Relevant bibliographies by topics / Thrombocytopenia – etiology

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

Academic literature on the topic 'Thrombocytopenia – etiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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Journal articles on the topic "Thrombocytopenia – etiology"

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Horrell, Cindy Jo, and Jan Rothman. "The etiology of thrombocytopenia." Dimensions of Critical Care Nursing 20, no. 4 (July 2001): 10–16. http://dx.doi.org/10.1097/00003465-200107000-00004.

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Santivasi, Wil L., Meghan M. Routt, and Alicia M. Terando. "Idiopathic Thrombocytopenic Purpura after Mastectomy and Axillary Lymph Node Dissection." Case Reports in Surgery 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/316064.

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First described in 1916, idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease resulting in the destruction of platelets. Here, we present a case of an 85-year-old patient diagnosed with invasive ductal carcinoma of the breast whose surgical treatment was complicated postoperatively by acute-onset thrombocytopenia with a resultant hematoma at the operative site. Diagnostic Workup revealed no clear etiology for the thrombocytopenia; therefore, a presumptive diagnosis of idiopathic thrombocytopenic purpura was made. Previous literature has associated the development of idiopathic thrombocytopenic purpura with breast cancer. However, to the authors’ knowledge, there are no reported cases of ITP presenting immediately following surgical intervention for breast cancer in the absence of other etiologic factors.
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Sillers, Laura, Charles Van Slambrouck, and Gabrielle Lapping-Carr. "Neonatal Thrombocytopenia: Etiology and Diagnosis." Pediatric Annals 44, no. 7 (July 1, 2015): e175-e180. http://dx.doi.org/10.3928/00904481-20150710-11.

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&NA;. "Establishing the Etiology of Thrombocytopenia." Nurse Practitioner 25, no. 6 (June 2000): 68. http://dx.doi.org/10.1097/00006205-200025060-00004.

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Gunnink, Suzanne F., Roos Vlug, Karin Fijnvandraat, Johanna G. van der Bom, Simon J. Stanworth, and Enrico Lopriore. "Neonatal thrombocytopenia: etiology, management and outcome." Expert Review of Hematology 7, no. 3 (March 25, 2014): 387–95. http://dx.doi.org/10.1586/17474086.2014.902301.

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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 (May 1, 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 was significantly elevated (greater than 1,280 IgG molecules per platelet) at all stages of the cycle, even during thrombocytosis. However, the highest values were observed during thrombocytopenia. Platelet-bindable IgG in plasma declined to normal immediately before platelet levels began to rise. IgG eluted from the platelets of this patient reacted strongly with autologous and homologous platelets in contrast to a “mock eluate” prepared from platelets of a normal subject. The eluate from the patient's platelets reacted strongly with immobilized autologous and homologous glycoprotein IIb/IIIa complex and weakly with GPIb but not with isolated GPIIIa alone. In each patient the decline in platelet levels was significantly delayed following administration of intravenous gamma globulin 0.4 g/kg body weight for five days. These findings suggest that platelet-reactive autoantibodies are of pathogenic significance in some patients with cyclic thrombocytopenia.
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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 (May 1, 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 significantly elevated (greater than 1,280 IgG molecules per platelet) at all stages of the cycle, even during thrombocytosis. However, the highest values were observed during thrombocytopenia. Platelet-bindable IgG in plasma declined to normal immediately before platelet levels began to rise. IgG eluted from the platelets of this patient reacted strongly with autologous and homologous platelets in contrast to a “mock eluate” prepared from platelets of a normal subject. The eluate from the patient's platelets reacted strongly with immobilized autologous and homologous glycoprotein IIb/IIIa complex and weakly with GPIb but not with isolated GPIIIa alone. In each patient the decline in platelet levels was significantly delayed following administration of intravenous gamma globulin 0.4 g/kg body weight for five days. These findings suggest that platelet-reactive autoantibodies are of pathogenic significance in some patients with cyclic thrombocytopenia.
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8

Butt, Muhammad Umer, Ahmad Jabri, and Samy Claude Elayi. "Azithromycin-Induced Thrombocytopenia: A Rare Etiology of Drug-Induced Immune Thrombocytopenia." Case Reports in Medicine 2019 (July 8, 2019): 1–3. http://dx.doi.org/10.1155/2019/6109831.

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Drug-induced thrombocytopenia requires a high suspicion for diagnosis and a broad investigation to exclude other etiologies of low platelets. Cessation of the offending agent often results in recovery of platelet counts. Many medications are known to cause a degree of thrombocytopenia. We present a rare case of severe thrombocytopenia associated with administration of azithromycin.
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9

Kaplan, Cécile, Francois Forestier, Marie Dreyfus, Marie-Christine Morel-Kopp, and Gil Tchernia. "Maternal Thrombocytopenia During Pregnancy: Diagnosis and Etiology." Seminars in Thrombosis and Hemostasis 21, no. 01 (January 1995): 85–94. http://dx.doi.org/10.1055/s-2007-1000382.

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10

Kapadia, Shital N., Harsh S. Patel, and Kartikey G. Parmar. "Effects of thrombocytopenia in pregnancy." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 3 (February 27, 2018): 1044. http://dx.doi.org/10.18203/2320-1770.ijrcog20180889.

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Background: Thrombocytopenia defined as platelet count of less than 1,50,000/cu.mm. Thrombocytopenia is divided according to severity into mild moderate and severe types. Multiple factors are responsible.Methods: This is a retrospective study of one-year period including 120 pregnant patients irrespective of their gestational age at civil hospital Ahmedabad. Etiology of this condition are identified and analyzed.Results: Gestational Thrombocytopenia is the most common etiology. This condition is self-limiting usually.Conclusions: Platelet count estimation should be a routine at first antenatal visit for timely diagnosis and to achieve favorable fetomaternal outcome.
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Dissertations / Theses on the topic "Thrombocytopenia – etiology"

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"Effects of lung injury on neonatal thrombocytopoiesis." 2002. http://library.cuhk.edu.hk/record=b6073424.

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Abstract:
Yang Jie.
"January, 2002."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2002.
Includes bibliographical references (p. 204-250).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.
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Books on the topic "Thrombocytopenia – etiology"

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McCrae, Keith R. Thrombocytopenia (Basic and Clinical Oncology). Informa Healthcare, 2006.

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Book chapters on the topic "Thrombocytopenia – etiology"

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Behr, Th, W. Becker, H. J. Bair, J. Schwab, and F. Wolf. "Thrombocytopenia in HIV, Idiopathic Thrombocytopenic Purpura (ITP), Vasculitis and Toxic Bone Marrow Injury: An Etiologic Entity ? Results of a Comparative Study." In Radioactive Isotopes in Clinical Medicine and Research, 45–50. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7340-6_7.

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Resch, Bernhard. "Thrombocytopenia in Neonates." In Platelets. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.92857.

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Thrombocytopenia defined as platelet count below 150,000/μL is not an uncommon event at the neonatal intensive care unit (NICU). In our region we calculated a prevalence of nearly 2 of 1000 live births. Early-onset neonatal thrombocytopenia (NT) occurring within the first 72 hours of life is more common than late-onset NT. Preterm infants are affected more often than term infants and bacterial infection is the most common diagnosis associated with NT. There are a lot of maternal, perinatal, and neonatal causes associated with NT and complications include bleedings with potentially life-threatening intracranial hemorrhage. Alloimmune thrombocytopenia (NAIT) often presents with severe thrombocytopenia (<30,000/μL) in otherwise healthy newborns and needs careful evaluation regarding HPA-1a antigen status and HLA typing. Platelet transfusions are needed in severe NT and threshold platelet counts might be at ≤25,000/μL irrespective of bleeding or not. Immune mediated NT recovers within 2 weeks with a good prognosis when there happened no intracranial hemorrhage. This short review gives an overview on etiology and causes of NT and recommendations regarding platelet transfusions.
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Teodorescu, Dana, and Caroline Larkin. "Coagulopathy in Cardiac Surgery: Etiology and Treatment Options." In Cardiothoracic Critical Care, 313–22. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190082482.003.0033.

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This chapter reviews the causes and outlines an approach to the management of coagulopathy following cardiac surgery. Bleeding after cardiac surgery is common and expected up to a rate of 2 mL/kg/h for the first 6 hours. A more significant hemorrhage needs to be investigated and treated. Causes are often multifactorial. It is imperative that surgical causes be excluded early concomitant to providing resuscitation, investigating other medical causes for bleeding, and treating coagulopathy empirically until laboratory testing becomes available. The most frequent causes for coagulopathy post–cardiac surgery are excess heparinization, prolonged cardiopulmonary bypass time, hypothermia, acidosis, and preexisting bleeding diathesis. The management of coagulopathy implies maintenance of the normal physiological conditions for coagulation, reversal of excess heparinization, treatment of hyperfibrinolysis, maintaining normal levels of coagulation factors, and transfusion of platelets if thrombocytopenia or platelet dysfunction occurs. The chapter reviews what is involved in standard laboratory testing (complete blood count, prothrombin time, activated partial thromboplastin time, fibrinogen level, etc.) for coagulopathy. Also discussed is point-of-care testing and how the results from these tests should be interpreted. The chapter details the various blood products that are required in this scenario and suggests doses and transfusion thresholds.
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Conference papers on the topic "Thrombocytopenia – etiology"

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Villians, Ph, J. L. Bouvier, G. Le Corff, A. Elias, I. Juhan-vague, and G. Serradimigni. "DO APTT AND ANTI Ila ACTIVITY PERMIT THE PREDICTION OF THE EFFICIENCY OF HEPARIN THERAPY IN PATIENTS WITH PROXIMAL DEEP VEIN THROMBOSIS?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644171.

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One hundred and forty two patients admitted for proximal deep venous thrombosis (PDVT)from 01.01.85 to 12.20.86 were treated with Na-heparin. After an initial bolus (100 units/kg), a continuous intravenous infusion was started (500 units/kg/24h). Heparin activity in daily drawn blood samples was determined by two different assays = APTT (general diagnostic) and anti Ila activity (clotting method). Doses of heparin were adjusted to maintain APTT ratio between 2 and 3 .A phlebography was performed for each patient at DO and D10. Two groups of patients with PDVT were identified : -Group I:n=14 increased thrombosis -Group II :n=26 partly or fully cleared thrombosisNo difference in localization or etiology of PDVT was found between the two groups. Thrombocytopenia was excluded in the two groups by platelet counts (D0, D5, D10).Daily mean values and mean of mean values were analyzed in each group for APTT ratio andanti Ila activity :Statistical analysis (student's T test) shows no difference between the two groups. It can be concluded that mean values of APTT and anti IIa activity in therapeutic range are not predictive of heparin efficiency for the treatment of PDVT
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