Relevant bibliographies by topics / Thrombocytopenia

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Thrombocytopenia'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 April 2023

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Journal articles on the topic "Thrombocytopenia"

1

Browning, James, and David James. "Immune thrombocytopenia in pregnancy." Fetal and Maternal Medicine Review 2, no. 2 (July 1990): 143–57. http://dx.doi.org/10.1017/s0965539500000334.

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Autoimmune thrombocytopenia (ITP)1) The risks to mother and fetus have previously been overstated.2) There is no maternal test which will accurately determine fetal thrombocytopenia.3) The only reliable test for fetal thrombocytopenia is cordocentesis – this carries a higher morbidity than that of fetal intracerebral haemorrhage from ITP.4) Contrary to received wisdom, there is no evidence that, even for the most severely thrombocytopenic infant, abdominal delivery protects against intracranial haemorrhage.5) Management therefore involves keeping the maternal platelet count above 50 × 1091 and choosing the route of delivery on normal obstetric grounds.Alloimmune thrombocytopenia1) Alloimmune thrombocytopenia is commoner than hitherto believed (0.15% all neonates).2) The fetal risks are considerable: intracranial haemorrhage occurs in 4% of cases antenatally and in 10% in labour. The risks are virtually confined to those with a platelet count of less than 30 × 109l−1.3) Cordocentesis is justified for the ‘at risk’ fetus; fetal immunoglobulin or platelet therapy can be given.4) When the fetal platelet count is below 50 × 109l−1, abdominal delivery should be planned.5) A maternal screening test for neonatal alloimmune thrombocytopenia exists (lack of P1A1 antigen).
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Gouin-Thibault, Isabelle, Bruno Cassinat, Christine Chomienne, Jean-Didier Rain, Yves Najean, and Marie-Hélène Schlageter. "Is the Thrombopoietin Assay Useful for Differential Diagnosis of Thrombocytopenia? Analysis of a Cohort of 160 Patients with Thrombocytopenia and Defined Platelet Life Span." Clinical Chemistry 47, no. 9 (September 1, 2001): 1660–65. http://dx.doi.org/10.1093/clinchem/47.9.1660.

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Abstract Background: Thrombopoietin (TPO), the major hormone controlling platelet production, has been measured in thrombocytopenias with discordant results. The aim of our work was to assess the value of the TPO assay for differential diagnosis of thrombocytopenias in a large cohort of patients classified according to the results of their platelet isotopic study. Methods: We measured TPO (R&D Systems) in serum of 160 thrombocytopenic patients referred to our department for platelet life span isotopic studies. We classified patients as follows: (a) idiopathic or autoimmune thrombocytopenia group (ITP; patients with increased platelet destruction and shortened platelet life span; n = 67); (b) pure genetic thrombocytopenia group (patients with decreased platelet production, normal platelet life span, and without bone marrow aplasia; n = 55); (c) bone marrow aplasia group (BM; patients with decreased platelet production, normal platelet life span, and bone marrow aplasia; n = 13). Results: In patients with pure genetic thrombocytopenia, TPO (median, 55 ng/L) was not different from TPO in patients with ITP (median, 58 ng/L) or controls (n = 54; median, 51 ng/L). Only in patients with bone marrow aplasia was TPO significantly higher (median, 155 ng/L) and negatively correlated to the platelet count (r2 = 0.5014). Conclusions: Although the median serum TPO is increased in thrombocytopenia with decreased platelet production from bone marrow aplasia, it does not differentiate patients with pure genetic thrombocytopenia from those with ITP.
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Weimann, Andreas, Andreas Lun, Gerhard Gaedicke, and Malte Cremer. "Immature Platelet Fraction (IPF) as Novel Laboratory Parameter for Managing Early Onset Thrombocytopenia in Very Low Birth Weight Infants." Blood 112, no. 11 (November 16, 2008): 4552. http://dx.doi.org/10.1182/blood.v112.11.4552.4552.

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Abstract Thrombocytopenia (platelet count <150/nl) is one of the most common hematologic problems in preterm and term neonates and affects 18 to 35% of all patients admitted to neonatal intensive care units (NICU). Thrombocytopenia is more than twice common in extremely low birth weight infants (ELBW; <1000g) as reported among the general NICU population. Among thrombocytopenic ELBW infants almost 40% suffer from severe thrombocytopenia as defined by a platelet count <50nl. The risk for hemorrhage, which may cause acute life-threatening complications and/or life-long disability in more than 15%, is difficult to assess, because it is closely related to the gestational and postnatal age of the neonate as well as the cause of the thrombocytopenia and the severity of concurrent conditions. From routine full blood counts of premature (birth weight <1500g) and full term babies we additionally determined platelet counts, IPF, MPV, NRBC and reticulocyte counts. On the basis of individual IPF and platelet counts we were able to predict the platelet counts of the following day. In non-thrombocytopenic preterm and term neonates no significant changes in IPF values were found during the first week of life. In the first week, thrombocytopenic neonates displayed higher IPF values than neonates with normal plaletet counts. We hypothesize that IPF is higher in neonates with chronic hypoxia as leading cause for thrombocytopenia and lower in case of perinatal infections. IPF could be a novel parameter in routine diagnostics available at a 24/7 basis in VLBW infants and may be valuable in identifying the underlying pathomechanism of various thrombocytopenias and in clinical decision making on platelet transfusions.
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4

Skupski, Daniel W., and James B. Bussel. "Antenatal treatment of fetal immune thrombocytopenias." Fetal and Maternal Medicine Review 10, no. 1 (February 1998): 1–19. http://dx.doi.org/10.1017/s0965539598000114.

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Advances in both imaging techniques and in treatments for immune thrombocytopenias affecting the fetus have allowed for more accurate antenatal predictions of severe disease and effective antenatal treatments for those fetuses who are at risk of sequelae. This article will review current knowledge of the diagnosis and treatment of affected fetuses in alloimmune thrombocytopenia and in immune thrombocytopenic purpura.
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5

Lee, S. H., S. Looareesuwan, J. Chan, P. Wilairatana, S. Vanijanonta, S. M. Chong, and B. H. Chong. "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 (n = 24). On admission, 69% of PF patients and 75% of PV patients were thrombocytopenic (platelets < 150 X 109/1). M-CSF was elevated in PF (3021 ± 1844 pg/ml) and PV (2602 ± 1668 pg/ml) patients, compared to controls (589 ± 200 pg/ml). The platelet count was inversely correlated with M-CSF in PF (r = -0.681), and in PV malaria (r = -0.548). Elevated P-selectin was found in severe PF malaria, but not in PV malaria. Severe PF malaria was associated with marked thrombocytopenia, very high M-CSF, elevated P-selectin and compelling evidence of disseminated intravascular coagulopathy (DIC). Platelet counts, M-CSF and P-selectin returned to control values in 7-14 days. These data suggest that elevated M-CSF in malaria, by enhancing macrophage activity, may result in increased macrophage-mediated platelet destruction. Further, platelet/endothelial activation or damage, as measured by P-selectin, or DIC could intensify thrombocytopenia in severe PF malaria, but does not appear to contribute to thrombocytopenia in uncomplicated PF or PV malaria.
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Ellahi, Ayesha, Muhammad Wasiullah Khan, Samra Shahid, Javaid Usman, Hassan Ikran, and Safoora Naveed. "Thrombocytopenia in Pregnancy: A Cross-Sectional Study in Northern Pakistan." Pakistan Armed Forces Medical Journal 72, no. 3 (June 26, 2022): 1013–17. http://dx.doi.org/10.51253/pafmj.v72i3.7048.

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Objective: To determine the association of thrombocytopenia (mild, moderate & severe) with pregnancy-related disorders. Study Design: Cross-sectional study. Place and Duration of Study: Department of Haematology of Pakistan Railway Hospital, Rawalpindi Pakistan, in collaboration with the Departments of Obstetrics and Gynecology of Pak Emirates Military Hospital and Fuji Foundation Hospital, Rawalpindi Pakistan, from Oct 2018 to Oct 2019. Methodology: Seventy-five pregnant females with platelet count <150x109/l were included. Blood samples were taken and analyzed for complete blood count, peripheral blood smear, manual count by Neubauer chamber, uric acid, urinary proteins, liver function tests (bilirubin & aspartate aminotransferase), lactate dehydrogenase, coagulation profile and viral serology (Hepatitis B & C). Results: Out of a total of 75 thrombocytopenic pregnant females, gestational thrombocytopenia was most common (74.7%), followed by preeclampsia (17.3%), HELLP syndrome (4%), immune thrombocytopenic purpura (4%) respectively. Mild thrombocytopenia was frequently observed in patients of G.T. (62.5%), while moderate thrombocytopenia (84.6%) was generally detected in preeclampsia patients. Severe thrombocytopenia was mostly identified in patients with HELLP syndrome (66.7%) and immune thrombocytopenic purpura (66.7%). Conclusion: Mild thrombocytopenia is mostly presented in gestational thrombocytopenia. Moderate thrombocytopenia was frequent in patients with preeclampsia, and severe thrombocytopenia was usually diagnosed in patients with HELLP syndrome and immune thrombocytopenic purpura, which require apposite and judicious management for the safety of mother and fetus.
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Komatsu, Norio. "1. Immune Thrombocytopenic Purpura (Immune Thrombocytopenia)." Nihon Naika Gakkai Zasshi 103, no. 7 (2014): 1593–98. http://dx.doi.org/10.2169/naika.103.1593.

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8

Özsoylu, Sinasi, Janine Campbell, and Christina Mitchell. "Autoimmune thrombocytopenia versus idiopathic thrombocytopenic purpura." European Journal of Haematology 53, no. 1 (April 24, 2009): 54–55. http://dx.doi.org/10.1111/j.1600-0609.1994.tb00181.x.

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9

Arnott, J., P. Horsewood, and JG Kelton. "Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia." Blood 69, no. 5 (May 1, 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. Nonimmune aregenerative thrombocytopenia was produced by irradiation of the animals; nonimmune consumptive thrombocytopenia was produced by injection of adenosine diphosphate (ADP). PAIgG was measured in a direct binding assay using 125I-labeled staphylococcal protein A (SpA). Washed platelets from normal, nonthrombocytopenic rabbits bound an average of 81 molecules of SpA per platelet (81 +/- 168, mean +/- 2 SD, n = 39). Infusion of the antiplatelet antiserum produced thrombocytopenia with a rise in PAIgG that was closely correlated with the level of PAIgG (r = 0.86, n = 12). The thrombocytopenia was consumptive, as shown by a very short platelet life span using 111In- labeled platelets. In contrast, both nonimmune thrombocytopenic states resulted in an equal or greater drop in the platelet count but no change in the level of PAIgG. The animals with aregenerative thrombocytopenia had normal or only moderately reduced platelet life spans; however, in every animal the level of PAIgG was not different from the nonthrombocytopenic controls, irrespective of the platelet count. Similarly, the level of PAIgG was unchanged in those rabbits with nonimmune consumptive thrombocytopenia following infusion of ADP (82 +/- 55 molecules of SpA per platelet, mean +/- SD, n = 6). These studies indicate that elevated PAIgG is a specific finding of immune thrombocytopenia and is not secondary to thrombocytopenia itself. Indirectly these results support our hypothesis that immune mechanisms contribute to more thrombocytopenic disorders than was once thought likely.
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Arnott, J., P. Horsewood, and JG Kelton. "Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia." Blood 69, no. 5 (May 1, 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 aregenerative thrombocytopenia was produced by irradiation of the animals; nonimmune consumptive thrombocytopenia was produced by injection of adenosine diphosphate (ADP). PAIgG was measured in a direct binding assay using 125I-labeled staphylococcal protein A (SpA). Washed platelets from normal, nonthrombocytopenic rabbits bound an average of 81 molecules of SpA per platelet (81 +/- 168, mean +/- 2 SD, n = 39). Infusion of the antiplatelet antiserum produced thrombocytopenia with a rise in PAIgG that was closely correlated with the level of PAIgG (r = 0.86, n = 12). The thrombocytopenia was consumptive, as shown by a very short platelet life span using 111In- labeled platelets. In contrast, both nonimmune thrombocytopenic states resulted in an equal or greater drop in the platelet count but no change in the level of PAIgG. The animals with aregenerative thrombocytopenia had normal or only moderately reduced platelet life spans; however, in every animal the level of PAIgG was not different from the nonthrombocytopenic controls, irrespective of the platelet count. Similarly, the level of PAIgG was unchanged in those rabbits with nonimmune consumptive thrombocytopenia following infusion of ADP (82 +/- 55 molecules of SpA per platelet, mean +/- SD, n = 6). These studies indicate that elevated PAIgG is a specific finding of immune thrombocytopenia and is not secondary to thrombocytopenia itself. Indirectly these results support our hypothesis that immune mechanisms contribute to more thrombocytopenic disorders than was once thought likely.
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Dissertations / Theses on the topic "Thrombocytopenia"

1

Johnson, Ben David. "Molecular genetic investigation into inherited thrombocytopenia." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7555/.

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Inherited thrombocytopenias are a heterogeneous group of disorders characterised by abnormally low platelet counts, often with secondary qualitative defects in platelet function, which can be associated with abnormal bleeding. Next generation sequencing has only previously been employed in small-scale studies and for the confirmation of suspected variants. This study presents the first large-scale approach to fully categorise inherited thrombocytopenia. Ninety-five patients were recruited to the UK-Genotyping and Phenotyping (GAPP) study with inherited thrombocytopenia of unknown genetic aetiology. An average platelet count of 88x109/L was observed across all individuals. Platelet function testing revealed a secondary phenotypic defect in addition to the reduction in platelet count in 71% (61/86). Of the 95 patients, 69 patients, encompassing 47 index cases, were analysed by whole exome sequencing. A variant with a positive prediction of pathogenicity was identified in 40% (19/47) of patients and overall plausible candidate variants of disease were identified in 69% of index cases. Subsequently an inherited thrombocytopenia specific gene panel was developed to serve as a pre-screen for patients prior to whole exome sequencing. In total, candidate variants in genes previously known to be implicated with disease were identified in 77% (20/26) of patients analysed. In conclusion, the application of a combined phenotyping and genotyping approach to patients with inherited thrombocytopenia is an effective and efficient means of complete diagnosis. It also has the added benefit of identifying novel candidate variants in genes not previously known to cause disease that may further our understanding of the processes surrounding haemostasis through subsequent functional studies.
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Ketchem, Shannon, Katie Prosser, Christine Colon, Diana Heiman, Kelly Covert, and David Stewart. "Thrombocytopenia Risk with Valproic Acid Therapy." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/asrf/2020/presentations/47.

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Valproic acid (Depakote) is an antiepileptic drug approved for the treatment of bipolar disorder, migraine prophylaxis, and seizure disorders. While the exact mechanism is still unknown, thrombocytopenia, defined as platelet counts < 150,000/uL, has been reported secondary to Depakote treatment. The frequency of Depakote-induced thrombocytopenia varies greatly, with reported rates ranging from 5 to 54%. This adverse effect is dose-dependent and possible risk factors include lower baseline platelet counts, female gender, and high VPA serum concentrations.Our team came across two patient cases where thrombocytopenia during Depakote therapy was observed. Patient information was gathered through electronic medical records. The first patient was a 65-year-old male who was started on 500 mg Depakote ER three tablets at night for bipolar affective disorder. After several months on this dose, the patient’s platelets decreased to 59 X 103per microliter. One month after the drug was discontinued, the platelets recovered to 160 X 103per microliter. The second patient was a 57-year-old woman who had two occurrences of thrombocytopenia while on Depakote. The patient was started on Depakote for a seizure disorder. She was later admitted for symptomatic bradycardia, hypotension, and concern for thrombocytopenia. Her Depakote dose was decreased from 500 mg three times a day to twice a day. Approximately 5 weeks later, she presented to the emergency room for decreased arousal and hypotension. She was again found to have thrombocytopenia with a platelet count of 28 X 103per microliter with a Depakote level of 101 mcg/mL. The team discovered she had been receiving Depakote 500 mg three times a day following discharge from her last admission, not the reduced dose prescribed. On day four of admission, her platelets had not improved and the Depakote dose was decreased further to 250 mg twice daily. After Depakote was discontinued her platelets gradually improved and returned to normal after four days, the eighth day of admission. Utilizing the Naranjo adverse drug reaction probability scale, the first patient case had a probable reliability that this adverse reaction was due to Depakote, while the second patient case had a definite reliability.These cases illustrate the potential for thrombocytopenia secondary to Valproic acid use. Although this adverse event isn’t well understood, these cases add to the evidence that it can occur. Recognition of this reaction is important and clinicians should monitor hematologic labs, including platelets, for patients receiving Valproic acid.
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Joutsi-Korhonen, Lotta. "Autoimmune thrombocytopenia : detection of platelet-associated IgG, reticulated platelets and platelet Fcg[gamma] receptor polymorphism in thrombocytopenic patients." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/joutsi-korhonen/.

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4

Newman, Peter Michael Pathology UNSW. "Antibody and Antigen in Heparin-Induced Thrombocytopenia." Awarded by:University of New South Wales. Pathology, 2000. http://handle.unsw.edu.au/1959.4/17485.

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Immune heparin-induced thrombocytopenia (HIT) is a potentially serious complication of heparin therapy and is associated with antibodies directed against a complex of platelet factor 4 (PF4) and heparin. Early diagnosis of HIT is important to reduce morbidity and mortality. I developed an enzyme immunoassay that detects the binding of HIT IgG to PF4-heparin in the fluid phase. This required techniques to purify and biotinylate PF4. The fluid phase assay produces consistently low background and can detect low levels of anti-PF4-heparin. It is suited to testing alternative anticoagulants because, unlike in an ELISA, a clearly defined amount of antigen is available for antibody binding. I was able to detect anti-PF4-heparin IgG in 93% of HIT patients. I also investigated cross-reactivity of anti-PF4-heparin antibodies with PF4 complexed to alternative heparin-like anticoagulants. Low molecular weight heparins cross-reacted with 88% of the sera from HIT patients while half of the HIT sera weakly cross-reacted with PF4-danaparoid (Orgaran). The thrombocytopenia and thrombosis of most of these patients resolved during danaparoid therapy, indicating that detection of low affinity antibodies to PF4-danaparoid by immunoassay may not be an absolute contraindication for danaparoid administration. While HIT patients possess antibodies to PF4-heparin, I observed that HIT antibodies will also bind to PF4 alone adsorbed on polystyrene ELISA wells but not to soluble PF4 in the absence of heparin. Having developed a technique to affinity-purify anti-PF4-heparin HIT IgG, I provide the first estimates of the avidity of HIT IgG. HIT IgG displayed relatively high functional affinity for both PF4-heparin (Kd=7-30nM) and polystyrene adsorbed PF4 alone (Kd=20-70nM). Furthermore, agarose beads coated with PF4 alone were almost as effective as beads coated with PF4 plus heparin in depleting HIT plasmas of anti-PF4-heparin antibodies. I conclude that the HIT antibodies which bind to polystyrene adsorbed PF4 without heparin are largely the same IgG molecules that bind PF4-heparin and thus most HIT antibodies bind epitope(s) on PF4 and not epitope(s) formed by part of a PF4 molecule and part of a heparin molecule. Binding of PF4 to heparin (optimal) or polystyrene/agarose (sub-optimal) promotes recognition of this epitope. Under conditions that are more physiological and sensitive than previous studies, I observed that affinity-purified HIT IgG will cause platelet aggregation upon the addition of heparin. Platelets activated with HIT IgG increased their release and surface expression of PF4. I quantitated the binding of affinity-purified HIT 125I-IgG to platelets as they activate in a plasma milieu. Binding of the HIT IgG was dependent upon heparin and some degree of platelet activation. Blocking the platelet Fc??? receptor-II with the monoclonal antibody IV.3 did not prevent HIT IgG binding to activated platelets. I conclude that anti-PF4-heparin IgG is the only component specific to HIT plasma that is required to induce platelet aggregation. The Fab region of HIT IgG binds to PF4-heparin that is on the surface of activated platelets. I propose that only then does the Fc portion of the bound IgG activate other platelets via the Fc receptor. My data support a dynamic model of platelet activation where released PF4 enhances further antibody binding and more release.
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Tytgat, Godelieve Andrea Maria. "[131I]Meta-iodobenzylguanidine ([131I]MIBG) related thrombocytopenia." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/57592.

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Apostu, Raluca. "Understanding cyclical thrombocytopenia : a mathematical modeling approach." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101834.

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Cyclical thrombocytopenia (CT) is a rare hematological disease characterized by periodic oscillations in the platelet count. Although first reported in 1936, the pathogenesis and an effective therapy remain to be identified. Since besides fluctuations in platelet levels the patients hematological profile have been consistently normal, a destabilization of a peripheral control mechanism might play an important role in the genesis of this disorder. In this thesis, we investigate through computer simulations the mechanisms underlying the platelet oscillations observed in CT. First, we collected the data published in the last 40 years and quantified the significance of the platelet fluctuations using Lomb-Scargle periodograms. Our analysis reveals that the incidence of the statistically significant periodic data is equally distributed in men and women. The mathematical model proposed in this thesis captures the essential features of hematopoiesis and successfully duplicates the characteristics of CT. With the same parameter changes, the model is able to fit the platelet counts and to qualitatively reproduce the TPO oscillations (when data is available). Our results indicate that a variation in the megakaryocyte maturity, a slower relative growth rate of megakaryocytes, as well as an increased random destruction of platelets are the critical elements generating the platelet oscillations in CT.
La thrombocytopénie cyclique (TC) est une rare maladie hématologique caracteriséepar des oscillations périodiques dans les plaquettes sanguines. Bien qu'elle fût évoquéepour la première fois en 1936, la maladie et une thérapie efficace restent à trouver.Puisque malgré les fluctuations au niveau des plaquettes, les profiles hématologiquesdes patients restent toujour normaux, une destabilisation du méchanisme de contrôlepériphérique peut jouer un rôle important dans la formation de ce maladie. Dans cettethèse, nous recherchons à travers des simulations informatiques les mechanismes sousjacentaux oscillations des plaquettes observées dans TC. En premier lieu, nous avonscollecté les données publiées ces 40 dernière années et quantifié l'importance des fluctuationsdes plaquettes en utilisant les périodograms Lomb-Scargle. Notre analysestatistique révèle que les données périodiques sont équitablement distribuée chez leshommes et les femmes. Le modèle mathématique proposé dans cette thèse prenden compte les caractéristiques essentielles de la production des cellules sanguineset reproduit avec succès les charactéristiques de TC. Avec les même changementde parametèrs, le modèle reproduit bien le comportement des plaquettes sanguineset donne qualitativement les même oscillations que TPO (quand les données sontdisponibles). Nos résultats indiquent que les éléments critiques générant les oscillationsdes plaquettes dans TC sont une variation dans la maturité du mégakaryocytes,un taux de croissance relativement lent des mégakaryo cytes , ainsi que une augmentationaléatoire de destruction des plaquettes.
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Desborough, Michael J. R. "Desmopressin for treatment of thrombocytopenia or platelet dysfunction." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:4de19720-328a-4d01-9153-02dec6202aff.

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The objective of the work presented in this thesis was to explore the role of potential alternatives to platelet transfusions and specifically to investigate whether desmopressin could be used for treatment of thrombocytopenia or platelet dysfunction. Patients with thrombocytopenia or platelet dysfunction are often treated with platelet transfusions to treat or prevent bleeding. However the evidence for the efficacy of platelet transfusion is limited and there is some evidence of harm. I have focused on thrombocytopenic patients with haematological malignancies or critically ill patients, who are amongst the groups most commonly treated with platelet transfusions. The aims of this research were to determine: 1. If levels of Von Willebrand factor (VWF) or other measures of haemostasis are predictive of bleeding in severe thrombocytopenia; 2. Whether VWF compensates for thrombocytopenia in vitro; 3. The evidence for the efficacy of desmopressin in all patients undergoing surgery or invasive procedures; 4. The evidence for desmopressin for platelet dysfunction or thrombocytopenia; 5. If it is feasible to use desmopressin to treat critically ill thrombocytopenic patients in a clinical trial. To identify derangements of haemostasis that may signify candidates for alternatives to platelet transfusions, I analysed blood samples from an observational trial of fifty patients with haematological malignancies and profound thrombocytopenia due to intensive chemotherapy. I used a panel of tests to investigate measures of primary haemostasis, thrombin generation, cross-linked fibrin formation and fibrinolysis. Using multivariable logistic regression, I found no consistent correlation between any measures of haemostasis and the risk of clinically significant bleeding. VWF antigen levels were the best predictor of clinically significant bleeding on the same day (odds ratio 0.31, 95% confidence interval 0.10 to 0.98, p=0.047) but were not predictive of severe bleeding over the 24 hours after the test (odds ratio 0.48, 95% confidence interval 0.10 to 2.34, p=0.36). In a separate set of experiments, I evaluated thrombus formation under flow in thrombocytopenia. This technique was sensitive to the platelet count . Addition of exogenous VWF to thrombocytopenic blood resulted in improvement in thrombus formation, suggesting that agents that affect or influence VWF pathways might have a role. Desmopressin can be used to increase VWF levels, so leading on from my laboratory experiments; I used systematic reviews and meta-analyses to assess whether desmopressin could be used in unselected patients to reduce bleeding peri-operatively. I identified 62 randomised controlled trials. Overall there was no evidence of benefit for administering desmopressin to unselected patients. However further analysis of eleven randomised controlled trials that focused on patients with platelet dysfunction found that desmopressin resulted in transfusion of fewer units of red cells (equivalent to a 25% reduction compared to control), less blood loss (equivalent to a 23% reduction compared to control) and a lower risk of requiring a re-operation due to bleeding (Peto odds ratio 0.39, 95% confidence interval 0.18 to 0.84). There was no evidence for an increase in thrombotic events. There was no randomised controlled trial evidence for perioperative desmopressin for patients with thrombocytopenia. These specific research gaps were addressed by designing new clinical trials. I have commenced a randomised controlled feasibility trial of desmopressin versus placebo for critically ill patients with thrombocytopenia undergoing invasive procedures. This trial is ongoing and is the first randomised trial evaluating peri-procedural desmopressin in thrombocytopenia. The programme of work arising from this research has the potential to benefit a large number of patients by preventing bleeding and reducing exposure to allogeneic blood components such as platelets. The results presented in this thesis are exploratory but are an important step on a path towards larger trials using desmopressin as an alternative, or adjunct to platelet transfusion.
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8

Antel, Katherine. "Splenectomy for immune thrombocytopenia : our 11-year experience." Master's thesis, University of Cape Town, 2015. http://hdl.handle.net/11427/14134.

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Splenectomy has been practiced for the treatment of ITP for the past few decades. Currently it is utilised when a patient is either dependent or resistant to steroid treatment and the platelet count remains less than 30×109/L. Recently new agents have been added to the armamentarium used to treat ITP, including immune-suppressants such as rituximab and the new thrombopoetin-receptor agonists. This has brought into question the role of surgery for the treatment of ITP, and the need to compare the response and complication rates of splenectomy to these newer agents. Historic studies done on splenectomy for the treatment of ITP have been performed in the setting of low HIV prevalence. There is a relative paucity of data on the response rate in HIV-associated thrombocytopenia to splenectomy and the durability of response to splenectomy is unclear in this patient population. We retrospectively analysed 73 consecutive patients who underwent splenectomy for ITP from 2001 to 2011. The primary objective was to determine the rate of complete response, this was defined as a platelet count greater than 100×109/L at one year post splenectomy. Results were compared between HIV positive and HIV negative patients. The secondary objectives were: to evaluate the intra-operative and post†operative complications and mortality in the HIV positive and HIV negative groups, and to investigate for associations between co-morbidities, pre-operative treatment and response to splenectomy.
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Chan, Ernest Ricky. "Genetic Analysis of Novel Models of Thrombocytopenia and Leucopenia." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1248212698.

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Lundin, Ann-Sofie. "QUALITY OF TACSI PLATELETS AND THEIR EFFECT ON THROMBOCYTOPENIA PATIENTS." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-126714.

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Conclusion:Medical treatment may have a role in platelet count after transfusion. Since the TACSI platelets passed the quality requirements, and the vast majority of patients platelet count increased after TACSI platelet transfusion, the TACSI platelets will replace the old method to produce platelets at the Uppsala University hospital.

 

 

Methods: A new approach that pools 8 buffy coats (TACSI platelets) that were separated into 2 units instead of 4-6 buffy coats pooled to 1 unit was investigated in this study. After the platelets were extracted from the buffy coats their quality was controlled and subsequently the platelet product was evaluated in 96 patients.

 

Results: The results showed that 80 % of the platelet units passed the European quality requirements. Further, the platelet count was increased in most patients that received TACSI platelets.

Conclusion: Medical treatment may have a role in platelet count after transfusion. Since the TACSI platelets passed the quality requirements, and the vast majority of patients platelet count increased after TACSI platelet transfusion, the TACSI platelets will replace the old method to produce platelets at the Uppsala University hospital.

 

 

 

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Books on the topic "Thrombocytopenia"

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Ishida, Yoji, and Yoshiaki Tomiyama, eds. Autoimmune Thrombocytopenia. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4142-6.

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1960-, Warkentin Theodore E., and Greinacher Andreas, eds. Heparin-induced thrombocytopenia. 2nd ed. New York: Dekker, 2001.

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1960-, Warkentin Theodore E., and Greinacher Andreas, eds. Heparin-induced thrombocytopenia. 4th ed. New York: Informa Healthcare USA, 2007.

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1960-, Warkentin Theodore E., and Greinacher Andreas, eds. Heparin-induced thrombocytopenia. 3rd ed. New York: Marcel Dekker, 2004.

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Warkentin, Theodore E., and Andreas Greinacher. Heparin-induced thrombocytopenia. 4th ed. New York: Informa Healthcare, 2007.

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H, Sutor Anton, and Thomas Kathy B, eds. Thrombocytopenia in childhood. Stuttgart: Schattauer, 1994.

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Saijo, Masayuki, ed. Severe Fever with Thrombocytopenia Syndrome. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9562-8.

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Handelsman, Harry. Protein A columns for immune thrombocytopenia. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1991.

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Parker, James N., and Philip M. Parker. The official patient's sourcebook on immune thrombocytopenic purpura. San Diego, Calif: Icon Health Publications, 2002.

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Parker, James N., and Philip M. Parker. Thrombocytopenia: A medical dictionary, bibliography, and annotated research guide to internet references. San Diego, CA: ICON Health Publications, 2004.

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Book chapters on the topic "Thrombocytopenia"

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Tsiara, Stavroula, Catherine Nelson-Piercy, and Nichola Cooper. "Thrombocytopenia in Pregnancy: Gestational Thrombocytopenia and Immune Thrombocytopenic Purpura." In Disorders of Thrombosis and Hemostasis in Pregnancy, 261–77. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15120-5_15.

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Tsiara, Stavroula, Catherine Nelson-Piercy, and Nichola Cooper. "Thrombocytopenia in Pregnancy: Gestational Thrombocytopenia and Idiopathic Thrombocytopenic Purpura." In Disorders of Thrombosis and Hemostasis in Pregnancy, 157–70. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-4411-3_11.

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Raj, Satish R., S. R. Wayne Chen, Robert S. Sheldon, Arti N. Shah, Bharat K. Kantharia, Ulrich Salzer, Bodo Grimbacher, et al. "Thrombocytopenia and Thrombotic Thrombocytopenic Purpura." In Encyclopedia of Molecular Mechanisms of Disease, 2051–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1737.

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Speer, Tod W., Rene Rubin, Iris Rusu, Iris Rusu, Yan Yu, Laura Doyle, Cheng B. Saw, et al. "Thrombocytopenia." In Encyclopedia of Radiation Oncology, 893. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_454.

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Brundige, Karyn. "Thrombocytopenia." In Pediatric Oncology, 179–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-87984-8_7.

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Kaplan, Elizabeth. "Thrombocytopenia." In The Perioperative Medicine Consult Handbook, 135–38. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09366-6_20.

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Hagan, Anna Fahy, and Scott Hagan. "Thrombocytopenia." In The Perioperative Medicine Consult Handbook, 181–87. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19704-9_22.

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Silver, Robert M. "Thrombocytopenia." In Queenan's Management of High-Risk Pregnancy, 102–7. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781119963783.ch14.

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Annamalai, Aniyizhai. "Thrombocytopenia." In Medical Management of Psychotropic Side Effects, 189–92. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51026-2_28.

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McMichael, Maureen. "Thrombocytopenia." In Textbook of Small Animal Emergency Medicine, 427–29. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119028994.ch67.

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Conference papers on the topic "Thrombocytopenia"

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Jaffar, Samia, Tekiyah Shabazz, and Frederick U. Eruo. "Gestational Thrombocytopenia." In 13th Philadelphia Prenatal Virtual Conference—Selected Abstracts. Thieme Medical Publishers, Inc., 2021. http://dx.doi.org/10.1055/s-0041-1735777.

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Casals, F. J., R. Moreno, L. Alfonso, A. Alonso, and R. Guerrero. "INCIDENCE AND CHARACTERISTICS OF MACROTHROMBOCYTOPENIA IN A MEDITERRANEAN AREA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644575.

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Idiopathic Thrombocytopenia Purpura (ITP) is diagnosed by exclusion in presence of a chronic thrombocytopenia, with evidence of bone marrow megakaryocytes and exclusion of associated diseases shortened platelet survival (PS), increased platelet volume (PV) and platelet associated immunoglobulin G (PAIgG) support this diagnosis. In subjects from mediterranean area, the idiopathic macrothrombocytopenia (IM) has been reported. This entity could be erroneously considered as a moderate type of ITP.To evaluate the incidence and characteristics of the IM we studied in 147 patients with not secondary megakaryocytic chronic thrombocytopenia, the PS by the 111-Indium-Oxine method, the PV distribution in citrated blood with the Coulter ZBI- Channelyzer C1000 and the PAIgG by the antiglobulin consumption assay.In 20 cases we found a macrothrombocytopenia, along with normal PS in 12 (Group A) or a near normal PS but marked facts of idiopathic hyperesplenism in the other eight (Group B ).25 % patients in the Group A and 57%in the Group B had increased PAIgG , more marked in the latter.Out of 147 patients studied, we found 40 with moderate thrombocytopenia (>40×10 plts/l) and 20 subjects were studied in remission (>100×10 plts/l), in all cases the PS was shortened.In conclusion we think that idiopathic macrothrombocytopenia and the idiopathic hypersplenic thrombocytopenia could be the broad spectrum of the same entity, with a high prevalence inthe mediterranean area. 14% of the patients studied had this alteration and this incidence increase to 35% when considering exclusively the moderate thrombocytopenias.
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Vollstaedt, J., M. T. Kashlan, and A. Saiyed. "Severe Trimethaprim Sulfamethaxole Induced Thrombocytopenia." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1681.

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Prasetia Nurwidda, Arvi Dian, Poernomo Boedi Setiawan, Iswan Abbas Nusi, Herry Purbayu, Titong Sugihartono, Ummi Maimunah, Ulfa Kholili, et al. "Thrombocytopenia in Chronic Hepatitis C." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007340404460452.

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Daffos, F., F. Forestier, C. Kaplan, and J. Y. Muller. "PERNATAL MANAGEMENT OF FETAL THROMBOCYTOPENIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644272.

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Fetal thrombocytopenia resulting from alloimmunisation (NAIT] or from autoimmune pathology (ITP) may contribute to morbidity from hemorrhage particularly when bleeding occurs into the central nervous system.Utilizing a safe procedure for in utero blood samplings i.e. directpuncture under ultrasound guidance, we are able to propose a prenatal management. Considering NAIT we haveuntil now treated 6 patients. We propose a screening protocol for highrisk group based on maternal antecedents and immunological grounds. Fetal blood sampling is performed at 20th week of gestation allowing platelet count and typing. If there isincompatibility between the fetus and his mother two ways can be consFdered : absence or presence of thrombocytopenia. If the platelet countis normal, nothing is done until 37th week of gestation. In the other case, frequent ultrasound examinations are done. At the 37e week, a fetal blood sampling is performed andin utero maternal platelet transfusion is done in the case of thrombocytopenia, before the delivery. It is possible with this prenatal treatment to have vaginal delivery. Considering ITP. when the maternal status permit it. fetal blood samplingslet us to know exactly the fetal platelet count. By this way. the indication of delivery can be documented.This procedure offers a new possibility of easily taking iterative samples. until the end of pregnancyand represents a particular interest in the prenatal treatment of suchhemorrhagic disorders.
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van den Heuvel, Robert. "Efgartigimod successful in immune thrombocytopenia." In 64th ASH Annual Meeting, edited by Gert Ossenkoppele. Baarn, the Netherlands: Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/ce435d9e.

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Slichter, Sherrill J. "PATHOPHYSIOLOGY OF THROMBOCYTOPENIA AND RESULTANT CLINICAL INDICATIONS FOR PLATELET TRANSFUSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643996.

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Careful evaluation of platelet survival data in normal individuals and patients with thrombocytopeniasecondary to marrow aplasia has demonstrated that platelets are lost from circulation by two mechanisms a fixed fraction of platelets, amounting to approxi mately 7,100 platelets/ul/day, are lost randomly while the remaining platelets are removed by senescent mechanisms. At platelet counts of <100,000/ul, platelet survival becomes progressively shorter as the fixed platelet loss becomes a proportionately greater fraction of the circulating platelets. Thus, there is a direct relationship between platelet count and platelet survival in thrombocytopenic patients. Therefore, when judging the effectiveness of platelet therapy in thrombocytopenic patients, the influence of platelet count on platelet survival must be considered. As yet, there have been no studies to determine if there are ways to interrupt this fixed platelet loss? whether such therapy might improve platelet support in thrombocyotpenic patients by prolonging platelet survival? or, alternatively, whether such therapy might enhance the bleeding risk if random platelet removal is related to physiologic platelet-endothelial cell interactions.Besides taking into account the effect of thrombocytopenia on the expected response to platelet transfusions, the risk of alloimmunization with platelet transfusion therapy requires a careful assessment of the indications for platelet transfusions for each patient.Based on 51Cr-labeled stool blood loss measurements, we have determined that the bleeding risk is minimal at platelet counts above 10,000 platelets/ul.Only when the platelet count falls to a lower level of 5,000/ul is GI bleeding significantly increased. However, there are certain medications that may enhance the bleeding risk and require platelet transfusions to be given at higher platelet counts.In those patients who are thrombocytopenic, not because of failure of marrow platelet production, but rather because of accelerated platelet removal, indications for platelet transfusions must be adjusted to meet the particular problem. For example, for patients with autoimmune thrombocytopenic purpura, platelet transfusions are rarely indicated (one exception being intracerebral bleeding) because of the rapid rate of platelet removal and because the patients are usually releasing young hyperfunctional platelets from the bone marrow reducing the hemorrhagic risk at any given platelet count. In some patients with consumptive coagulopathies, even though platelet removal is rapid, platelets may have to be provided until specific therapy resolves the underlying disease process causing the platelet consumption. For these patients, increased levels of fibrinogen/fibrin degregation products, as well as various medications they maybe receiving, may produce platelet dysfunction necessitating platelet transfusions at higher platelet levels. Finally, massive transfusion patients may develop a dilution thrombocytopenia requiring platelet transfusions.
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Chediak, J., J. Eldridge, D. Sobel, B. Maxey, J. Baron, and M. C. Telfer. "FURTHER EVIDENCES OF VON WILLEBRAND FACTOR INVOLVEMENT IN THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644587.

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Laboratory findings of TTP include severe thrombocytopenia and marked anemia due to intravascular hemolysis. The pathogenesis of the thrombocytopenia is poorly understood. Possible mechanisms include the presence of a platelet aggregating factor (JCI 76:1330, 1935), a calcium dependent protease (Blood 63:310a, 1986), abnormal prostaglandin production or metabolism, and an excessive consumption of high molecular weight forms of von Uillebrand factor (VUF). Von Willebrand factor proteins from 12 patients (pts) diagnosed as having TTP were studied. They include 8 females and 4 males; nine were studied during the acute presentation and seven pts also during the remission period. Three pts died during the acute event. None of the pts had a recurrence. Control subjects include both normal individuals and thrombocytopenic pts due to a variety of underlying diseases including marrow aplasia and immune thrombocytopenia, but excluding pts with DIC or suffering infection. Plasmas were tested for VWF antigen and Ristocetin Cofactor (RiCof) activity. The electrophoretic mobility (CIE) of VWF:Ag was also assessed and the ratio VWF:RiCof to VWF:Ag was determined. Statistical analysis including p values will be reported. Results:These results suggest that during the acute event there is an excessive consumption of large VWF multimers and the ratio VWF:RiCof/VWF:Ag could be used to corroborate the diagnosis of TTP and by doing sequential measurements to monitor the response to therapy.
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Taboada, Dolores, Carmen Treacey, Karen Sheares, Nicholas W. Morrell, and Joanna Pepke Zaba. "Thrombocytopenia In Idiopathic Pulmonary Arterial Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1883.

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Christiaens, G. C. M. L. "DIAGNOSIS AND MANAGEMENT OF ITP DURING THE PERINATAL PERIOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644762.

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Although maternal and perinatal mortality and morbidity in pregnant patients with ITP are lower than previously assumed, they are not negligable. Significant postpartum hemorrhage occurs in 7% of the mothers with ITP. Thrombocytopenia is found in 51% of the newborns born from mothers with ITP and 6% of these have serious bleeding problems. Tests which predict which fetuses are at risk, are not yet available. Thrombocyte counts in a fetal blood sample are falsely low in 40% of cases.A prospective controlled randomized study done in the Netherlands failed to show an effect of antenatal corticosteroid treatment on neonatal platelet counts. Elective caesarean section has not been shown to protect against intracranial bleeding in thrombocytopenic newborns. The choice between vaginal delivery and caesarean section in ITP patients should be made on obstetric grounds with one exception: no other assisted vaginal delivery than the easy outlet forceps should be done. All cases of slow progress of the second stage of labour with insufficient descent should be terminated by caesarean section as well as breech delivery with suboptimal progress. Newborn thrombocyte counts should be done daily during the first week of life, since lowest platelet counts are often found between the 3rd and 5th postpartum day. Newborn thrombocytopenia is transient and does not warrant splenectomy, but can necessitate treatment with corticosteroids and/or high doses of immunoglobulin 6. Current data do not justify to dissuade breastfeeding.The recurrence of neonatal thrombocytopenia in subsequent patients is unknown.
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Reports on the topic "Thrombocytopenia"

1

Pai, Menaka, Allan Grill, Noah Ivers, Antonina Maltsev, Katherine J. Miller, Fahad Razak, Michael Schull, et al. Vaccine Induced Prothrombotic Immune Thrombocytopenia (VIPIT) Following AstraZeneca COVID-19 Vaccination. Ontario COVID-19 Science Advisory Table, March 2021. http://dx.doi.org/10.47326/ocsat.2021.02.17.1.0.

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This Science Brief provides information for health care professionals about Vaccine Induced Prothrombotic Immune Thrombocytopenia (VIPIT), a rare adverse event following the AstraZeneca vaccine. This brief describes the pathophysiology, presentation, diagnostic work-up and treatment of VIPIT. Figure 1 presents a decision tree for diagnosis and rule out of VIPIT.
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Pai, Menaka, Benjamin Chan, Nathan M. Stall, Allan Grill, Noah Ivers, Antonina Maltsev, Katherine J. Miller, et al. Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT) Following Adenovirus Vector COVID-19 Vaccination: Lay Summary. Ontario COVID-19 Science Advisory Table, May 2021. http://dx.doi.org/10.47326/ocsat.2021.02.16.2.0.

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Pai, Menaka, Benjamin Chan, Nathan M. Stall, Allan Grill, Noah Ivers, Antonina Maltsev, Katherine J. Miller, et al. Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT) Following Adenovirus Vector COVID-19 Vaccination. Ontario COVID-19 Science Advisory Table, May 2021. http://dx.doi.org/10.47326/ocsat.2021.02.17.2.0.

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Pai, Menaka, Allan Grill, Noah Ivers, Antonina Maltsev, Katherine J. Miller, Fahad Razak, Michael Schull, et al. Vaccine Induced Prothrombotic Immune Thrombocytopenia (VIPIT) Following AstraZeneca COVID-19 Vaccination: Lay Summary. Ontario COVID-19 Science Advisory Table, March 2021. http://dx.doi.org/10.47326/ocsat.2021.02.16.1.0.

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Ding, Mengyuan, Bing Li, and Meng Yang. Meta-analysis on Effectiveness of Shengxuexiaoban Capsules Combined with Hormone Therapy for Immune Thrombocytopenia. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0031.

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Chan, Benjamin, Ayodele Odutayo, Peter Juni, Nathan M. Stall, Pavlos Bobos, Adalsteinn D. Brown, Allan Grill, et al. Risk of Vaccine-Induced Thrombotic Thrombocytopenia (VITT) following the AstraZeneca/COVISHIELD Adenovirus Vector COVID-19 Vaccines. Ontario COVID-19 Science Advisory Table, May 2021. http://dx.doi.org/10.47326/ocsat.2021.02.28.1.0.

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Published estimates of the risk of vaccine-induced thrombotic thrombocytopenia (VITT) from countries with moderate to high data quality range from 1 case per 26,500 to 1 case per 127,300 first doses of AstraZeneca/COVISHIELD administered (Table 1). The risk of VITT in Canada as of May 8, 2021 has been estimated to be approximately 1 per 55,000 doses, but several presumptive cases are still under investigation.
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Liu, Yin, Jianyong Fu, Xiaoyang Wang, and Shaokai Zhang. Efficacy and Safety of Thrombopoietin Receptor Agonists in Adults with Immune Thrombocytopenia: A Systematic Review and Network Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0054.

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Dong, Yu, and Mengjiao Hu. The efficacy and safety of different dosages of rituximab for adults with immune thrombocytopenia: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0024.

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Pai, Menaka, Allan Grill, Noah Ivers, Antonina Maltsev, Katherine J. Miller, Fahad Razak, Michael Schull, et al. Vaccine-Induced Prothrombotic Immune Thrombocytopenia (VIPIT) following AstraZeneca COVID-19 Vaccination: Interim Guidance for Healthcare Professionals in the Outpatient Setting. Ontario COVID-19 Science Advisory Table, April 2021. http://dx.doi.org/10.47326/ocsat.2021.02.20.1.0.

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Pai, Menaka, Allan Grill, Noah Ivers, Nathan M. Stall, Katherine J. Miller, Ullanda Niel, Benjamin Chan, et al. Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT) Following Adenovirus Vector COVID-19 Vaccination: Interim Guidance for Healthcare Professionals in the Outpatient Setting. Ontario COVID-19 Science Advisory Table, May 2021. http://dx.doi.org/10.47326/ocsat.2021.02.20.2.0.

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