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1

Mazurov, A. V., S. G. Khaspekova, and S. A. Vasiliev. "Diagnostics of thrombocytopenias." Terapevticheskii arkhiv 90, no. 7 (2018): 4–13. http://dx.doi.org/10.26442/terarkh20189074-13.

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Laboratory methods used for the diagnostics of thrombocytopenias are reviewed. Differential diagnosis is usually carried out between immune and hypoproductive forms of thrombocytopenia. Immune thrombocytopenias are caused by appearance in blood of antiplatelet abtibodies and accelerated destruction of platelets sensibilized by those antibodies, and hypoproductive thrombocytopenias - by impaired platelet production in the bone marrow. Main directions of the laboratory diagnostics of thrombocytopenias - analysis of auto - and alloautoantibodies and evaluation of platelet production and turnover
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2

Alugupalli, Kishore R., Alan D. Michelson, Isabelle Joris, et al. "Spirochete-platelet attachment and thrombocytopenia in murine relapsing fever borreliosis." Blood 102, no. 8 (2003): 2843–50. http://dx.doi.org/10.1182/blood-2003-02-0426.

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Abstract Thrombocytopenia is common in persons infected with relapsing fever Borreliae. We previously showed that the relapsing fever spirochete Borrelia hermsii binds to and activates human platelets in vitro and that, after platelet activation, high-level spirochete-platelet attachment is mediated by integrin αIIbβ3, a receptor that requires platelet activation for full function. Here we established that B hermsii infection of the mouse results in severe thrombocytopenia and a functional defect in hemostasis caused by accelerated platelet loss. Disseminated intravascular coagulation, immune
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3

Sun, Siyu, Rolf T. Urbanus, Hugo ten Cate, et al. "Platelet Activation Mechanisms and Consequences of Immune Thrombocytopenia." Cells 10, no. 12 (2021): 3386. http://dx.doi.org/10.3390/cells10123386.

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Autoimmune disorders are often associated with low platelet count or thrombocytopenia. In immune-induced thrombocytopenia (IIT), a common mechanism is increased platelet activity, which can have an increased risk of thrombosis. In addition, or alternatively, auto-antibodies suppress platelet formation or augment platelet clearance. Effects of the auto-antibodies are linked to the unique structural and functional characteristics of platelets. Conversely, prior platelet activation may contribute to the innate and adaptive immune responses. Extensive interplay between platelets, coagulation and c
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4

Vinholt, Pernille J. "The role of platelets in bleeding in patients with thrombocytopenia and hematological disease." Clinical Chemistry and Laboratory Medicine (CCLM) 57, no. 12 (2019): 1808–17. http://dx.doi.org/10.1515/cclm-2019-0380.

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Abstract This review evaluates the role of platelets in bleeding risk among patients with hematological disease and thrombocytopenia. Platelets are pivotal in primary hemostasis, and possess non-hemostatic properties involved in angiogenesis, tissue repair, inflammation and metastatis. Also, platelets safeguard vascular integrity in inflamed vessels. Overall, bleeding risk depends on the underlying disease, and patients with cancer and platelet count <6–10 × 109/L have a markedly increased bleeding risk, while the platelet count does not correlate with bleeding risk at higher platelet count
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5

Arnott, J., P. Horsewood, and JG Kelton. "Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia." Blood 69, no. 5 (1987): 1294–99. http://dx.doi.org/10.1182/blood.v69.5.1294.1294.

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Abstract Platelet-associated IgG (PAIgG) is elevated in idiopathic thrombocytopenic purpura (ITP), but it also is elevated in other thrombocytopenic disorders traditionally considered to be nonimmune. Consequently it is possible that elevated PAIgG is a nonspecific finding secondary to thrombocytopenia. To study this issue we developed a rabbit model of immune and nonimmune mediated thrombocytopenia. The mechanism of the thrombocytopenia was validated by platelet survival studies. Immune thrombocytopenia was produced by injection of antirabbit platelet serum that was raised in guinea pigs. Non
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6

Arnott, J., P. Horsewood, and JG Kelton. "Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia." Blood 69, no. 5 (1987): 1294–99. http://dx.doi.org/10.1182/blood.v69.5.1294.bloodjournal6951294.

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Platelet-associated IgG (PAIgG) is elevated in idiopathic thrombocytopenic purpura (ITP), but it also is elevated in other thrombocytopenic disorders traditionally considered to be nonimmune. Consequently it is possible that elevated PAIgG is a nonspecific finding secondary to thrombocytopenia. To study this issue we developed a rabbit model of immune and nonimmune mediated thrombocytopenia. The mechanism of the thrombocytopenia was validated by platelet survival studies. Immune thrombocytopenia was produced by injection of antirabbit platelet serum that was raised in guinea pigs. Nonimmune ar
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7

Tavares, FL, ME Peichoto, JR Marcelino, et al. "Platelet participation in the pathogenesis of dermonecrosis induced by Loxosceles gaucho venom." Human & Experimental Toxicology 35, no. 6 (2015): 666–76. http://dx.doi.org/10.1177/0960327115597983.

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Loxosceles gaucho spider venom induces in vitro platelet activation and marked thrombocytopenia in rabbits. Herein, we investigated the involvement of platelets in the development of the dermonecrosis induced by L. gaucho venom, using thrombocytopenic rabbits as a model. L. gaucho venom evoked a drop in platelet and neutrophil counts 4 h after venom injection. Ecchymotic areas at the site of venom inoculation were noticed as soon as 4 h in thrombocytopenic animals but not in animals with initial normal platelet counts. After 5 days, areas of scars in thrombocytopenic animals were also larger,
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8

Nishimoto, Tetsuya, Takashi Satoh, Elisa Simpson, Heyu Ni, Tsutomu Takeuchi, and Masataka Kuwana. "Emergence of polyclonal autoantibody responses to multiple platelet surface glycoproteins in regulatory T cell-deficient mice. (115.28)." Journal of Immunology 186, no. 1_Supplement (2011): 115.28. http://dx.doi.org/10.4049/jimmunol.186.supp.115.28.

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Abstract Naturally occurring CD4+CD25+Foxp3+ regulatory T cells (Tregs) are known to play an important role in preventing pathogenic autoimmune responses. Recently, we have found that approximately one third of mice deficient of CD4+CD25+Foxp3+ Tregs spontaneously develop thrombocytopenia with increased platelet-associated IgG, analogous to patients with immune thrombocytopenia. To identify platelet autoantigens in Treg-deficient mice, plasma samples from thrombocytopenic and non-thrombocytopenic Treg-deficient mice were subjected to immunoblots using platelets as an antigen in reduced and non
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9

Brandt, John T., Craig E. Isenhart, Jeanne M. Osborne, Alaa Ahmed та Clark L. Anderson. "On the Role of Platelet FcγRIIa Phenotype in Heparin-Induced Thrombocytopenia". Thrombosis and Haemostasis 74, № 06 (1995): 1564–72. http://dx.doi.org/10.1055/s-0038-1649983.

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SummaryHeparin induced thrombocytopenia (HIT) is characterized by the formation of antibodies that activate normal donor platelets in vitro in the presence of heparin. We asked whether the commonly observed donor-specific variation in the platelet aggregation response to HIT antibodies is influenced by the density of FcγRII on platelets or by the Arg/His 131 allelic polymorphism of platelet FcγRII. We found that platelets with the His/Hisl31 FcγRII phenotype were unresponsive to HIT antibody (0/9) whereas platelets with the Arg/Argl31 phenotype responded well (7/9). His/Hisl31 platelets were l
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10

Mithun, M., and V. Rajashekaraiah. "Antioxidants as supplements during drug-induced thrombocytopenia: a comparative analysis of Vanillic acid, L-carnitine and Caripill™." Ukrainian Biochemical Journal 96, no. 1 (2024): 49–59. http://dx.doi.org/10.15407/ubj96.01.049.

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Drug-induced thrombocytopenia (DIT) is a disorder where platelet count declines as an adverse effect of therapeutic drugs. Plant extract of C. papaya Caripill™ is known to elevate platelet count under thrombocytopenic conditions. To evaluate the contribution of supplements with antioxidant potential to treat DIT, the comparative study of Caripill™, vanillic acid L-carnitine effect on platelet count and indices of oxidative stress in a model of rat thrombocytopenia induced through oral administration of hydroxyurea was performed. Wistar rats were grouped into four categories with five animals i
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11

Lassandro, Giuseppe, Francesco Carriero, Domenico Noviello, et al. "Successful Eltrombopag Therapy in a Child with MYH9-Related Inherited Thrombocytopenia." Children 9, no. 12 (2022): 1839. http://dx.doi.org/10.3390/children9121839.

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Inherited thrombocytopenias represents a heterogenous group of diseases characterized by a congenital reduction in the platelet count that could lead to a bleeding tendency. MYH9-related disorders are characterized by large platelets and congenital thrombocytopenia. Thrombopoietin-receptor agonists: eltrombopag and romiplostim are currently approved in many countries for the treatment of different forms of acquired thrombocytopenia, such as immune thrombocytopenia. We report, instead, the successful use of eltrombopag to treat inherited thrombocytopenia in a patient with an MHY9-related diseas
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12

Lo, S. K., K. E. Burhop, J. E. Kaplan, and A. B. Malik. "Role of platelets in maintenance of pulmonary vascular permeability to protein." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 4 (1988): H763—H771. http://dx.doi.org/10.1152/ajpheart.1988.254.4.h763.

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We examined the role of platelets in maintenance of pulmonary vascular integrity by inducing thrombocytopenia in sheep using antiplatelet serum (APS). A causal relationship between thrombocytopenia and increase in pulmonary vascular permeability was established by platelet repletion using platelet-rich plasma (PRP). Sheep were chronically instrumented and lung lymph fistulas prepared to monitor pulmonary lymph flow (Qlym). A balloon catheter was positioned in the left atrium to assess pulmonary vascular permeability to protein after raising the left atrial pressure (Pla). Thrombocytopenia was
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13

Dale, David C., Janet L. Nichol, Douglas A. Rich, et al. "Chronic Thrombocytopenia Is Induced in Dogs by Development of Cross-Reacting Antibodies to the MpL Ligand." Blood 90, no. 9 (1997): 3456–61. http://dx.doi.org/10.1182/blood.v90.9.3456.

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Abstract The MpL ligand (ML) is a potent stimulus for thrombocytopoiesis. To create an in vivo model of ML deficiency, we injected dogs with a recombinant human ML (rhML) to determine whether cross-reacting antibodies would develop and cause thrombocytopenia. RhML was administered subcutaneously for 8 weeks to three normal dogs (mean platelets, 197 ± 5.5 × 103/μL). Within 5 days their platelet counts were twice baseline and greater than 4 times baseline by day 21. Then, uniformly, chronic thrombocytopenia developed. At 1 week after terminating rhML, mean platelets were 0.5 times baseline and a
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14

Reusswig, Friedrich, Amin Polzin, Meike Klier, et al. "Only Acute but Not Chronic Thrombocytopenia Protects Mice against Left Ventricular Dysfunction after Acute Myocardial Infarction." Cells 11, no. 21 (2022): 3500. http://dx.doi.org/10.3390/cells11213500.

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Background: Platelets are major players of thrombosis and inflammation after acute myocardial infarction (AMI). The impact of thrombocytopenia on platelet-induced cellular processes post AMI is not well defined. Methods: The left anterior descending artery was ligated in C57/Bl6 mice and in two thrombocytopenic mouse models to induce AMI. Results: Platelets from STEMI patients and from C57/Bl6 mice displayed enhanced platelet activation after AMI. This allows platelets to migrate into the infarct but not into the remote zone of the left ventricle. Acute thrombocytopenia by antibody-induced pla
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15

Setarehaseman, Alireza, Abbas Mohammadi, and Robert W. Maitta. "Thrombocytopenia in Sepsis." Life 15, no. 2 (2025): 274. https://doi.org/10.3390/life15020274.

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Platelets, traditionally known for their role in hemostasis, have emerged as key players in immune response and inflammation. Sepsis, a life-threatening condition characterized by systemic inflammation, often presents with thrombocytopenia, which at times, can be significant. Platelets contribute to the inflammatory response by interacting with leukocytes, endothelial cells, and the innate immune system. However, excessive platelet activation and consumption can lead to thrombocytopenia and exacerbate the severity of sepsis. Understanding the multifaceted roles of platelets in sepsis is crucia
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16

Stoll, D., DB Cines, RH Aster, and S. Murphy. "Platelet kinetics in patients with idiopathic thrombocytopenic purpura and moderate thrombocytopenia." Blood 65, no. 3 (1985): 584–88. http://dx.doi.org/10.1182/blood.v65.3.584.584.

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Abstract We studied ten normal subjects and 20 patients with stable, untreated idiopathic thrombocytopenic purpura (ITP) and platelet counts in the range of 35,000 to 110,000/microL. The diagnosis was made by clinical criteria. Platelet-associated IgG was increased in all nine of the nine patients studied. Autologous platelets were labeled with chromium 51 and reinfused for measurement of mean cell life and platelet production rate. Mean cell life was calculated by two methods, weighted mean and multiple hit, with excellent agreement between the two. As expected, mean cell life was significant
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17

Stoll, D., DB Cines, RH Aster, and S. Murphy. "Platelet kinetics in patients with idiopathic thrombocytopenic purpura and moderate thrombocytopenia." Blood 65, no. 3 (1985): 584–88. http://dx.doi.org/10.1182/blood.v65.3.584.bloodjournal653584.

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We studied ten normal subjects and 20 patients with stable, untreated idiopathic thrombocytopenic purpura (ITP) and platelet counts in the range of 35,000 to 110,000/microL. The diagnosis was made by clinical criteria. Platelet-associated IgG was increased in all nine of the nine patients studied. Autologous platelets were labeled with chromium 51 and reinfused for measurement of mean cell life and platelet production rate. Mean cell life was calculated by two methods, weighted mean and multiple hit, with excellent agreement between the two. As expected, mean cell life was significantly reduce
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18

Goerge, Tobias, Benoit Ho-Tin-Noe, Carla Carbo, et al. "Inflammation induces hemorrhage in thrombocytopenia." Blood 111, no. 10 (2008): 4958–64. http://dx.doi.org/10.1182/blood-2007-11-123620.

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Abstract The role of platelets in hemostasis is to produce a plug to arrest bleeding. During thrombocytopenia, spontaneous bleeding is seen in some patients but not in others; the reason for this is unknown. Here, we subjected thrombocytopenic mice to models of dermatitis, stroke, and lung inflammation. The mice showed massive hemorrhage that was limited to the area of inflammation and was not observed in uninflamed thrombocytopenic mice. Endotoxin-induced lung inflammation during thrombocytopenia triggered substantial intra-alveolar hemorrhage leading to profound anemia and respiratory distre
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19

Mazahir, Rufaida, Neha Kumari, Shahzad Alam, and Rupa Singh. "Severe autoimmune thrombocytopenia in a neonate secondary to maternal immune thrombocytopenia: a case report." International Journal of Scientific Reports 8, no. 8 (2022): 240. http://dx.doi.org/10.18203/issn.2454-2156.intjscirep20221839.

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<p>Neonatal thrombocytopenia is one of the common haematological problems encountered in neonatal intensive care unit. Severe neonatal thrombocytopenia is defined as a platelet count <50×10<sup>3</sup>/µl and is relatively uncommon. Based on the time-of-onset, neonatal thrombocytopenia can be categorized into early-onset (<72 h after birth) and late-onset (>72 h after birth) thrombocytopenia. Neonatal autoimmune thrombocytopenia should be considered in any neonate who has early-onset thrombocytopenia and a maternal history of either immune thrombocytopeni
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20

Hanson, SR, and SJ Slichter. "Platelet kinetics in patients with bone marrow hypoplasia: evidence for a fixed platelet requirement." Blood 66, no. 5 (1985): 1105–9. http://dx.doi.org/10.1182/blood.v66.5.1105.1105.

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Abstract We have studied 16 normal subjects and 27 patients with stable, untreated thrombocytopenia secondary to bone marrow failure and platelet counts ranging from 12,000 to 70,000/microL. Autologous platelets were labeled with 51Cr for measurement of mean platelet life span in the normal subjects and in 20 patients. Labeled donor cells were used in the remaining subjects. Platelet survival, as determined with both autologous and homologous platelets, correlated directly with platelet count in the thrombocytopenic patients. Platelet life span was only modestly reduced in patients having coun
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21

Hanson, SR, and SJ Slichter. "Platelet kinetics in patients with bone marrow hypoplasia: evidence for a fixed platelet requirement." Blood 66, no. 5 (1985): 1105–9. http://dx.doi.org/10.1182/blood.v66.5.1105.bloodjournal6651105.

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We have studied 16 normal subjects and 27 patients with stable, untreated thrombocytopenia secondary to bone marrow failure and platelet counts ranging from 12,000 to 70,000/microL. Autologous platelets were labeled with 51Cr for measurement of mean platelet life span in the normal subjects and in 20 patients. Labeled donor cells were used in the remaining subjects. Platelet survival, as determined with both autologous and homologous platelets, correlated directly with platelet count in the thrombocytopenic patients. Platelet life span was only modestly reduced in patients having counts in the
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22

Mesawara, Hend B. E., Neven N. M. Bayomy, Tamer A. E. Elbedewy, and Mahmoud F. Selim. "Effect of helicobacter pylori eradication on hepatitis C virus associated thrombocytopenia." Tanta Medical Journal 53, no. 2 (2025): 171–76. https://doi.org/10.4103/tmj.tmj_25_24.

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Background The infection with the hepatitis C virus is a common cause of chronic hepatitis and liver cirrhosis, causing many hepatic and extra hepatic complications such as thrombocytopenia. Helicobacter pylori is a gram-negative organism, which is complicated by gastric and extra gastric diseases as chronic immune thrombocytopenic purpura. Aim Showing the effect of eradication of H. pylori on platelet count in cases of hepatitis C associated thrombocytopenia. Patients and methods This study was consisted of 150 patients subdivided into two groups. Group 1, including 100 patients with chronic
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23

Jesudas, Rohith, and Clifford M. Takemoto. "Where have all the platelets gone? HIT, DIC, or something else?" Hematology 2023, no. 1 (2023): 43–50. http://dx.doi.org/10.1182/hematology.2023000465.

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Abstract Thrombocytopenia in ill children is common; accurately diagnosing the underlying etiology is challenging and essential for appropriate management. Triggers for accelerated consumption of platelets are numerous; common downstream mechanisms of clearance include platelet trapping in microvascular thrombi, phagocytosis, and platelet activation. Thrombocytopenia with microangiopathic hemolytic anemia (MAHA) is frequently due to disseminated intravascular coagulation. Thrombotic microangiopathy (TMA) is a subgroup of MAHA. Specific TMA syndromes include thrombotic thrombocytopenic purpura,
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24

Nevzorova, Tatiana A., Elmira R. Mordakhanova, Anastasia A. Ponomareva, et al. "Apoptosis Might Contribute to the Thrombocytopenia in Heparin-Induced Thrombocytopenia." Blood 128, no. 22 (2016): 2545. http://dx.doi.org/10.1182/blood.v128.22.2545.2545.

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Abstract Heparin-induced thrombocytopenia (HIT) is a prothrombotic autoimmune complication of heparin therapy. Thrombocytopenia and thrombosis in HIT patients are caused by immune complexes containing pathogenic antibodies against platelet factor 4 (PF4)/glycosaminoglycan complexes. Mechanisms of platelet activation and/or destruction in HIT are not fully understood. Phosphatidylserine expression is a marker of platelet activation that contributes to the procoagulant function. On the other hand, phosphatidylserine expression is generally an early marker of cell apoptosis, which, similarly to o
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25

Li, Chen, Sara Ture, Sara Blick-Nitko, et al. "Platelet CD47 Maintains Circulating Monocyte Immune Homeostasis." Blood 142, Supplement 1 (2023): 675. http://dx.doi.org/10.1182/blood-2023-179997.

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In addition to their well-studied hemostatic functions, platelets are immune cells. Platelets circulate at the interface between the vascular wall and white blood cells, and transient platelet-leukocyte complexes are found in both healthy and disease states, positioning platelets to provide physiologic cues of both vascular health and injury. Roles for activated platelets in inducing and amplifying immune responses have received an increasing amount of research attention, but our past studies also showed that normal platelet counts are needed in healthy conditions to maintain immune homeostasi
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26

Hammer, Hannes, Christoph Bührer, Christof Dame, Malte Cremer, and Andreas Weimann. "Immature platelet values indicate impaired megakaryopoietic activity in neonatal early-onset thrombocytopenia." Thrombosis and Haemostasis 103, no. 05 (2010): 1016–21. http://dx.doi.org/10.1160/th09-03-0148.

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SummaryNewly released platelets, referred to as immature platelets, can be reliably quantified based on their RNA content by flow cytometry in an automated blood analyser. The absolute number of immature platelets (IPF#) and the immature platelet fraction (IPF%) reflect megakaryopoietic activity. We aimed to analyse the implication of these parameters in analysing the pathomechanism of early-onset neonatal thrombocytopenia. Platelet counts and IPF were determined at day 1 to 3 (d1 to d3) in 857 neonates admitted to intensive care. In thrombocytopenic patients (platelet counts<150 x 109/l, n
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27

Anil, Kumar, Bharti Pranav, and Mishra Asim. "A Prospective Study of Platelet Indices and Their Interpretation in Thrombocytopenia at a Tertiary Care Hospital." International Journal of Pharmaceutical and Clinical Research 15, no. 10 (2023): 1334–39. https://doi.org/10.5281/zenodo.11288767.

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<strong>Background:</strong>&nbsp;Thrombocytopenia is defined as a platelet count of &lt;150 &times; 10<sup>9</sup>/L, although patients with a platelet count &gt;50 &times; 10<sup>9</sup>/L are usually asymptomatic. Severe spontaneous bleeding is rare in thrombocytopenia. It is more common when the platelet count is &lt;20 &times; 10<sup>9</sup>/L, and particularly when &lt;10 &times; 10<sup>9</sup>/L.&nbsp;<strong>Aims and Objectives:</strong>&nbsp;The present study was conducted to evaluate platelet indices and their interpretation in thrombocytopenia in a tertiary care hospital.&nbsp;<stro
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28

Lee, S. H., S. Looareesuwan, J. Chan, et al. "Plasma Macrophage Colony-Stimulating Factor and P-Selectin Levels in Malaria-Associated Thrombocytopenia." Thrombosis and Haemostasis 77, no. 02 (1997): 289–93. http://dx.doi.org/10.1055/s-0038-1655955.

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SummaryThrombocytopenia is a common finding in malaria. In clinical trials, recombinant macrophage colony-stimulating factor (M-CSF) causes a reversible, dose-dependent thrombocytopenia, and high M-CSF has been reported in autoimmune thrombocytopenias. P-selectin, which is secreted into the plasma following platelet/endothelial activation or damage, is elevated in certain consumptive thrombocytopenic disorders. The relationships between thrombocytopenia, M-CSF and P-selectin were analysed in 63 patients with severe (n = 13) or uncomplicated (n = 26) P. falciparum (PF) or P. vivax (PV) malaria
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29

Goodnough, Lawrence T., David J. Kuter, Jeffrey McCullough, et al. "Prophylactic platelet transfusions from healthy apheresis platelet donors undergoing treatment with thrombopoietin." Blood 98, no. 5 (2001): 1346–51. http://dx.doi.org/10.1182/blood.v98.5.1346.

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Many patients receiving dose-intensive chemotherapy acquire thrombocytopenia and need platelet transfusions. A study was conducted to determine whether platelets harvested from healthy donors treated with thrombopoietin could provide larger increases in platelet counts and thereby delay time to next platelet transfusion compared to routinely available platelets given to thrombocytopenic patients. Community platelet donors received either 1 or 3 μg/kg pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) or placebo and then donated platelets 10 to 15 days later.
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30

Yoneyama, Akiko, Jun Shirai, Tateru Ishida, et al. "Evaluation of Thrombopoiesis in Thrombocytopenic Disorders by Simultaneous Measurement of Reticulated Platelets of Whole Blood and Serum Thrombopoietin Concentrations." Thrombosis and Haemostasis 79, no. 06 (1998): 1106–10. http://dx.doi.org/10.1055/s-0037-1615024.

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SummaryTo evaluate thrombopoiesis in thrombocytopenic disorders, we simultaneously determined reticulated platelet counts in whole blood by FACScan flow cytometry and serum thrombopoietin (TPO) concentrations by a sensitive sandwich ELISA. The subjects were 40 healthy volunteers and 45 thrombocytopenic patients. In idiopathic thrombocytopenic purpura (ITP), the percentage of reticulated platelets was significantly elevated (5.61 ± 2.02%: mean ± SD) relative to normal controls (2.17 ± 0.90%), but serum TPO concentrations (1.91 ± 1.27 fmol/l) did not differ significantly from the normal range (1
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31

Out, HJ, PG de Groot, M. van Vliet, GC de Gast, HK Nieuwenhuis, and RH Derksen. "Antibodies to platelets in patients with anti-phospholipid antibodies." Blood 77, no. 12 (1991): 2655–59. http://dx.doi.org/10.1182/blood.v77.12.2655.2655.

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Abstract Binding of anti-phospholipid antibodies to circulating platelets and its consequences on platelet activation and aggregation was investigated in 11 patients with anti-phospholipid antibodies. Seven patients had mild thrombocytopenia. Nine healthy donors served as controls. Binding to platelets was investigated by performing enzyme- linked immunosorbent assays (ELISAs) with phospholipids as antigen on platelet eluates. Platelet activation was measured by flow cytofluorometry using monoclonal antibodies to an activation-specific lysosomal membrane protein. Findings in ELISA were compare
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32

Out, HJ, PG de Groot, M. van Vliet, GC de Gast, HK Nieuwenhuis, and RH Derksen. "Antibodies to platelets in patients with anti-phospholipid antibodies." Blood 77, no. 12 (1991): 2655–59. http://dx.doi.org/10.1182/blood.v77.12.2655.bloodjournal77122655.

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Binding of anti-phospholipid antibodies to circulating platelets and its consequences on platelet activation and aggregation was investigated in 11 patients with anti-phospholipid antibodies. Seven patients had mild thrombocytopenia. Nine healthy donors served as controls. Binding to platelets was investigated by performing enzyme- linked immunosorbent assays (ELISAs) with phospholipids as antigen on platelet eluates. Platelet activation was measured by flow cytofluorometry using monoclonal antibodies to an activation-specific lysosomal membrane protein. Findings in ELISA were compared with re
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33

Garibaldi, Brian T., Rupal B. Malani, Hsin-Chieh Yeh, et al. "The Immature Platelet Fraction in HIV Patients with Thrombocytopenia." Blood 110, no. 11 (2007): 2095. http://dx.doi.org/10.1182/blood.v110.11.2095.2095.

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Abstract Thrombocytopenia is a common clinical feature of HIV infection. Given the number of possible etiologies of thrombocytopenia in a patient with known HIV, a peripheral blood test effective in determining the likely pathophysiologic basis of the thrombocytopenia would be a valuable clinical tool. Immature platelets are released early from the bone marrow in response to increased platelet turnover. These platelets contain residual megakaryocyte mRNA and have been termed reticulated platelets. A new assay, the Immature Platelet Fraction (IPF), measures the reticulated platelet count in per
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34

Psaila, Bethan, James B. Bussel, Matthew D. Linden, et al. "Comparison of Platelet Function and Bleeding in Thrombocytopenic Patients with Immune Thrombocytopenic Purpura (ITP) and Chemotherapy-Induced Thrombocytopenia (CIT)." Blood 110, no. 11 (2007): 2094. http://dx.doi.org/10.1182/blood.v110.11.2094.2094.

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Abstract Because of methodologic problems, platelet function in thrombocytopenic patients has never been adequately studied, and therefore individual differences in bleeding risk are poorly understood. Whole blood flow cytometry analyzes the function of individual platelets, thereby enabling assessment of platelet function in severe thrombocytopenia (Michelson, A. Platelets, 2nd ed, Elsevier, 2007). In this study, platelet function was compared in 31 ITP patients, 14 CIT patients, and 16 healthy controls. Clinical bleeding was related to platelet function testing. The immature platelet fractio
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Aslam, Rukhsana, Edwin R. Speck, Michael Kim та ін. "Platelet Toll-like receptor expression modulates lipopolysaccharide-induced thrombocytopenia and tumor necrosis factor-α production in vivo". Blood 107, № 2 (2006): 637–41. http://dx.doi.org/10.1182/blood-2005-06-2202.

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AbstractToll-like receptors (TLRs) play a critical role in stimulating innate immunity by recognizing pathogen-associated molecular patterns (PAMPs) on invading microorganisms. Platelets also play a role in innate immunity, and we studied whether they express TLR. Results show that human and murine platelets variably expressed TLR2, TLR4, and TLR9 by flow cytometry and Western blotting. TLR4 expression was confirmed by demonstrating murine platelet binding to lipopolysaccharide (LPS). Thrombin activation of the platelets significantly enhanced the expression of TLR9, suggesting that at least s
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36

Marini, Irene, Jan Zlamal, Christoph Faul, et al. "Autoantibody-mediated desialylation impairs human thrombopoiesis and platelet lifespan." Haematologica 106, no. 1 (2019): 196–207. http://dx.doi.org/10.3324/haematol.2019.236117.

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Immune thrombocytopenia is a common bleeding disease caused by autoantibody-mediated accelerated platelet clearance and impaired thrombopoiesis. Accumulating evidence suggests that desialylation affects platelet life span in immune thrombocytopenia. Herein, we report on novel effector functions of autoantibodies from immune thrombocytopenic patients which might interfere with the clinical picture of the disease. Data from our study show that a subgroup of autoantibodies is able to induce cleave of sialic acid residues from the surface of human platelets and megakaryocytes. Moreover, autoantibo
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Miyazaki, Koji, Miyako Taira, Tomiteru Togano, et al. "Immature Platelet Fraction in Different Diagnosis of Thrombocytopenic States: An Approach to Distinguish Idiopathic Thrombocytopenic Purpura from Myelodysplastic Syndrome with Isolated Thrombocytopenia." Blood 108, no. 11 (2006): 1085. http://dx.doi.org/10.1182/blood.v108.11.1085.1085.

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Abstract It is sometimes confusing to distinguish idiopathic thrombocytopenic purpura (ITP) from thrombocytopenia due to dysmegakaryopoiesis, as seen in myelodysplastic syndrome (MDS) patients, especially MDS with isolated thrombocytopenia. In this study, we investigated the useful parameters for the different diagnosis of thrombocytopenia. The number of reticulated platelets reflects the rate of thrombopoiesis, and this clinical utility has been established in the laboratory diagnosis of thrombocytopenia due to increased peripheral platelet destruction, such as autoimmune thrombocytopenic pur
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38

Nishimoto, Tetsuya, Takashi Satoh, Yasuo Ikeda, and Masataka Kuwana. "A Critical Role of CD4+CD25+ Regulatory T Cells In Prevention of Murine Autoantibody-Mediated Thrombocytopenia." Blood 116, no. 21 (2010): 381. http://dx.doi.org/10.1182/blood.v116.21.381.381.

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Abstract Abstract 381 Immune thrombocytopenic purpura (ITP) is a T cell-mediated autoimmune disorder, in which IgG autoantibodies to platelet surface glycoproteins promote platelet clearance in the reticuloendthelial system. Since CD4+CD25+ regulatory T cells (Tregs) are known to play a crucial role in the maintenance of immune homeostasis to self-antigens, it has been believed that Treg dysfunction contributes to the development of a various forms of human autoimmune disorders. Several lines of recent evidence have shown that Tregs are decreased in number and are functionally impaired in pati
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39

Kocfa, Chung-Delgado, Revilla-Montag Alejandro, Guillén-Bravo Sonia, Ríos-Díaz Hugo, and C. Alva-Muñoz José. "Refractory Thrombocytopenia Responds to Octreotide Treatment in a Case of Evans Syndrome with Gastric Neuroendocrine Tumor." Case Reports in Hematology 2013, ID 391086 (2015): 5. https://doi.org/10.1155/2013/391086.

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A 37-year-old woman with history of Evans Syndrome with poor response to high-dose corticoid treatment presented to the emergency department with gastrointestinal and vaginal bleeding. The patient was later diagnosed with severe thrombocytopenia and a stage G1, well-differentiated gastric neuroendocrine tumor, confirmed by a biopsy. A total gastrectomy was performed to eradicate the tumor. After being treated with a total splenectomy for her Evans Syndrome with no clinical or laboratory improvement, she began regular treatment with octreotide on the basis of a possible hepatic metastasis. Days
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Menitove, JE, J. Pereira, R. Hoffman, T. Anderson, W. Fried, and RH Aster. "Cyclic thrombocytopenia of apparent autoimmune etiology." Blood 73, no. 6 (1989): 1561–69. http://dx.doi.org/10.1182/blood.v73.6.1561.1561.

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Abstract Serial studies were performed in two patients with cyclic thrombocytopenia to investigate the pathogenesis of this disorder. Mean life span of autologous platelets when platelet levels were declining was subnormal (2.4 and 0.8 days), and megakaryocytes were abundant in the bone marrow during thrombocytopenia. Megakaryocyte colony- stimulating activity could not be detected in the serum of either patient at any point of their cycles. In each patient, total platelet- associated IgG varied inversely with platelet levels. Surface platelet- associated IgG was measured only in patient 2 and
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41

Menitove, JE, J. Pereira, R. Hoffman, T. Anderson, W. Fried, and RH Aster. "Cyclic thrombocytopenia of apparent autoimmune etiology." Blood 73, no. 6 (1989): 1561–69. http://dx.doi.org/10.1182/blood.v73.6.1561.bloodjournal7361561.

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Serial studies were performed in two patients with cyclic thrombocytopenia to investigate the pathogenesis of this disorder. Mean life span of autologous platelets when platelet levels were declining was subnormal (2.4 and 0.8 days), and megakaryocytes were abundant in the bone marrow during thrombocytopenia. Megakaryocyte colony- stimulating activity could not be detected in the serum of either patient at any point of their cycles. In each patient, total platelet- associated IgG varied inversely with platelet levels. Surface platelet- associated IgG was measured only in patient 2 and was sign
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42

Parmar, Riddhi A., and Keval A. Patel. "Immune Thrombocytopenic Purpura (ITP): A Comprehensive Review." GAIMS Journal of Medical Sciences 4, no. 1 (2023): 103–7. https://doi.org/10.5281/zenodo.10253600.

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Immune thrombocytopenic purpura (ITP) is a condition where the body's immune system mistakenly attacks and destroys platelets, resulting in a decreased platelet count. This leads to the development of purpura on the skin and may cause bleeding episodes due to the presence of antibodies that target and damage platelets. Excluding the usual suspects helps in identifying the underlying causes of thrombocytopenia. The diagnosis of immune thrombocytopenia (ITP) relies on clinical suspicion and the presence of thrombocytopenia, as indicated on a normal peripheral smear. Bone marrow examination is pe
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Sen Gupta, Anirban. "Synthetic Platelets for Treatment of Traumatic Hemorrhage and Thrombocytopenia." Blood 134, Supplement_1 (2019): SCI—37—SCI—37. http://dx.doi.org/10.1182/blood-2019-121079.

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Platelets are primarily responsible for staunching bleeding by forming a 'platelet plug' and further amplifying thrombin generation on its surface to facilitate fibrin formation, leading to hemostatic clot formation at the site of vascular breach. Therefore, platelet transfusions are clinically used to mitigate bleeding risks in thrombocytopenia (prophylactic transfusion) and to mitigate hemorrhage in traumatic injuries (emergency transfusion). Currently these transfusions utilize donor-derived platelets, stored at 20-24oC with gentle agitation. In this condition, platelets have high risk of b
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Yamada, Shinya, and Hidesaku Asakura. "How We Interpret Thrombosis with Thrombocytopenia Syndrome?" International Journal of Molecular Sciences 25, no. 9 (2024): 4956. http://dx.doi.org/10.3390/ijms25094956.

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Platelets play an important role in hemostasis, and a low platelet count usually increases the risk of bleeding. Conditions in which thrombosis occurs despite low platelet counts are referred to as thrombosis with thrombocytopenia syndrome, including heparin-induced thrombocytopenia, vaccine-induced immune thrombotic thrombocytopenia, paroxysmal nocturnal hemoglobinuria, antiphospholipid syndrome, thrombotic microangiopathy (TMA), and disseminated intravascular coagulation. TMA includes thrombotic thrombocytopenic purpura, Shiga toxin-producing Escherichia coli-associated hemolytic uremic synd
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Abdalhadi, Haneen, Yazan Fahmawi, Abhijin Das, and Brian Fouty. "Life-Threatening Intrapulmonary Hemorrhage due to Vancomycin-Induced Thrombocytopenia: A Case Report." Case Reports in Critical Care 2020 (September 30, 2020): 1–3. http://dx.doi.org/10.1155/2020/8890335.

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Thrombocytopenia is a rare and sometimes life-threatening complication of Vancomycin. A 52-year-old male patient with acute kidney injury was treated with Vancomycin for ventilator-associated pneumonia. Three days later, his platelets decreased from 172×109/L to 3×109/L over a 36-hour period. The patient developed significant intrapulmonary bleeding leading to profound hypoxemia. Workup was negative for thrombotic thrombocytopenic purpura, disseminated intravascular coagulopathy, atypical hemolytic uremic syndrome, heparin-induced thrombocytopenia, and autoimmune diseases. All recently started
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46

Kochieva, Marina Leonidovna. "Modern approach to the diagnosis and treatment of thrombocytopenia." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 12 (November 20, 2021): 28–34. http://dx.doi.org/10.33920/med-10-2112-04.

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Normally, the number of platelets in a healthy adult is in the range of 150-320 x 10⁹. A condition in which their number falls below 150x10⁹ is called thrombocytopenia. It can be both associated with a violation of the process of platelet formation in the bone marrow (in particular, with aplastic anemia, hemoblastosis, thrombocytopenic purpura), and be a concomitant pathology, for example, be a consequence of drug treatment of a number of somatic diseases. In the pathogenesis of thrombocytopenia, three main directions are distinguished: a decrease in platelet production, an acceleration of the
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Chen, Yuhan, Michael Kim, Arata Tabuchi, et al. "The Role of Recipient Platelets In the Prevention of Antibody-Mediated Transfusion Related Acute Lung Injury (TRALI)." Blood 116, no. 21 (2010): 3351. http://dx.doi.org/10.1182/blood.v116.21.3351.3351.

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Abstract Abstract 3351 Transfusion related acute lung injury (TRALI) is a serious complication of transfusion. The pathogenesis of TRALI is not fully understood but previous findings have suggested that platelet depletion can protect mice in a two-hit model of TRALI (Looney et al J Clin Invest 119:3450, 2009). To further understand the role of platelets in preventing antibody-mediated TRALI, two mouse models of immune thrombocytopenia (ITP) were utilized. In the passive ITP model, SCID mice were injected with a monoclonal anti-platelet antibody (MWReg30) intraperitoneally (ip, 18 h before TRAL
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48

Warkentin, TE, CP Hayward, LK Boshkov, et al. "Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia." Blood 84, no. 11 (1994): 3691–99. http://dx.doi.org/10.1182/blood.v84.11.3691.bloodjournal84113691.

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Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a hep
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Oyaizu, N., R. Yasumizu, M. Miyama-Inaba, et al. "(NZW x BXSB)F1 mouse. A new animal model of idiopathic thrombocytopenic purpura." Journal of Experimental Medicine 167, no. 6 (1988): 2017–22. http://dx.doi.org/10.1084/jem.167.6.2017.

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A decrease in thrombocyte count was observed in (NZW x BXSB)F1 (W/B F1) mice at the age of greater than 5 mo, whereas megakaryocyte counts were found to increase in such mice. FACS analyses revealed the presence of both platelet-associated antibodies (PAA) and circulating antiplatelet antibodies. There is a correlation between the presence of these antibodies and the degree of thrombocytopenia. The transplantation of normal bone marrow cells from BALB/c nu/nu mice to W/B F1 mice was found to have preventative and curative effects on thrombocytopenia; the mice showed normal platelet counts and
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50

Nishiyama, Uichi, Haruhiko Morita, Yoshifumi Torii, et al. "Platelets Exposed to Elevated Levels of Endogenous Thrombopoietin In Vivo Have a Reduced Response to Megakaryocyte Growth and Development Factor In Vitro." Thrombosis and Haemostasis 85, no. 01 (2001): 152–59. http://dx.doi.org/10.1055/s-0037-1612918.

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SummaryThrombopoietin (TPO), or megakaryocyte growth and development factor (MGDF), has been shown to potentiate the sensitivity of normal human platelets to various agonists in vitro. The present study investigated the functional and biochemical properties of platelets from mice rendered thrombocytopenic by sublethal irradiation with regard to the reactivity to recombinant murine MGDF (rmMGDF) in vitro. During the course of reversible thrombocytopenia following irradiation, platelets from irradiated mice which had lower platelet counts and reciprocally higher plasma TPO levels showed lower re
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