) is a bleeding disorder characterized by a lack of normal platelet dense granule function, as evidenced by decreased platelet aggregation in response to ADP, epinephrine and collagen. Platelet SPD has been studied most extensively in humans and rodents with Hermansky-Pudlak syndrome (HPS), whose phenotype is a result of defects in granule trafficking, leading to oculocutanous albinism, lysosomal storage diseases, and platelet dysfunction. We have been characterizing the fawn-hooded hypertensive (FHH) rat, which has been previously shown

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19

Nieuwenhuis, HK, KS Sakariassen, WP Houdijk, PF Nievelstein, and JJ Sixma. "Deficiency of platelet membrane glycoprotein Ia associated with a decreased platelet adhesion to subendothelium: a defect in platelet spreading." Blood 68, no. 3 (1986): 692–95. http://dx.doi.org/10.1182/blood.v68.3.692.692.

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Abstract A bleeding disorder with absent collagen-induced platelet aggregation and adhesion has been described in a patient whose platelets failed to express surface glycoprotein Ia. We studied the interaction of her platelets with subendothelium in an annular perfusion chamber and the interaction with purified human collagen type III in a rectangular perfusion system under flow conditions. Platelet adherence was almost completely absent both at low and high shear rates. The few platelets which adhered remained in the contact stage without subsequent spreading and aggregate formation. Addition

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Nieuwenhuis, HK, KS Sakariassen, WP Houdijk, PF Nievelstein, and JJ Sixma. "Deficiency of platelet membrane glycoprotein Ia associated with a decreased platelet adhesion to subendothelium: a defect in platelet spreading." Blood 68, no. 3 (1986): 692–95. http://dx.doi.org/10.1182/blood.v68.3.692.bloodjournal683692.

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A bleeding disorder with absent collagen-induced platelet aggregation and adhesion has been described in a patient whose platelets failed to express surface glycoprotein Ia. We studied the interaction of her platelets with subendothelium in an annular perfusion chamber and the interaction with purified human collagen type III in a rectangular perfusion system under flow conditions. Platelet adherence was almost completely absent both at low and high shear rates. The few platelets which adhered remained in the contact stage without subsequent spreading and aggregate formation. Addition of a mon

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21

Andrews, Robert K., Michael C. Berndt, and Ismael Elalamy. "Platelets — From Function to Dysfunction in Essential Thrombocythaemia." European Oncology & Haematology 07, no. 02 (2011): 125. http://dx.doi.org/10.17925/eoh.2011.07.02.125.

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Platelets are an important component of blood. The main biological role of platelets is to respond to vascular injury and promote thrombus formation to prevent bleeding. However, we now know that platelets also have additional functions in a variety of processes such as immunity, inflammation, coagulation, atherogenesis and tumour metastasis. Platelet disorders commonly lead to defects in haemostasis. Of particular interest is the myeloid proliferative disorder, essential thrombocythaemia (ET). In ET the increased number of platelets leads to an increased risk of blood clot formation and subse

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Hassan, Amy A., and Michael H. Kroll. "Acquired Disorders of Platelet Function." Hematology 2005, no. 1 (2005): 403–8. http://dx.doi.org/10.1182/asheducation-2005.1.403.

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Abstract A qualitative abnormality of platelet function should be considered in patients with mucocutaneous bleeding in the absence of thrombocytopenia or von Willebrand disease. Antiplatelet drugs are the most common cause of acquired platelet disorders leading to bleeding. Uremia, hepatic cirrhosis, myeloma and related disorders, polycythemia vera, essential thrombocythemia, and cardiopulmonary bypass have long been recognized as clinical situations in which platelet dysfunction may contribute to bleeding. When an acquired platelet disorder is suspected, it is useful to examine platelet func

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Frojmovic, Mony M., and Truman Wong. "The Platelet Extinction Coefficient Measured by Aggregometry Is Dependent on Platelet Composition rather than Size: Implications for Studies of Platelet Heterogeneity and Abnormalities." Thrombosis and Haemostasis 64, no. 04 (1990): 582–88. http://dx.doi.org/10.1055/s-0038-1647362.

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SummaryExtinction (E) or light transmission measurements of platelet suspensions have been widely used to evaluate platelet structure and aggregation for platelet populations of varying mean platelet size (V). However, useful comparisons of platelet suspensions from donors having abnormally-sized platelets with those from healthy controls require a knowledge of the dependence of E on V. We have analyzed the extinction per platelet (e) as a function of the geometric scattering cross-section of equivalent spheres, V2/3, related to the apparent mean platelet optical efficiency, k. Such an analysi

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Tubman, Venée N., Jason E. Levine, Dean R. Campagna, et al. "X-linked gray platelet syndrome due to a GATA1 Arg216Gln mutation." Blood 109, no. 8 (2007): 3297–99. http://dx.doi.org/10.1182/blood-2006-02-004101.

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AbstractWe identified a family with gray platelet syndrome (GPS) segregating as a sex-linked trait. Affected males had a mild bleeding disorder, thrombocytopenia, and large agranular platelets characteristic of GPS, while obligate carrier females were asymptomatic but had dimorphic platelets on peripheral smear. Associated findings included mild erythrocyte abnormalities in affected males. Linkage analysis revealed a 63 cM region on the X chromosome between markers G10578 and DXS6797, which segregated with the platelet phenotype and included the GATA1 gene. Sequencing of GATA1 revealed a G-to-

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Canault, Matthias, and Marie-Christine Alessi. "RasGRP2 Structure, Function and Genetic Variants in Platelet Pathophysiology." International Journal of Molecular Sciences 21, no. 3 (2020): 1075. http://dx.doi.org/10.3390/ijms21031075.

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RasGRP2 is calcium and diacylglycerol-regulated guanine nucleotide exchange factor I that activates Rap1, which is an essential signaling-knot in “inside-out” αIIbβ3 integrin activation in platelets. Inherited platelet function disorder caused by variants of RASGRP2 represents a new congenital bleeding disorder referred to as platelet-type bleeding disorder-18 (BDPLT18). We review here the structure of RasGRP2 and its functions in the pathophysiology of platelets and of the other cellular types that express it. We will also examine the different pathogenic variants reported so far as well as s

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Abraham, Shirley M., Dong Chen, Karen Simon, Thomas Markello, and William A. Gahl. "GFI1B Mutation Associated Alpha-Delta Platelet Storage-Pool Deficiency: A Case Report and Its Potential Important Implication." Blood 128, no. 22 (2016): 3727. http://dx.doi.org/10.1182/blood.v128.22.3727.3727.

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Abstract Background: In addition to NBEAL2, a single dominant-negative mutation in the GFIB1 gene has been associated with grey platelet syndrome but no association has been mentioned with dense granule deficiency. Here we describe a child with thrombocytopenia, alpha-delta granule deficiency, and a homozygous missense mutation in GFIB1. Case Report:The patient is an 8y/o Hispanic male born to non-consanguineous parents. Prenatal and birth history were unremarkable. No family history of blood disorders or pediatric malignancies. The boy has 2 healthy older siblings, no dysmorphic features, and

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Althaus, K., M. Wagner, I. Marini, T. Bakchoul, and L. Pelzl. "Flow Cytometric Assessment of AKT Signaling in Platelet Activation: An Alternative Diagnostic Tool for Small Volumes of Blood." Hämostaseologie 40, S 01 (2020): S21—S25. http://dx.doi.org/10.1055/a-1282-1989.

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Abstract Introduction The diagnosis of platelet function disorder in children is challenging. Light transmission aggregometry is the gold standard for platelet function disorders. However, large blood volumes are required. Currently, there are no existing tools for the diagnosis of platelet function disorders that use small blood volumes. AKT signaling plays a central role in platelet activation during hemostasis and might be visualized by flow cytometry. Methods Platelet-rich plasma obtained by centrifugation of citrated blood from healthy volunteers was activated with arachidonic acid, throm

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Dziedzic, Angela, Elzbieta Miller, Michal Bijak, Lukasz Przyslo, and Joanna Saluk-Bijak. "Increased Pro-Thrombotic Platelet Activity Associated with Thrombin/PAR1-Dependent Pathway Disorder in Patients with Secondary Progressive Multiple Sclerosis." International Journal of Molecular Sciences 21, no. 20 (2020): 7722. http://dx.doi.org/10.3390/ijms21207722.

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Epidemiological studies confirm the high risk of ischemic events in multiple sclerosis (MS) that are associated with increased pro-thrombotic activity of blood platelets. The most potent physiological platelet agonist is thrombin, which activates platelets via cleavage of specific protease-activated receptors (PARs). Our current study is aimed to determine the potential genetics and proteomic abnormalities of PAR1 in both platelets and megakaryocytes, which may have thromboembolic consequences in the course of MS. The obtained results were correlated with the expression level of platelet and m

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Baruch, Dominique, Theo Lindhout, Evelyne Dupuy, and Jacques P. Caen. "Thrombin-Induced Platelet Factor Va Formation in Patients with a Gray Platelet Syndrome." Thrombosis and Haemostasis 58, no. 02 (1987): 768–71. http://dx.doi.org/10.1055/s-0038-1645967.

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SummaryThe present study was initiated to establish the functional factor V concentration in platelets of patients with a mild bleeding disorder ascribed to a gray platelet syndrome. This inherited platelet disorder has been characterized by a specific deficiency of alpha-granules and subsequent deficiencies in the alpha-granule proteins. We found that the concentration of plasma factor V was slightly decreased (70% of normal values). In contrast, platelet factor Va formation was severely impaired. Besides a much lower factor V content than in control platelets (10-20% of normal), the dependen

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Rand, Margaret L., Guy C. Le Breton, Tara Paton, et al. "A Novel Inherited Platelet Function Disorder Involving the Thromboxane A2 Pathway of Platelet Activation." Blood 106, no. 11 (2005): 2175. http://dx.doi.org/10.1182/blood.v106.11.2175.2175.

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Abstract Thromboxane A2 (TXA2) is a short-lived metabolite of the fatty acid arachidonate that is formed upon platelet activation; it stimulates platelet responses including shape change, aggregation and secretion of granule contents. The TXA2 pathway of platelet activation is important clinically as demonstrated by the beneficial effect of aspirin, that inhibits TXA2 formation, in preventing arterial thrombotic events. TXA2 elicits its stimulatory responses on platelets by binding to the G protein-coupled thromboxane prostanoid (TP) receptor (approximately 55 kD). Of the α and β isoforms of t

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Lee, Robert H., Raymond Piatt, Ankita Dhenge, et al. "Impaired hemostatic activity of healthy transfused platelets in inherited and acquired platelet disorders: Mechanisms and implications." Science Translational Medicine 11, no. 522 (2019): eaay0203. http://dx.doi.org/10.1126/scitranslmed.aay0203.

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Platelet transfusions can fail to prevent bleeding in patients with inherited platelet function disorders (IPDs), such as Glanzmann’s thrombasthenia (GT; integrin αIIbβ3 dysfunction), Bernard-Soulier syndrome [BSS; glycoprotein (GP) Ib/V/IX dysfunction], and the more recently identified nonsyndromic RASGRP2 variants. Here, we used IPD mouse models and real-time imaging of hemostatic plug formation to investigate whether dysfunctional platelets impair the hemostatic function of healthy donor [wild-type (WT)] platelets. In Rasgrp2−/− mice or mice with platelet-specific deficiency in the integrin

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Pai, Menaka, Grace Wang, Karen A. Moffat, et al. "Diagnostic Utility of Platelet Secretion Testing by ATP Release Assays: Results From a Prospective Study of Individuals Referred for Bleeding Disorder Assessments." Blood 114, no. 22 (2009): 1314. http://dx.doi.org/10.1182/blood.v114.22.1314.1314.

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Abstract Abstract 1314 Poster Board I-338 Background Platelet secretion defects are a common type of inherited platelet disorder. Experts agree that ATP release assays are often helpful to assess for platelet secretion disorders among individuals with suspected bleeding problems. However, the diagnostic utility of ATP release assays has not been established, and it is unclear if the findings correlate with aggregation results. Our goal was to evaluate the incidence and spectrum of platelet release abnormalities in a prospective cohort of individuals referred for testing as part of a bleeding d

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Khakwani, Sadia, Claire Winton, Nosheen Aslam, and Suzanne Taylor. "Platelet storage pool disorder: multidisciplinary planning in pregnancy." BMJ Case Reports 14, no. 5 (2021): e239321. http://dx.doi.org/10.1136/bcr-2020-239321.

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A 32-year old primigravida woman presented for antenatal care giving a history that her mother had platelet storage pool disorder (PSPD). The patient was subsequently diagnosed with PSPD during her pregnancy and had a caesarean delivery for breech presentation at 39 weeks. In this paper, we discuss the basic science, inheritance pattern, symptoms and management of this condition, alongside the antenatal and intrapartum and postnatal management specific to it, highlighting the need for a multidisciplinary approach to care. PSPD refers to a group of rare conditions involving defects in platelet

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Takahashi, H., W. Tatewaki, M. Hanano, R. Nagayama, and A. Shibata. "Further Studies on Aggregation of Platelet-Type von Willebrand’s Disease Platelets by Human von Willebrand Factor." Thrombosis and Haemostasis 55, no. 03 (1986): 338–41. http://dx.doi.org/10.1055/s-0038-1661559.

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SummaryPlatelet-type von Willebrand’s disease (vWD) is a bleeding disorder characterized by a heightened interaction between platelets and von Willebrand factor (vWF) as the result of an intrinsic platelet abnormality (probably in GPIb). Platelet aggregability was nearly normal in response to thrombin, wheat germ agglutinin and Ricinus communis agglutinin in this disorder. Unmodified platelets showed no aggregation upon the addition of peanut agglutinin. Partially purified human vWF induced little aggregation of washed patient platelets, but the aggregation was greatly enhanced in the presence

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Han, Jong Hyeok, Inkwon Yoon, and Hee-Jae Jeon. "Microfluidic System-Based Quantitative Analysis of Platelet Function through Speckle Size Measurement." Biomolecules 14, no. 6 (2024): 612. http://dx.doi.org/10.3390/biom14060612.

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Platelets play essential roles in the formation of blood clots by clumping with coagulation factors at the site of vascular injury to stop bleeding; therefore, a reduction in the platelet number or disorder in their function causes bleeding risk. In our research, we developed a method to assess platelet aggregation using an optical approach within a microfluidic chip’s channel by evaluating the size of laser speckles. These speckles, associated with slowed blood flow in the microfluidic channel, had a baseline size of 28.54 ± 0.72 µm in whole blood. Removing platelets from the sample led to a

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Mannion, Laura, Desmond Nugent, and Brian Leonard. "Platelet studies in panic disorder: A review." Irish Journal of Psychological Medicine 14, no. 4 (1997): 139–43. http://dx.doi.org/10.1017/s0790966700003372.

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AbstractObjective: The blood platelet has been proposed as a model of central neurons and may therefore be used as a peripheral marker of psychiatric illness. One method of investigating serotonin function in panic disorder has relied on the use of the platelet as a model of serotonergic neurons. This article reviews the studies of platelet function in panic disorder.Method: A literature search and review of relevant papers was undertaken.Result: Studies examining platelet serotonin uptake and concentration in panic disorder patients have to date yielded conflicting results, with some investig

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Varon, David, Jacob Luboshits, Gili Kenet, Boris Shenkman, Naphtali Savion, and Aharon Lubetsky. "Platelet Adrenergic Receptor Dysfunction Is Associated with Both Aggregation and Adhesion Defects: Application of the Cone and Plate(let) Analyzer for Diagnosis and Monitoring of the Response to DDAVP Therapy." Blood 104, no. 11 (2004): 3039. http://dx.doi.org/10.1182/blood.v104.11.3039.3039.

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Abstract Diagnosis of platelet function disorders is based on the nature of bleeding symptoms, a positive family history and abnormal laboratory tests. However, currently available methods are time and labour consuming and lack sensitivity and specificity. In the present study we evaluated the performance of the Cone and Plate (let) analyzer (CPA) for screening patients with a suspected platelet function disorder and for monitoring therapy. Consecutive patients presenting with spontaneous or post surgical bleeding were studied. All patients underwent primary and secondary hemostasis evaluation

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Fábián, Balázs, Ildiko Fanny Horváth, Amir Houshang Shemirani, and Zoltán Csiki. "Depression and Anxiety Symptoms Are Associated with Mean Platelet Volume in Autoimmune Disorders." International Journal of Environmental Research and Public Health 19, no. 17 (2022): 11006. http://dx.doi.org/10.3390/ijerph191711006.

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Platelets are increasingly considered a bridge between mental and immunological disorders. However, data relating to platelet parameters in patients with autoimmune disorders are limited. The aim of the present study was to investigate, for the first time, the association of platelet parameters with the symptoms of affective disorders in patients with autoimmune conditions. In this cross-sectional study, we measured the complete blood count (CBC), the Generalized Anxiety Disorder Scale for anxiety (GAD-7), and the Beck Depression Inventory for depression (BDI) in 121 patients with autoimmune d

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Meyer, M., C. M. Kirchmaier, A. Schirmer, P. Spangenberg, Ch Ströhl, and K. Breddin. "Acquired Disorder of Platelet Function Associated with Autoantibodies against Membrane Glycoprotein IIb-IIIa Complex - 1. Glycoprotein Analysis." Thrombosis and Haemostasis 65, no. 05 (1991): 491–96. http://dx.doi.org/10.1055/s-0038-1648178.

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SummaryA patient with idiopathic thrombocytopenic purpura developed after splenectomy a thrombasthenia-like severe haemor-rhagic 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) lib and Ilia 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 we

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Moka, Nagabhishek, Dong Chen, Chen Han, et al. "Novel Hermanksky-Pudlak Syndrome Type 6 Missense Variant Associated with Subclinical Oculocutaneous Albinism and Mild Bleeding." Blood 132, Supplement 1 (2018): 1153. http://dx.doi.org/10.1182/blood-2018-99-109829.

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Abstract Qualitative disorders of platelets are often missed at clinical evaluation. Hermansky-Pudlak (HPS) syndrome is a rare genetic metabolic disorder with subtype specific clinical associations most prevalent in Puerto Rico with strong link to consanguinity. HPS is usually associated with albinism, visual impairment and a qualitative platelet dysfunction due to absence of dense granules. Ceroid accumulation can be associated with inflammatory bowel disease, pulmonary fibrosis and kidney disease. Ten variants have been described with types 1, 2 and 4 associated with severe disease whilst ty

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Kahr, Walter H. A., Shilun Zheng, Prameet M. Sheth, et al. "Platelets from patients with the Quebec platelet disorder contain and secrete abnormal amounts of urokinase-type plasminogen activator." Blood 98, no. 2 (2001): 257–65. http://dx.doi.org/10.1182/blood.v98.2.257.

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The Quebec platelet disorder (QPD) is an autosomal dominant platelet disorder associated with delayed bleeding and α-granule protein degradation. The degradation of α-granule, but not plasma, fibrinogen in patients with the QPD led to the investigation of their platelets for a protease defect. Unlike normal platelets, QPD platelets contained large amounts of fibrinolytic serine proteases that had properties of plasminogen activators. Western blot analysis, zymography, and immunodepletion experiments indicated this was because QPD platelets contained large amounts of urokinase-type plasminogen

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Kufrin, Dubravka, Don E. Eslin, Khalil Bdeir, et al. "Antithrombotic thrombocytes: ectopic expression of urokinase-type plasminogen activator in platelets." Blood 102, no. 3 (2003): 926–33. http://dx.doi.org/10.1182/blood-2003-01-0054.

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Abstract Arterial occlusive disorders are a leading cause of human morbidity. We hypothesized that ectopic expression of fibrinolytic proteins in platelets could be used to favorably alter the hemostatic balance at sites of thrombosis. To test our hypothesis, we directed murine urokinase-type plasminogen activator transgene expression to platelets using a platelet factor 4 promoter. Urokinase was selectively expressed and stored in the platelets of these mice. These transgenic mice had altered platelet biology and a bleeding diathesis similar to that seen in patients with Quebec platelet disor

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Shlebak, Abdul, Anthony Poles, Richard Manning, et al. "A Novel Homozygous c.800C>G Substitution in GP1BA Exon 2 in a Kuwaiti Family with Bernard-Soulier Syndrome." Acta Haematologica 134, no. 3 (2015): 193–98. http://dx.doi.org/10.1159/000381328.

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Background: Bernard-Soulier syndrome (BSS) is a congenital bleeding disorder characterised by thrombocytopenia, giant platelets and decreased platelet adhesion resulting from genetic alterations of the glycoprotein (GP) Ib/IX/V complex. Objectives: Three sisters with a lifelong bleeding history and a provisional diagnosis of BSS were referred for further characterisation of their bleeding diathesis. The siblings' symptoms varied in severity from skin and gum bleeding to menorrhagia associated with iron-deficiency anaemia requiring regular transfusion of red cells and platelets. The parents wer

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Izzi, Benedetta, Alfonsina Tirozzi, Chiara Cerletti, et al. "Beyond Haemostasis and Thrombosis: Platelets in Depression and Its Co-Morbidities." International Journal of Molecular Sciences 21, no. 22 (2020): 8817. http://dx.doi.org/10.3390/ijms21228817.

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Alongside their function in primary haemostasis and thrombo-inflammation, platelets are increasingly considered a bridge between mental, immunological and coagulation-related disorders. This review focuses on the link between platelets and the pathophysiology of major depressive disorder (MDD) and its most frequent comorbidities. Platelet- and neuron-shared proteins involved in MDD are functionally described. Platelet-related studies performed in the context of MDD, cardiovascular disease, and major neurodegenerative, neuropsychiatric and neurodevelopmental disorders are transversally presente

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Bhattarai, Abhinav, Sangam Shah, Sara Bagherieh, et al. "Endothelium, Platelets, and Coagulation Factors as the Three Vital Components for Diagnosing Bleeding Disorders: A Simplified Perspective with Clinical Relevance." International Journal of Clinical Practice 2022 (August 27, 2022): 1–10. http://dx.doi.org/10.1155/2022/5369001.

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Bleeding disorders are a major group of hematological disorders, which are highly prevalent in the world. Excessive bleeding can result in serious consequences including hypoperfusion and cardiac arrest. The body has its selfmechanism to control excessive bleeding which is termed hemostasis. Hemostasis is achieved in two major steps, the formation of the primary and secondary hemostatic plugs. Endothelium, platelets, and coagulation factors are three components involved in hemostasis. Endothelium and platelets have a major role in forming the primary hemostatic plug. Consequently, the first st

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Kosheed, I. V., A. N. Mamaev, Y. G. Motin, A. V. Kudinov, A. P. Momot, and T. N. Babaeva. "Platelet Delta granules storage pool defi ciency in female patient with severe hemorrhagic syndrome." Russian journal of hematology and transfusiology 68, no. 1 (2023): 90–97. http://dx.doi.org/10.35754/0234-5730-2023-68-1-90-97.

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Introduction. Platelet dense granule disorders are a group of rare heterogeneous disorders of the blood coagulation system in which bleeding occurs due to functional and morphological disorders of platelet organelles accumulating phosphates and bioactive amines. Aim — to present a clinical case of a 37-year-old patient with severe hemorrhagic syndrome. Basic information. An observation of the occurrence of hemorrhagic manifestations of unspecified genesis in a patient is described. The results of 25 healthy volunteer examinations of both sexes were used as a control for testing methods of diag

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Xu, Peipei, Ying Jiang, Huaqin Zuo, et al. "Vincristine-loaded platelets coated with anti-CD41 mAbs: a new macrophage targeting proposal for the treatment of immune thrombocytopenia." Biomaterials Science 7, no. 11 (2019): 4568–77. http://dx.doi.org/10.1039/c9bm01026b.

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Jennings, LK, RA Ashmun, WC Wang, and ME Dockter. "Analysis of human platelet glycoproteins IIb-IIIa and Glanzmann's thrombasthenia in whole blood by flow cytometry." Blood 68, no. 1 (1986): 173–79. http://dx.doi.org/10.1182/blood.v68.1.173.173.

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Abstract Antibodies that bind to human platelet membrane glycoproteins IIb and IIIa were used to develop methods for analyzing platelet membrane components by flow cytometry. Platelets were tentatively identified by their low-intensity light scatter profiles in whole blood or platelet- rich plasma preparations. Identification of this cell population as platelets was verified by using platelet-specific antibodies and fluorescein-conjugated antiimmunoglobulin. Two-parameter analysis of light scatter versus fluorescence intensity identified greater than 98% of the cells in the “platelet” light sc

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49

Jennings, LK, RA Ashmun, WC Wang, and ME Dockter. "Analysis of human platelet glycoproteins IIb-IIIa and Glanzmann's thrombasthenia in whole blood by flow cytometry." Blood 68, no. 1 (1986): 173–79. http://dx.doi.org/10.1182/blood.v68.1.173.bloodjournal681173.

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Antibodies that bind to human platelet membrane glycoproteins IIb and IIIa were used to develop methods for analyzing platelet membrane components by flow cytometry. Platelets were tentatively identified by their low-intensity light scatter profiles in whole blood or platelet- rich plasma preparations. Identification of this cell population as platelets was verified by using platelet-specific antibodies and fluorescein-conjugated antiimmunoglobulin. Two-parameter analysis of light scatter versus fluorescence intensity identified greater than 98% of the cells in the “platelet” light scatter pro

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50

Chaudhari, Atul L., Prakash A Kumbar, Rinjin G. Krishna, and Patel Kajalben. "A case study on Ayurvedic management of Immune Thrombocytopenic Purpura w.s.r to Tiryaka Raktapitta." International Journal of Ayurvedic Medicine 13, no. 1 (2022): 233–37. http://dx.doi.org/10.47552/ijam.v13i1.2411.

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Immune Thrombocytopenic Purpura is an autoimmune disorder which is characterized by destruction and decrease in the number of platelets count due to the presence of autoantibodies directed against platelet. There are two types of Idiopathic thrombocytopenic purpura i.e. acute and chronic forms which are characterized by mucocutaneous bleeding such as oral mucosa, heavy menstrual bleeding or gastrointestinal bleeding and low platelet count with normal peripheral blood cells and smear. Clinical features of ITP are ecchymosis and petechiae or thrombocytopenia incidentally found on a routine CBC.

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