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1
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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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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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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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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Chitra, K. S., and C. Shanthi. "Etiology, Obstetrical Risk Factors, Complications and Outcomes of Pregnancies Affected by Thrombocytopenia." Indian Journal of Obstetrics and Gynecology 6, no. 4 (2018): 359–62. http://dx.doi.org/10.21088/ijog.2321.1636.6418.3.
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Subtil, Simone Filipa Carrasqueira, Jorge Miguel Bastos Mendes, Ana Luísa Fialho de Amaral Areia, and José Paulo Achando Silva Moura. "Update on Thrombocytopenia in Pregnancy." Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics 42, no. 12 (December 2020): 834–40. http://dx.doi.org/10.1055/s-0040-1721350.
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AbstractThrombocytopenia, defined as platelet count < 150,000 mm3, is frequently diagnosed by obstetricians since this parameter is included in routine surveillance during pregnancy, with an incidence of between 7 and 12%. Therefore, decisions regarding subsequent examination and management are primordial. While most of the cases are due to physiological changes, as gestational thrombocytopenia, other causes can be related to severe conditions that can lead to fetal or maternal death. Differentiating these conditions might be challenging: they can be pregnancy-specific (pre-eclampsia/HELLP syndrome [hemolysis, elevated liver enzymes, low platelets]), or not (immune thrombocytopenia purpura, thrombotic thrombocytopenic purpura or hemolytic uremic syndrome). Understanding the mechanisms and recognition of symptoms and signs is essential to decide an adequate line of investigation. The severity of thrombocytopenia, its etiology and gestational age dictates different treatment regimens.
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Smedile, LE, DM Houston, SM Taylor, K. Post, and GP Searcy. "Idiopathic, asymptomatic thrombocytopenia in Cavalier King Charles spaniels: 11 cases (1983-1993)." Journal of the American Animal Hospital Association 33, no. 5 (September 1, 1997): 411–15. http://dx.doi.org/10.5326/15473317-33-5-411.
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The medical records of 11 Cavalier King Charles spaniels with idiopathic, asymptomatic thrombocytopenia and large-to-giant platelets were identified from a 10-year retrospective search using the Veterinary Medical Data Base at Purdue University. Eight of the dogs had been treated with various immunosuppressive drugs. Six of the treated dogs remained thrombocytopenic, one was not reevaluated, and one developed a normal platelet count. The underlying etiology of idiopathic, asymptomatic thrombocytopenia in Cavalier King Charles spaniels has not been identified, but this condition could represent a congenital macrothrombocytopenic disorder.
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Drachman, Jonathan G. "Inherited thrombocytopenia: when a low platelet count does not mean ITP." Blood 103, no. 2 (January 15, 2004): 390–98. http://dx.doi.org/10.1182/blood-2003-05-1742.
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Abstract Congenital thrombocytopenias, once considered rare and obscure conditions, are today recognized with increasing frequency, especially due to the measurement of platelet number as part of routine blood testing. The clinical spectrum of congenital thrombocytopenia ranges from severe bleeding diatheses, recognized within the first few weeks of life, to mild conditions that may remain undetected even in adulthood. For the latter group of diseases, distinguishing between inherited (primary) and acquired (secondary) thrombocytopenia, especially immune thrombocytopenia purpura (ITP), is essential to avoid unnecessary and potentially harmful treatments. In this review, the congenital thrombocytopenia syndromes are discussed with specific attention focused on diagnostic criteria, clinical presentations, genetic etiology, and current medical management. The mutated genes responsible for each syndrome are reviewed as well as the potential implications for using gene therapy or gene repair in the future.
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Madhavi, Deepak, Shamama Subuhi, and Mohammed Zubai. "Outcome of neonatal thrombocytopenia in tertiary care NICU." Journal of Pediatrics & Neonatal Care 10, no. 3 (June 29, 2020): 92–96. http://dx.doi.org/10.15406/jpnc.2020.10.00418.
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Thrombocytopenia is one of the commonest haematological disorders in the neonatal period, affecting up to a third of those admitted to neonatal intensive care units. It is well recognized that many fetomaternal and neonatal conditions are associated with thrombocytopenia. The majority of episodes of neonatal thrombocytopenia are relatively mild, self-limiting and of short duration but it may cause severe morbidity & mortality due to severe complication like IVH. Methods & material: 140 Newborn admitted in tertiary care NICU were selected to find out outcome and etiology of neonatal thrombocytopenia. Detail maternal history and neonatal physical examination done and Neonates were followed for outcome, relevant investigation done according to cases. Result: Out of 140 neonates 63 neonates had thrombocytopenia (45%).42.8% neonates were premature out of which 63.3% had thrombocytopenia. Other neonatal risk factor for thrombocytopenia are sepsis 38 (74.5%), SGA/IUGR 28(80%) and NEC 9(100%). Maternal risk factor for thrombocytopenia are eclampsia81.8% and infection during pregnancy 72.72%. 95.5 % of all study population were discharged.4.5 % cases of whole study population didn’t survive. 4.54% of mild, 9.09% of moderate and 60 % of severe thrombocytopenic babies didn’t survive. Conclusion: Bleeding manifestations i.e. mucosal, cutaneous and intracranial bleed were significantly associated with severe thrombocytopenia. 60% of mortality was found in severe thrombocytopenic group. Thus, severe thrombocytopenia was found to be a predictor of poor outcome in sick neonates of NICU.
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Rosenbaum, Hanna, Tina Napso, and Lilach Bonstein. "Immune Thrombocytopenia in Type I Gaucher Disease." Blood 110, no. 11 (November 16, 2007): 3200. http://dx.doi.org/10.1182/blood.v110.11.3200.3200.
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Abstract Backgound: Type I Gaucher disease (GD) the non-neuronopathic form is characterized by hepatosplenomegaly, pancytopenia and skeletal complications due to the accumulation of glucocerebroside in macrophages. Thrombocytopenia is usually related to hypersplenism and/or infiltration of bone marrow by the lipid-laden macrophages namely Gaucher cells. Enzyme replacement therapy (ERT) restores the hemoglobin and platelet count in treated GD patients within 12–24 months of treatment. In GD patients, including ERT treated, with persistent low platelet counts other ethiological factors should be considered. Goals: To determine the etiology of persistent thrombocytopenia in Type I GD patients and to evaluate their clinical course and hematological parameters. Methods: Flow cytometric technique was used to detect platelet-surface associated IgG/M (PSIgG/M) in a cohort of 24 Type I GD patients followed at the Gaucher clinic in Haifa, Israel. The evaluated hematological parameters of the thrombocytopenic GD patients include: bleeding phenomena, concurrence of autoimmune phenomena, hematological malignancies and bone marrow findings. Results: Twenty four Type I GD patients, 15 females and 9 males with an age range of 35 to 80 years (median 53 years) were included in the study. Seventeen of the evaluated 24 patients were thrombocytopenic with platelet counts less than <100×109/l and 7/24 were in the normal range. Bone marrow aspirate was performed in 16 of the 17 thrombocytopenic patients and showed normal or hyperplasic megakariopoiesis together with Gaucher cells infiltrates. Six of the 17 thrombocytopenic patients received ERT for at least 24 months with no effect on the low platelet counts. Elevated platelet surface IgG was detected in 16/17(94%) of GD patients with thrombocytopenia and in only 1/7 (14%) of non thrombocytopenic patients (p<0.0001). In 6/17 of the thrombocytopenic patients, surface IgM (PSIgM) was found, in addition to the PSIgG. Those six patients are known with monoclonal IgM (concomitant Waldenstrom macroglobulinemia), markedly elevated polyclonal IgM levels, or lupus like autoimmune disorder which may have been responsible for the positive PSIgM. Only three thrombocytopenic patients with platelet counts less than 40×109/l had bleeding tendency (mainly purpura) with no response to steroid treatment (two of them were also resistant to ERT concerning their thrombocytopenia). Conclusions: Thrombocytopenia in Type I GD is related to either infiltration of bone marrow compromising megakariopoiesis or hypersplenism, but immune factors should also be considered. Despite the lack of response to steroids, the observed megakaryocytic hyperplasia in Gaucher infiltrated marrows, the failure to respond to ERT, and the presence of platelet surface antibodies in the thrombocytopenic patients, strongly implicate autoimmune etiology. The present study demonstrates that surface platelet antibodies may play a role in refractory thrombocytopenic GD patients. Since the role of splenectomy is controversial in GD, immune modulation approach should be considered.
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Toyama, Keisuke. "Recent Advances in Etiology and Management of Thrombocytopenia." TRENDS IN THE SCIENCES 5, no. 12 (2000): 84–86. http://dx.doi.org/10.5363/tits.5.12_84.
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Hayashino, Yasuaki, Hiroyasu Ishimaru, Kazuhiro Hatta, and Yosiaki Kohri. "Thrombotic thrombocytopenic purpura as an etiology of thrombocytopenia in systemic lupus erythematosus: case report." Modern Rheumatology 13, no. 3 (September 2003): 256–60. http://dx.doi.org/10.3109/s10165-003-0232-y.
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Cuker, Adam, and Douglas B. Cines. "Immune Thrombocytopenia." Hematology 2010, no. 1 (December 4, 2010): 377–84. http://dx.doi.org/10.1182/asheducation-2010.1.377.
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Immune thrombocytopenia (ITP) comprises a heterogeneous group of disorders characterized by autoimmune-mediated platelet destruction and impairment of thrombopoiesis. ITP may occur in the absence of an evident predisposing etiology (primary ITP) or secondary to a growing list of associated conditions (secondary ITP), and must be differentiated from other causes of thrombocytopenia. This review focuses on primary ITP in adults. The traditional goal of therapy in this population is to achieve a hemostatic platelet count of 30 × 109/L or above for most patients while minimizing treatment-related morbidity. This approach has been called into question by the recent advent of well-tolerated and effective agents for the management of ITP, including pulse-dose dexamethasone, rituximab, and the thrombopoietin receptor agonists. Recent studies suggest the potential for aggressive therapy at the time of diagnosis to alter the natural history of ITP and point to the importance of quality-of-life considerations in therapeutic decision making.
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Cuker, Adam, and Douglas B. Cines. "Immune Thrombocytopenia." Hematology 2010, no. 1 (December 4, 2010): 377–84. http://dx.doi.org/10.1182/asheducation.v2010.1.377.3643150.
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Abstract Immune thrombocytopenia (ITP) comprises a heterogeneous group of disorders characterized by autoimmune-mediated platelet destruction and impairment of thrombopoiesis. ITP may occur in the absence of an evident predisposing etiology (primary ITP) or secondary to a growing list of associated conditions (secondary ITP), and must be differentiated from other causes of thrombocytopenia. This review focuses on primary ITP in adults. The traditional goal of therapy in this population is to achieve a hemostatic platelet count of 30 × 109/L or above for most patients while minimizing treatment-related morbidity. This approach has been called into question by the recent advent of well-tolerated and effective agents for the management of ITP, including pulse-dose dexamethasone, rituximab, and the thrombopoietin receptor agonists. Recent studies suggest the potential for aggressive therapy at the time of diagnosis to alter the natural history of ITP and point to the importance of quality-of-life considerations in therapeutic decision making.
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Xu, Yiqing, Ying-Yi Xiao, Michael Simon, Than Than Aye, Komal Khiani, Yang Liu, Yiwu Huang, and Jack Burton. "Plasma Vascular Endothelial Growth Factor (VEGF) Levels Correlate with Thrombocytopenia of Various Etiology." Blood 124, no. 21 (December 6, 2014): 4991. http://dx.doi.org/10.1182/blood.v124.21.4991.4991.
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Abstract The mechanisms leading to thrombocytopenia include (1) decreased platelet production; (2) splenic sequestration due to splenomegaly; and (3) increased peripheral consumption and/or destruction. VEGF, physiologically secreted by endothelial cells, is also produced in the alpha-granules of platelets. VEGF measured in plasma will presumably reflect its level in in vivo circulation, released from both endothelial cells and platelets. We hypothesized that thrombocytopenic disorders characterized by increased platelet destruction would manifest with increased plasma VEGF level; whereas disorders characterized by decreased platelet production or platelet sequestration would show low or normal plasma VEGF level. Methods: This is a prospective study approved by IRB. Patients were eligible if they had platelet counts less than 150,000/ul at diagnosis. Plasma and serum specimens were collected at baseline and multiple time points towards recovery, and VEGF levels were determined using commercial ELISA kit from RayBiotech and BioRad according to manufacturer’s instructions. We enrolled 69 patients and 50 were included in the analysis. Nineteen patients were excluded from the analysis due to the following: the specimen was yielding non detectable serum VEGF value, or higher plasma VEGF level than serum level (both of above were used as internal controls for the validity of the experiment), or platelet count more than 150,000/ul. Five healthy controls were also enrolled. Results: Among the patients, the diagnoses were (A) 18 with ITP, (B) 13 with sepsis, (C) 4 with TTP, (D) 6 with MDS or AML (E) 6 with splenomegaly and (G) 3 with gestational thrombocytopenia. There was wide inter-patient variation in each group. The inter-experiment variation on the same specimen was less than 30% in most of the cases. The mean plasma VEGF value in the ITP, sepsis, TTP and groups were 49.2 ± 36.1 ng/ml, 158.9± 380.5 ng/ml, 204.5±222.6 ng/ml respectively, and were statistically higher than that of the control group 9.1±18.1 ng/ml, (p= 0.032, 0.029 and 0.022 respectively, Mann-Whitney test). On the other hand, the mean plasma VEGF value in the MDS, splenomegaly and gestational thrombocytopenia groups were 29.8±49.1 ng/ml, 13.2±21.3ng/ml and 3.0±1.8 ng/ml respectively, similar to that of the control group (p> 0.05 in all three groups, Mann-Whitney test). One patient in the sepsis group showed an extremely high plasma VEGF value (1447 ng/ml). Conclusion: Plasma VEGF value is a potential biomarker which can aide in the differential diagnosis of thrombocytopenia of various etiologies. Plasma VEGF levels were increased in most patients with thrombocytopenia from ITP, sepsis and TTP, but not in patients who have thrombocytopenia from MDS, splenomegaly or gestational thrombocytopenia. The elevation of plasma VEGF in those conditions could be due to increased epithelial production or release from platelet activation or destruction, the differentiation of which will need further study. A larger scale study is warranted to confirm the above result. Disclosures No relevant conflicts of interest to declare.
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Fogerty, Annemarie E. "Thrombocytopenia in Pregnancy: Approach to Diagnosis and Management." Seminars in Thrombosis and Hemostasis 46, no. 03 (April 2020): 256–63. http://dx.doi.org/10.1055/s-0040-1708842.
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AbstractThe impact of thrombocytopenia varies widely depending on the underlying pathophysiology driving it. The biggest challenge in managing thrombocytopenia in pregnancy is accurately identifying the responsible pathophysiology—a task made difficult given the tremendous overlap in clinical and laboratory abnormalities associated with different thrombocytopenia processes. The most common etiologies of thrombocytopenia in pregnancy range from physiology deemed benign to those that are life-threatening to the mother and fetus. Even in cases in which the responsible etiology is deemed benign, such as gestational thrombocytopenia, there are still implications for the management of labor and delivery, a time where hemostatic challenges may prove life-threatening. In most institutions, a minimum platelet count will be mandated for epidural anesthesia to be deemed a safe option. The causes of thrombocytopenia can also include diagnoses that are pregnancy-specific (such as preeclampsia or gestational thrombocytopenia), potentially triggered by pregnancy (such as thrombotic thrombocytopenic purpura), or unrelated to or predating the pregnancy (such as liver disease, infections, or immune thrombocytopenia purpura). It is imperative that the source of thrombocytopenia is identified accurately and expeditiously, as intervention can range from observation alone to urgent fetal delivery. In this review, the approach to diagnosis and the pathophysiological mechanisms of the most common etiologies of thrombocytopenia in pregnancy and associated management issues are presented.
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Simoes, Ana Teresa, Rogério Barreira, Ana Cristina Oliveira, Ana Cristina Pinheiro, Patrícia Ferreira, Marta Duarte, Ramón Salvado, Maria Leticia Ribeiro, and Susana Almeida Santos. "Reticulated Platelets Quantification In An Automatic CBC Counter and Its Role In Thrombocytopenia Etiology Assessment." Blood 116, no. 21 (November 19, 2010): 4672. http://dx.doi.org/10.1182/blood.v116.21.4672.4672.
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Abstract Abstract 4672 INTRODUCTION: Reticulated platelets (rP) are young platelets, recently released from the bone marrow, and contain more cytoplasmic RNA elements than mature platelets. Considerable amount of evidence suggests that rP analysis may be useful in the investigation of platelet disorders. Automatic quantification methods have been developed; however, the methodology has not yet been standardized and validated in clinical practice. STUDY PURPOSE To analyze the rP percentage (rP%) in 168 samples, using software version v3 in Cell Dyn® Sapphire, in correlation with clinical data. MATERIAL AND METHODS: 168 samples analyzed in Cell Dyn® Sapphire, between March and August 2010, using CBC+RET methodology in the determination of: rP%, reticulocytes % (Ret%), platelet optical counts (PLTo) and mean platelet volume (VPM). Normal control samples (C) n=73; Patients: 20 with auto-immune haemolytic anemia (IHA); 8 with thrombocytopenic thrombotic purpura (TTP); 45 with immune thrombocytopenia (IT), 4 with bone marrow aplasia (BMA) and 18 thrombocythopenias of unknown cause (TUC). Mean difference between rP% in controls vs TUC samples calculated by t-student. Statistical analysis by StatView 5.0. RESULTS: C samples: median rP % =1.6, range=0.2-4.1, mean PLTo= 263×109/L, median MPV=8.5fL. IHA: median rP%= 1.9, range =0.6 – 12.5, mean PLTo=284×109/L, median MPV= 8.6, mean Ret%=12. TTP: median rP%=5.1, range=0.3-16.5, mean PLTo=185×109/L, median MPV=8.5. IT: median rP%=3.8, range=0.4-27.8, mean PLTo=56.8×109/L, median MPV=11.4. BMA: median rP%=4.1, range=0.3-6, mean PLTo=66.2×109/L, median MPV=11. TUC: median rP%=2.7, range=0.2-13.6, mean PLTo= 80.5×109/L, median MPV=11.1 Mean difference between rP% in C vs TUC samples: t=2.5, p=0.02. CONCLUSIONS: Median rP% values obtained in control group are in agreement with published data, despite the variation in the “normal” values between the authors. MPV and rP% in destructive thrombocytopenias (IT and TTP) are higher than in control group, in accord to immature platelets release by the bone marrow. IHA patients, despite the high Ret%, have a median rP% similar to the control group, demonstrating that rP counts are not over-estimated by the high number of reticulocytes. In BMA rP% is higher than expected, however the number of samples analyzed is very low. The statistically significant mean difference between rP% in Control vs TUC samples makes the immune cause for the thrombocytopenia very likely. Due to its simplicity, ready availability and information provided by this methodology, it has a good potential to be a useful tool in the investigation of thrombocytopenias of unknown cause. Disclosures: No relevant conflicts of interest to declare.
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Fountain, Eric M., and Gowthami M. Arepally. "Etiology and complications of thrombocytopenia in hospitalized medical patients." Journal of Thrombosis and Thrombolysis 43, no. 4 (January 4, 2017): 429–36. http://dx.doi.org/10.1007/s11239-016-1467-8.
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Arias, Valerie, Allison Miller, Christina Moll, Shalom Barishansky, and James B. Bussel. "A Survey of the Etiology of Immune Thrombocytopenia (ITP)." Blood 118, no. 21 (November 18, 2011): 4688. http://dx.doi.org/10.1182/blood.v118.21.4688.4688.
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Abstract Abstract 4688 Background: Immune Thrombocytopenia (ITP) is a disease whose etiology remains unclear. Numerous socioeconomic, environmental, lifestyle, and genetic factors have been related to ITP, however their presence is variable and their relationship to ITP is not well understood. A questionnaire was created to study these relationships, to better understand what causes ITP and to relate this information to the course of disease, including response to treatment. Method: A literature search, 60 ITP patient interviews and multiple reviews by project coordinators, nurse practitioner, Platelet Disorder Support Association (PDSA) members, hematologists, and patients were performed to design a questionnaire. A pilot study was then conducted where 55 ITP patients from Cornell completed the questionnaire with the aim to further improve it. The next step will be to post a final version on the PDSA web site for 1,000 patients to complete it so that a database can be created. The questionnaire will also be given to a non-ITP patient population to serve as controls. Result: A 30 minute 93 item questionnaire that encompasses both children and adult patients was developed. The questionnaire documents factors that correlate with ITP and were present prior to diagnosis with the disease. It documents whether any of these factors changed and the effect of this change on ITP symptoms (worsening or improving). Among the factors addressed are nationality; country where the patient grew up; income; occupational hazards; neighborhood (e.g. Urban, Suburban, etc.); changes in job/school (e.g. remodeling or building damage); exposure to environmental hazards; travel history; medications taken; accidents; animal bites; pets; diet (e.g. increase/decrease in daily caloric intake, eliminating a type of food); allergies; exercise; sleep; stress level/stress reduction activities; alcohol consumption; smoking; drug abuse; consumption of certain foods (e.g. tonic water, sugar substitutes); vitamin deficiencies; vaccinations; general health state and medical history; pregnancy; infections; past history and family history of blood diseases, bone marrow diseases, inflammatory diseases, malignancies, autoimmune disorders and platelet production disorders; and past surgeries/procedures/hospitalizations. A few quality of life factors are also documented, among these are: the patient’s understanding of the disease and treatment options, resources, support network and side effects to ITP treatment. Finally, the questionnaire documents the severity of ITP symptoms, treatments received for ITP and the patient’s response to these treatments. Conclusion: This questionnaire is meant to capture a snapshot of different factors that correlate with ITP and treatment responses. It attempts to understand whether a patient’s response to different treatment modalities relates to the presence or absence of any of these factors. The questionnaire will also be given to a control group to see whether these socioeconomic, environmental, life-style and genetic factors are over-represented in ITP patients, when their prevalence is compared to a non-ITP population. This tool is meant to be broad in order to identify multiple significant factors that could be further investigated in more detail, and including molecular studies. Disclosures: Bussel: Portola: Consultancy; Eisai: Consultancy, Membership on an entity’s Board of Directors or advisory committees, Research Funding; GlaxoSmithKline: Consultancy, Equity Ownership, Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Amgen: Equity Ownership, Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Cangene: Research Funding; Genzyme: Research Funding; Immunomedics: Research Funding; Ligand: Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Shionogi: Membership on an entity’s Board of Directors or advisory committees, Research Funding, Speakers Bureau; Sysmex: Research Funding.
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Arias, Valerie, Ehsan Shabbir, Daniel Victorio, Emily Sperling, Naznin Haq, and James B. Bussel. "A Survey of the Etiology of Immune Thrombocytopenia (ITP)." Blood 120, no. 21 (November 16, 2012): 2239. http://dx.doi.org/10.1182/blood.v120.21.2239.2239.
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Abstract Abstract 2239 Introduction: Socioeconomic, environmental, lifestyle and genetic factors play a role in the etiology of ITP but are poorly understood. A self-reported questionnaire was designed to study these relationships and how these factors prior to the diagnosis of ITP relate to treatment response and disease progression in order to gain insight into the etiology of ITP. Methods: To design the questionnaire that would address topics of interest: 1) 60 ITP patient interviews were performed and 2) the questionnaire was reviewed by project coordinators, nurse practitioners, Platelet Disorder Support Association (PDSA) members, and hematologists. The input was incorporated into a further-revised questionnaire, which was then administered to both “pediatric” (patients <18 years of age at the time of diagnosis) and adult ITP patients from the Platelet Disorders Center at Weill Cornell - New York Presbyterian Hospital. Formal statistical analysis to relate responses to one question to responses of another to define sub-groups of patients is ongoing. Results: 109 patients were enrolled. Ages ranged from 2–78 years of age; median age was 55 years, with 21 females and 33 “pediatric” patients. The most frequent environmental exposures in adults were automotive exhaust (n=14) and Teflon (n=12). In pediatrics, preservatives and insecticides (n=8) and Teflon (n=7) were most common. The most prevalent hazardous substances in both groups were cleaning supplies (n=16 adults, n=9 “pediatric”) and chlorinated water (n=13 adult, n=9 “pediatric”). 13 adults also had exposure to gasoline or diesel fumes. Refer to figure 1. 51(47%) patients reported at least one infection prior to diagnosis with ITP. The most common were Strep throat (n=12); influenza (n=9), and respiratory tract infections (n=8). Twenty-four (22%) patients reported at least one autoimmune disease, including celiac (n=2) and discoid lupus (n=2).Twenty-one patients reported a family history of Type II diabetes, 12 Type I diabetes, 13 osteoarthritis and 10 rheumatoid arthritis. Eight (7%) patients reported at least one inflammatory disease including: Crohn's disease (n=3), Inflammatory bowel disease (n=7), Systemic lupus erythematous and Vitiligo(each n=1). Thirty-seven (34%) patients reported surgeries prior to diagnosis of ITP, especially: appendectomy (n=8) and tonsil removal (n=8). Twenty-three patients traveled close to date of diagnosis, 58 patients reported more stress than usual (i.e. death of a relative, loss of employment); 13 patients reported a drastic change in diet (i.e. decreasing calories (n=7) or becoming vegetarian (n=5)). Vitamin supplementation for vitamin C and D (each n=17), E (n=12) and B (n=11) were common. In addition, 11 vitamin deficiencies were reported, vitamin D (n=5), vitamin B12 (n=3) and other (n=3). The most frequent allergic reactions included: 31 (28%) patients with hay fever, 9 patients with allergies to milk, 7 patients with poison ivy or skin irritation, 6 patients with eczema, and 4 with allergic rhinitis. Other medical conditions reported were: hypothyroidism (n=10), hyperthyroidism (n=9), high blood pressure (N=16), high cholesterol (N=14), and anemia (N=13) [9 additional patients included 4 with iron deficiency anemia and 5 with a family history of iron deficiency anemia]. Seven patients reported a lack of prenatal care in their mothers' pregnancy and 7 were premature. Medications reported include: acetaminophen (n=53), antibiotics (n=36), antihistamines (n=22), and hormone therapy (n=17). Vaccinations received close to date of diagnosis include: flu vaccine (n=10) and T-dap (n=9). Prednisone was reported most frequently as both the best therapy to minimize symptoms (n=18) and the worst (n=16). Conclusion: Our pilot study intended to capture critical information and to further development of the questionnaire. We can see if there are groups of patients in whom onset and other characteristics relate to outcomes including response to treatment. Following formal statistical analysis of the material acquired (in progress and anticipated by early September), the next step will be for a final updated version of the questionnaire to be posted on the PDSA web site in order to accrue responses from a much larger number of patients. The questionnaire will also be given to a non-ITP patient population to serve as controls. Disclosures: Bussel: Amgen: Family owns Amgen stock Other, Membership on an entity's Board of Directors or advisory committees, Research Funding; Cangene: Research Funding; GlaxoSmithKline: Family owns GSK stock, Family owns GSK stock Other, Membership on an entity's Board of Directors or advisory committees, Research Funding; Genzyme: Research Funding; IgG of America: Research Funding; Immunomedics: Research Funding; Ligand: Membership on an entity's Board of Directors or advisory committees, Research Funding; Eisai: Membership on an entity's Board of Directors or advisory committees, Research Funding; Shionogi: Membership on an entity's Board of Directors or advisory committees, Research Funding; Sysmex: Research Funding; Portola: Consultancy. Off Label Use: The use of romiplostim in pediatric patients was examined in this study.
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Parker, Robert I. "Etiology and Significance of Thrombocytopenia in Critically Ill Patients." Critical Care Clinics 28, no. 3 (July 2012): 399–411. http://dx.doi.org/10.1016/j.ccc.2012.04.007.
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Meena, Sumarth Lal, Kanwar Singh, Sanjiv Jain, Anil Jain, and B. S. Karnawat. "Clinical profile and outcome of neonatal thrombocytopenia in a tertiary care hospital." International Journal of Contemporary Pediatrics 6, no. 3 (April 30, 2019): 1344. http://dx.doi.org/10.18203/2349-3291.ijcp20192041.
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Background: Thrombocytopenia (platelet count <1,50,000/µL) is one of the most common haematological problems in neonatal intensive care units. In contrast, only 2% of the normal neonates are thrombocytopenic at birth with severe thrombocytopenia (platelet count <50,000/µL) occurring in less than 3/1000 term infants. Multiple disease processes can cause thrombocytopenia in neonates. The important causes of thrombocytopenia in neonates are sepsis, birth asphyxia, prematurity, intra-uterine growth retardation, hyperbilirubinemia, respiratory distress syndrome, meconium aspiration syndrome and low birth weight. Apart from platelet count, bleeding manifestations depend on underlying ailments. The aims and objective were to study the clinical profile, etiology and outcome of neonatal thrombocytopenia in a tertiary care hospital.Methods: Prospective study involving 100 neonates with or developed neonatal thrombocytopenia in NICU.Results: In present study, 100 new-borns with thrombocytopenia 46% were mild, 35% were moderate and 19% were severe thrombocytopenia. 51 (51%) had early onset neonatal thrombocytopenia and 49 (49%) babies had late onset neonatal thrombocytopenia. Anaemia was the dominant maternal predisposing risk factor. Sepsis was the most common cause of neonatal thrombocytopenia. Most common symptom was apnoea. Sepsis, RDS and NEC had significantly contributed to mortality. Most common cause of death was sepsis followed by RDS and NEC.Conclusions: Neonatal thrombocytopenia is a treatable and reversible condition. Hence, it is important to identify neonates at risk and initiate transfusion therapy to prevent severe bleeding and potentially significant morbidity. Anaemia and PROM were the commonest maternal risk factors. Therefore, author recommended that babies born to mothers with these risk factors should be closely monitored for thrombocytopenia.
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Fadiloglu, Erdem, Canan Unal, Atakan Tanacan, Oytun Portakal, and Mehmet Sinan Beksac. "5 Yearsʼ Experience of a Tertiary Center with Thrombocytopenic Pregnancies: Gestational Thrombocytopenia, Idiopathic Thrombocytopenic Purpura and Hypertensive Disorders of Pregnancy." Geburtshilfe und Frauenheilkunde 80, no. 01 (July 24, 2019): 76–83. http://dx.doi.org/10.1055/a-0865-4442.
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Abstract Aim To evaluate thrombocytopenic pregnancies including gestational thrombocytopenia (GT), idiopathic thrombocytopenic purpura (ITP), and hypertensive disorders of pregnancy (HDP). Materials and Methods We evaluated the pregnancy outcomes and laboratory findings of 385 patients diagnosed with GT, ITP, or HDP whose thrombocyte levels were < 150 000/µL. Results GT, ITP, and HDP were the final diagnoses in 315 (81.8%), 35 (9.1%), and 35 (9.1%) cases, respectively. Patients diagnosed during the 1st trimester and diagnosed with ITP had significantly lower minimal platelet counts during the antenatal period and prior to delivery (p < 0.001; p < 0.001; p < 0.001; p < 0.001). Transfusion of any kind of blood product was given in 9.9% (n = 38) of all cases. Twelve patients had methylprednisolone and/or intravenous immunoglobulin treatments during the antenatal period. All patients who had undergone medical treatment were also found to have ITP. Four out of 385 patients underwent hysterectomy post partum due to refractory hemorrhage. Analysis of newborn platelet levels showed no statistical differences between any of the groups. Despite the lack of statistical significance, the rate of thrombocytopenia in newborns was 50% in patients with severe thrombocytopenia, while rates were 25.6 and 18.1% in patients with moderate and mild thrombocytopenia, respectively. Conclusion Thrombocytopenic pregnancies must be carefully evaluated with regard to the severity of thrombocytopenia, gestational period at initial diagnosis, and etiology. In particular, patients with ITP must be evaluated carefully as these patients are more likely to require transfusions and have platelet counts < 50 × 103/µl.
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Xiao, Ying-Yi, Yang Liu, Thanthanaye Zeng, Komal Khiani, Jack Burton, Yiwu Huang, and Yiqing Xu. "Plasma VEGF Levels and Etiology of Thrombocytopenia, a Biomarker Study." Blood 118, no. 21 (November 18, 2011): 4684. http://dx.doi.org/10.1182/blood.v118.21.4684.4684.
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Abstract Abstract 4684 Background: Thrombocytopenia is a major medical problem associated with bleeding. Etiology of thrombocytopenia includes myelosuppression, splenic sequestration and increased peripheral consumption and/or destruction. Vascular Endothelial Growth Factor (VEGF) is produced in both endothelial cells and platelets and is stored in alpha granules in the platelets. It plays multiple roles in the regulation of vascular endothelial cell proliferation and vascular integrity. Hypothesis: VEGF release from the platelets in vivo due to platelet activation or destruction may result in changes in plasma and serum VEGF levels, and the level could be associated with various etiologies of thrombocytopenia. Methods: This was a prospective IRB approved on-going study. Eligibility includes platelet count less than 120,000/ul, no current diagnoses of solid tumor and thrombocytopenia is not due to chemotherapy. Blood was collected at the time of diagnosis, and VEGF was measured in serum and plasma specimens using a commercial ELISA kit from Ray Biotech (Norcross, GA). Plasma adjusted VEGF levels are defined as plasma VEGF value divided by the platelet count. Results: Forty seven patients were enrolled, the clinical diagnoses included AML or MDS (designated as A/M, n=6), hypersplenism (n=13), ITP (n=14), sepsis (n=11) and confirmed TTP (n=3). Blood was also collected from 4 healthy volunteers as controls. Plasma VEGF levels and plasma adjusted VEGF levels (defined as plasma VEGF value divided by the number of platelets) were selected as the main measurements of outcome as shown below Conclusion: Plasma VEGF adjusted with platelet count should be the measurement for in vivo release of VEGF from endothelial or platelet sources. Plasma adjusted VEGF level has a wide range of variation in patients with thrombocytopenia, about 50% of our test subjects had undetectable VEGF plasma levels. Although not statistically significant, patients with thrombocytopenia due to AML or MDS had lowest plasma VEGF values and least variation, while patients with sepsis had highest plasma VEGF readings and variations, probably due to increased endothelial cell production. The study is ongoing in large scales, and we are also interested in following the trend of serial plasma adjusted VEGF levels along with platelet recovery. Disclosures: No relevant conflicts of interest to declare.
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Mansuri, Benazeer, and Komal P. Thekdi. "A prospective study on morphological alteration of megakaryocytes amongst megaloblastic anemia cases along with their clinic-haematological manifestations." International Journal of Research in Medical Sciences 5, no. 9 (August 26, 2017): 4127. http://dx.doi.org/10.18203/2320-6012.ijrms20173996.
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Background: Megaloblastic anemias are hematologic disorders in which abnormal DNA synthesis causes blood and bone marrow disorders. The cause of thrombocytopenia in megaloblastic anemia has been postulated as hypoproduction in some studies, whereas ineffective thrombopoeisis has been proposed in other. Objective was to study spectrum of clinic-hematological features in megaloblastic anemia and comparative bone marrow aspiration study of thrombocytopenia secondary to megaloblastic anemia, hypoproduction and hyper-destruction. This study was done to understand the various megakaryocytic alterations in hematological disorders presenting with thrombocytopenia due to different mechanisms.Methods: Total 85 cases of thrombocytopenia included in the study. Bone marrow finding in 33 cases of thrombocytopenia of megaloblastic etiology were compared with 34 cases of marrow proven hypo productive thrombocytopenia (aplastic anemia, acute leukemia) and 19 cases of hyper destructive thrombocytopenia (immune thrombocytopenia).Results: Most common age group presenting megaloblastic anemia is 11-20 year, with male to female ratio is1.2:1, most common complaint were generalized weakness and fever. In megaloblastic anemia 24.33%, 60% and 15.67% of the cases shows increase, decrease and normal megakaryocytes respectively. Dysplastic megakaryocytes were observed in 24.3%, 27% and 20.5% of the cases of megaloblastic anemia, acute leukaemia and immune thrombocytopenic purpura respectively.Conclusions: Both hypoproduction and ineffective thrombopoiesis are the underlying path mechanisms in megaloblastic thrombocytopenia as evidenced by the marrow findings. We hereby infer that megaloblastic thrombocytopenia is to be included as a separate category apart from hypo proliferative and hyper destructive groups. The presence of dysplastic megakaryocyte should not prompt an interpretation
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Hohlfeld, P., F. Forestier, C. Kaplan, JD Tissot, and F. Daffos. "Fetal thrombocytopenia: a retrospective survey of 5,194 fetal blood samplings." Blood 84, no. 6 (September 15, 1994): 1851–56. http://dx.doi.org/10.1182/blood.v84.6.1851.1851.
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Abstract Fetal platelet counts were retrospectively studied in a series of 5,194 consecutive fetal blood samplings (FBS). The mean value was 245 +/- 65 x 10(9)/L, without significant variation between 17 and 41 weeks' gestation. After exclusion of false thrombocytopenia due to contamination with amniotic fluid, 247 fetuses had platelet counts less than 150 x 10(9)/L. In 70 cases, thrombocytopenia was due to congenital infectious diseases (toxoplasmosis, rubella, and cytomegalovirus). It was related to immune causes in 45 cases: anti-HPA-1a (n = 23), anti- HPA-5b (n = 2) or possible anti-HLA (n = 2) alloimmunizations, and immune thrombocytopenic purpura (n = 18). Chromosomal abnormality was the etiology in 43 cases (trisomy 13, 18, and 21, Turner's syndrome, triploidy), and other disorders (multiple birth defects, intrauterine growth retardation, rhesus disease, and gestational thrombocytopenia) in 62 cases. No specific cause for the low platelet count could be established in 27 fetuses (range, 115 to 149 x 10(9)/L). Severe thrombocytopenia (< or = 50 x 10(9)/L) occurred mainly in immune cases (16%), congenital infectious diseases (7%), and chromosomal abnormalities (1%). Diagnosis, prognosis, and management of fetal thrombocytopenia are presented in the different clinical situations. In this series, FBS was never associated with serious bleeding, and no fetal exsanguination was observed.
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Hohlfeld, P., F. Forestier, C. Kaplan, JD Tissot, and F. Daffos. "Fetal thrombocytopenia: a retrospective survey of 5,194 fetal blood samplings." Blood 84, no. 6 (September 15, 1994): 1851–56. http://dx.doi.org/10.1182/blood.v84.6.1851.bloodjournal8461851.
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Fetal platelet counts were retrospectively studied in a series of 5,194 consecutive fetal blood samplings (FBS). The mean value was 245 +/- 65 x 10(9)/L, without significant variation between 17 and 41 weeks' gestation. After exclusion of false thrombocytopenia due to contamination with amniotic fluid, 247 fetuses had platelet counts less than 150 x 10(9)/L. In 70 cases, thrombocytopenia was due to congenital infectious diseases (toxoplasmosis, rubella, and cytomegalovirus). It was related to immune causes in 45 cases: anti-HPA-1a (n = 23), anti- HPA-5b (n = 2) or possible anti-HLA (n = 2) alloimmunizations, and immune thrombocytopenic purpura (n = 18). Chromosomal abnormality was the etiology in 43 cases (trisomy 13, 18, and 21, Turner's syndrome, triploidy), and other disorders (multiple birth defects, intrauterine growth retardation, rhesus disease, and gestational thrombocytopenia) in 62 cases. No specific cause for the low platelet count could be established in 27 fetuses (range, 115 to 149 x 10(9)/L). Severe thrombocytopenia (< or = 50 x 10(9)/L) occurred mainly in immune cases (16%), congenital infectious diseases (7%), and chromosomal abnormalities (1%). Diagnosis, prognosis, and management of fetal thrombocytopenia are presented in the different clinical situations. In this series, FBS was never associated with serious bleeding, and no fetal exsanguination was observed.
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Pandey, Anubha, and Roma Singh. "Thrombocytopenia during pregnancy: an institutional based prospective study of one year." International Journal of Research in Medical Sciences 5, no. 8 (July 26, 2017): 3502. http://dx.doi.org/10.18203/2320-6012.ijrms20173550.
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Background: Platelets are non-nucleated cellular fragments of megakaryocytes, they play a critical role in haemostasis. Thrombocytopenia, defined as blood platelet count below 150.000/μL is the second leading cause of blood disorders in pregnancy after anemia. It complicates 7 to 10% of all pregnancies. Gestational thrombocytopenia explains 70-80% of all cases of thrombocytopenia in pregnancy. Hypertensive disorders account for approximately 20% and immune thrombocytopenic purpura for about 3-4%. Other etiologies are considered rare in pregnancy.Methods: The study was conducted in the tertiary institute over a period of one year, from January 2016 to December 2016. The samples of blood were collected from the Antenatal out-patient department and from indoor patients of the department of gynecology and obstetrics of the J.K. Hospital, Bhopal, Madhya Pradesh India.Results: Maximum number of patients had moderate degree of anemia around 58%. Most of the cases presented during 30-34 weeks of gestation. The most common etiology was gestational thrombocytopenia.Conclusions: Thrombocytopenia in pregnancy may occur secondary to a variety of causes. Most of these cases occur during specific periods of gestation. Management of pregnant women with platelet disorders requires a multidisciplinary approach and close collaboration between obstetric and hepatologist.
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Schmidt, Brian M., and Crystal M. Holmes. "Retrospective Cohort Analysis of Pedal Procedures in the Thrombocytopenic Patient." International Journal of Lower Extremity Wounds 16, no. 4 (November 16, 2017): 284–88. http://dx.doi.org/10.1177/1534734617740483.
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Thrombocytopenia is an important medical condition to understand prior to performing procedures in the foot and ankle. We have set forth to highlight factors a physician should take into consideration before performing procedures in the thrombocytopenic patient. A retrospective cohort analysis at a large academic institution was undertaken utilizing a cohort discovery tool to discover incidence and management strategies for patients with foot-related conditions that require in-office procedures. We demonstrate that a full history and physical are important to guide treatment along with complete blood count testing prior to intervention. We included all patients at the institution that underwent a foot and ankle procedure in-office with podiatric surgery over 10 years where thrombocytopenia was demonstrable via complete blood count within 3 months of the procedure. Patients’ charts were reviewed for 1 year following podiatric intervention and outcomes were recorded. The cohort reveals that patients with thrombocytopenia have many advanced comorbidities but performing procedures in this cohort is safe. Complications from procedures included erythrocyte transfusion, ulcer recurrence, need for formal surgical intervention, infection, falls, and death. We then provide a brief discussion about the etiology and management options available for thrombocytopenia.
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Laber, Damian A., and Monte E. Martin. "Etiology of thrombocytopenia in all patients treated with heparin products." European Journal of Haematology 75, no. 2 (August 2005): 101–5. http://dx.doi.org/10.1111/j.1600-0609.2005.00503.x.
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Delhumeau, A., X. Moreau, C. Chapotte, N. Houi, and J. C. Bigorgne. "Heparin-associated thrombocytopenia syndrome: An underestimated etiology of adrenal hemorrhage." Intensive Care Medicine 19, no. 8 (August 1993): 475–77. http://dx.doi.org/10.1007/bf01711091.
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Kakanale, Mahesh, Manoj A. G., Prabhakar K., and Raveesha A. "Clinical, etiological and laboratory profile of febrile thrombocytopenia and correlation of platelet count with outcome in a South Indian tertiary hospital." International Journal of Research in Medical Sciences 8, no. 2 (January 27, 2020): 672. http://dx.doi.org/10.18203/2320-6012.ijrms20200255.
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Background: Febrile thrombocytopenia is commonly encountered by doctors especially during monsoon and peri-monsoon period, many of these patients have a turbulent cthisse with multi organ dysfunction and might land up in ICU with significant morbidity and mortality. Infections are the commonest causes of thrombocytopenia and they vary with season and geographical location. A systematic approach, carried out with an awareness of causes, clinical presentation and laboratory profile of febrile thrombocytopenia can shorten the duration of investigations and bring out the diagnosis early, reducing morbidity and mortality of patients and reducing burden on hospital resthisces. The objective of the study is to study the underlying etiology, the various clinical presentations, laboratory profile and complications of fever with thrombocytopenia in this community during monsoon period and to correlate thrombocytopenia with outcome, co morbidities and its etiology.Methods: The prospective observational study was conducted in tertiary centre in Kolar between June-December 2017. Patients meeting inclusion and exclusion criteria were grouped into 4 groups based on platelet counts, and correlated with comorbidities, etiology and outcome. Detailed clinical and laboratory examination were done in all patients and p value of <0.05 was considered statistically significant.Results: Among 465 patients were included in the study. Dengue was the most common cause for febrile thrombocytopenia and mortality. Hepatic complications and petechiaes were the most common complications and bleeding manifestations. 135 patients received platelet transfusion but there was no relationship between platelet transfusion and outcome, there were 9 deaths in the study and there was no association between death and platelet count at admission.Conclusions: There was no relation between platelet count on admission and mortality and also there was no relationship between platelet transfusion and outcome. Knowing the clinical presentation, etiology, complications and its monitoring can significantly reduce the morbidity and mortality due to febrile thrombocytopenia.
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George, James N., and Richard H. Aster. "Drug-induced thrombocytopenia: pathogenesis, evaluation, and management." Hematology 2009, no. 1 (January 1, 2009): 153–58. http://dx.doi.org/10.1182/asheducation-2009.1.153.
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AbstractAlthough drugs are a common cause of acute immune-mediated thrombocytopenia in adults, the drug etiology is often initially unrecognized. Most cases of drug-induced thrombocytopenia (DITP) are caused by drug-dependent antibodies that are specific for the drug structure and bind tightly to platelets by their Fab regions but only in the presence of the drug. A comprehensive database of 1301 published reports describing 317 drugs, available at www.ouhsc.edu/platelets, provides information on the level of evidence for a causal relation to thrombocytopenia. Typically, DITP occurs 1 to 2 weeks after beginning a new drug or suddenly after a single dose when a drug has previously been taken intermittently. However, severe thrombocytopenia can occur immediately after the first administration of antithrombotic agents that block fibrinogen binding to platelet GP IIb-IIIa, such as abciximab, tirofiban, and eptifibatide. Recovery from DITP usually begins within 1 to 2 days of stopping the drug and is typically complete within a week. Drug-dependent antibodies can persist for many years; therefore, it is important that the drug etiology be confirmed and the drug be avoided thereafter.
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Melikyan, Anait L., Elena K. Egorova, Elena I. Pustovaya, Tamara I. Kolosheynova, Irina N. Subortseva, Elena A. Gilyazitdinova, and Valeriy G. Savchenko. "The Frequency of Primary Immune Thrombocytopenia (idiopathic thrombocytopenic purpura) in Patients with Isolated Thrombocytopenia." Blood 132, Supplement 1 (November 29, 2018): 4982. http://dx.doi.org/10.1182/blood-2018-99-111654.
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Abstract CONTEXT: Many hematological and non-hematological diseases can be hidden under the mask of isolated thrombocytopenia. The choice of therapeutic tactics is determinated by correct diagnosis. OBJECTIVE: to define the frequency of occurrence of primary immune thrombocytopenia (idiopathic thrombocytopenic purpura-ITP) in the group of patients with isolated thrombocytopenia. Materials and methods: We analysed clinical and laboratory data of 301 patients who applied to the outpatient department of National Research Center for hematology, Russian Federation with thrombocytopenia of unspecified origin. The first group is 183 patients who applied for the first time. The second group is 118 patients with long history of ITP. All patients were examined according to the extended differential diagnostic protocol used in isolated thrombocytopenia and based on international and National clinical recommendations for the diagnosis and treatment of ITP in adults. Results: Median age of patients in both groups was 36 years, male/female ratio in group 1 was 1:2, in group 2 - 1:4. In group 1, the count of platelets in the blood was more than 50*109/l in 87% of cases, while in the second group, in most cases (94%), there was a decrease in the count of platelets <50*109/l. Among the patients of the first group, haemorrhagic syndrome was absent in 50% of cases, even with platelet count less than 50*109/l. In the second group, 88% of patients complained of haemorrhages on the skin and mucosa, in 2% of cases life-threatening bleeding (uterine and gastrointestinal) developed (table 1). The examination carried out according to the protocol allowed to establish the diagnosis of ITP in group 1 in 88 (48%) patients, in group 2 in 100 (85%). Thus, the ratio of primary and secondary thrombocytopenia in group 1 was 1:1, in group 2 - 6:1. (fig. 1). The causes of secondary thrombocytopenia in group 1 were: increased consumption syndrome with thrombogenic complications in 16 (9%) patients, autoimmune diseases, occurring with isolated thrombocytopenia in 13 (7%) cases, virus-associated thrombocytopenia in 12 (7%) patients, drug-induced thrombocytopenia in 8 (4%) patients with diseases of the cardiovascular system, long-taking anticoagulants and disaggregants, in 7 (4%) cases of chronic viral hepatitis C, in 4 (2%) - liver cirrhosis of non-viral etiology, in 4 (2%) HIV infection, in 4 (2%) lymphoproliferative disease, in 2 (1%) acute leukemia, in 3 (2%) cases myelodysplastic syndrome (MDS), 14 (8%) women were diagnosed with gestational thrombocytopenia, EDTA-associated false thrombocytopenia was detected in 8 (4%) patients. Repeated examination of patients of the second group was carried out in the following cases: early relapse, resistance to corticosteroid therapy or loss of response after any line of therapy, incompliance of haemorrhagic syndrome with the count of platelets, the presence of thrombosis in the history, causing doubts in the diagnosis of ITP. The diagnosis of ITP in this group was changed to antiphospholipid syndrome in 4 patients, MDS in 4 cases, in 2 - systemic lupus erythematosus, in 3 - primary immunodeficiency and 2 patients, aged 40 and 44 years were found to have a genetic abnormality - abnormality Meya-Hegglina and thrombasthenia Glanzmann. A comparison of the number of patients diagnosed with ITP and secondary thrombocytopenia by age groups showed that secondary thrombocytopenia are more common at the age of 60 years (38% versus 19%, respectively) (Fig. 2). Conclusion: This study clearly presents a variety of hematological and non-hematological diseases occurring with isolated thrombocytopenia, which indicates the ambiguity of such concepts as the symptom of isolated thrombocytopenia and primary immune thrombocytopenia and requires a complete examination not only in the onset of the disease, but also in the recurrence of ITP. Disclosures No relevant conflicts of interest to declare.
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Sumarokov, A. B., L. I. Buryachkovskaya, and N. V. Lomakin. "Thrombocytopenia and prospective endovascular intervention in a patient with coronary artery disease." Medical Council, no. 21 (January 20, 2019): 16–21. http://dx.doi.org/10.21518/2079-701x-2018-21-16-21.
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Thrombocytopenia in blood count may be a reflex of haemostatic problems of different origin – from autoimmune disease to iatrogenic nature. Sometimes, thrombocytopenia may be revealed in patient with coronary heart disease before PCI procedure as well as some hours or days later. Dual antithrombotic therapy and thrombocytopenia have the same main side effect – bleeding. Etiology of disease and details of medical decision before percutаneous coronary intervention (PCI) in CHD patients are discussed.
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Djordjevic, Jelena, Petar Svorcan, Dusica Vrinic, and Branka Dapcevic. "Splenomegaly and thrombocytopenia in patients with liver cirrhosis." Vojnosanitetski pregled 67, no. 2 (2010): 166–69. http://dx.doi.org/10.2298/vsp1002166d.
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Backgroud/Aim. Splenomegaly is a frequent finding in patients with liver cirrhosis and portal hypertension and may cause hypersplenism. The occurrence of thrombocytopenia in those patients can be considered as an event with multiple etiologies. Two mechanisms may act alone or synergistically with splenic sequestration. One is central which involves either myelosuppression because of hepatitis viruses or the toxic effects of alcohol abuse on the bone marrow. The second one involves the presence of antibodies against platelets. It also depends upon the stage and etiology of liver disease. The aim of the study was to investigate a correlation between the platelet count and spleen size and the risk factors for thrombocytopenia in patients with liver cirrhosis. Methods. We studied 40 patients with decompensated liver cirrhosis who were hospitalized in the Department of Gastroenterohepatology. The liver function was graded according to Child Pugh score. Spleen size was defined ultrasonografically on the basis of craniocaudal length. Suspicion of portal hypertension was present when longitudinal spleen length was more than 11 cm. Thrombocytopenia was determined by platelet count under 150 000/mL. Results. We did not find any significant correlation between hepatic dysfunction and spleen size (p = 0.9), and between hepatic dysfunction and thrombocytopenia (p = 0.17). Our study did not find any significant correlation between spleen size and peripheral platelet count (p = 0.5), but we found a significant correlation between thrombocytopenia and etiology of cirrhosis - decreased platelet count was more common among patients with cirrhosis of alcoholic etiology than in other etiologies of cirrhosis (p = 0.001). Conclusion. According to our study, liver cirrhosis, portal hypertension and thrombocytopenia could be present even in the absence of enlarged spleen suggesting the involvement of other mechanisms of decreasing platelet account.
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Srikant S Kandagatla and Swati Aundhakar. "A study on the Clinical profile of fever with thrombocytopenia." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 20, 2020): 176–83. http://dx.doi.org/10.26452/ijrps.v11ispl4.3765.
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Common manifestations during monsoon conditions in tropical regions are specified with fever and thrombocytopenia. With this, viral disease like dengue, chikungunya, malaria is more common. Hence it is important to evaluate and diagnose the manifestation thereby bringing in early treatment and reduced mortality. The present study was designed to evaluate the clinical profile of patients with fever and thrombocytopenia and its clinical outcome. Prospective non-interventional observational study was conducted in a tertiary care hospital with 160 patients by random sampling. Patients with fever were involved for the study, their clinical data (symptoms during presentation, signs of fever), laboratory examinations for platelet count, total leukocyte count, and liver function tests were performed. Follow-up was maintained until patients were discharged or with record of mortality. Data was analysed using Chi-square test and Cramer’s V test. Out of total 160 patients, majority were male with gender ratio of 7:3 (male:female0 and mean age was 32.53±15.23 years. Majority of patients depicted that the total platelet count was in the range of 40001-60000/ccum and was significantly dependent on etiology (P=0.03198). Similarly, total leukocyte count was also significantly dependent on etiology (P=0.0004998). Fever and thrombocytopenia are the early manifestations of the major viral diseases. Hence it is important to systemically study the clinical and laboratory data to determine its etiology and early diagnosis for treatment.
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Brassard, Jacqueline, Brian Curtis, Richard Cooper, John Ferguson, Wendy Komocsar, Maria Ehardt, Stuart Kupfer, et al. "Acute Thrombocytopenia in Patients Treated with the Oral Glycoprotein IIb/IIIa Inhibitors Xemilofiban and Orbofiban: Evidence for an Immune Etiology." Thrombosis and Haemostasis 88, no. 12 (2002): 892–97. http://dx.doi.org/10.1055/s-0037-1613330.
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SummaryThrombocytopenic episodes occurring in 18,845 patients treated with the GPIIb/IIIa inhibitors xemilofiban and orbofiban (“fibans”) were analyzed by a blinded review panel and 73 patients were classified as having “possible fiban-induced thrombocytopenia”. When the treatment codes were broken, a significant association between drug exposure and assignment to this group was found (p <0.001). Twenty-eight (82%) of 34 archived serum samples from these patients contained fiban-dependent antibodies specific for GPIIb/IIIa, but no such antibodies were found in 61 drug treated patients not classified as having “possible fiban-induced thrombocytopenia” (p <0.001). We conclude that fiban-dependent antibodies were the major cause of acute, severe thrombocytopenia in patients judged on the basis of clinical findings to have thrombocytopenia “possibly-induced” by xemilofiban and orbofiban. Measurement of drug-dependent antibodies may be helpful in determining the basis for acute thrombocytopenia in fiban-treated patients and possibly for identification of patients at risk to develop thrombocytopenia.
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Azrieh, Bahjat, Arwa Alsaud, Khaldun Obeidat, Amr Ashour, Seham Elebbi, Shehab F. Mohamed, Mohamed Adel Abdelaty, Abdelraouf Akkari, Abdurrahman Ali Elbuzidi, and Mohamed A. Yassin. "Rituximab Twice Weekly for Refractory Thrombotic Thrombocytopenic Purpura in a Critically Ill Patient with Acute Respiratory Distress Syndrome." Case Reports in Oncology 13, no. 1 (February 17, 2020): 153–57. http://dx.doi.org/10.1159/000505236.
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Thrombotic thrombocytopenic purpura (TTP) is a rare, serious, life-threatening disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and hypercoagulability. The etiology is a deficiency of ADAMTS13 which is usually caused by acquired antibodies. Plasma exchange and steroids is the standard of care in the treatment of TTP. However, there are refractory cases of TTP which require further management. Rituximab appears to be a safe and effective therapy for refractory and relapsing TTP. Here we report a challenging case of TTP that responded to treatment with rituximab twice weekly. According to our knowledge, rituximab twice weekly has never been used for TTP before.
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Kumar, Dr Sampat, Dr Anushree CN, and Dr Divya Nagaram. "The prevalence, etiology and patterns of thrombocytopenia among geriatric age group." International Journal of Clinical and Diagnostic Pathology 2, no. 1 (January 1, 2019): 361–64. http://dx.doi.org/10.33545/pathol.2019.v2.i1f.94.
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Sniecinski, Roman M., Marcie J. Hursting, Michael J. Paidas, and Jerrold H. Levy. "Etiology and Assessment of Hypercoagulability with Lessons from Heparin-Induced Thrombocytopenia." Anesthesia & Analgesia 112, no. 1 (January 2011): 46–58. http://dx.doi.org/10.1213/ane.0b013e3181ff0f7f.
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Boxer, Michael. "Consultation for Thrombocytopenia in Hospitalized Patients." Blood 120, no. 21 (November 16, 2012): 4659. http://dx.doi.org/10.1182/blood.v120.21.4659.4659.
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Abstract Abstract 4659 Thrombocytopenia is a frequent cause for hematologic consultation in an acute care hospital. During a 22 month period one hematologist assessed 93 patients with thrombocytopenia. Thrombocytopenia was the sole reason for the consultation. No previous thrombocytopenia had been recognized previously in any if these patients. The cause for thrombocytopenia was liver diease in 21 patients, sepsis in 12, immune (ITP) in 12, antimetabolites or antiseizure medications in 7, heparin induced thrombocytopenia (HIT) in 6, platelet clumping in 4, thrombotic thrombocytopenic purpura (TTP) in 3, myelodysplasia (MDS) in 3, acute progranulocytic leukemia (APL) in 3, rhabdomyolysis in 2, viral infections in 2, systemic lupus (SLE) in 2, and intravenous antibiotics in 2. The following conditions were each diagnosed once as the cause for thrombocytopenia:pregnancy, disseminated intravascular coagulation (DIC), post coronary bypass grafting, brain injury, acute myelogenous leukemia (AML-M5), antiphospholipid syndrome (APLS), and intra aortic ballon pump. No diagnosis could be made in 13 patients. In 28 patients the initial diagnosis was incorrect. No diagnosis could be made in 13 patients. In 6 patients two causes for thrombocytopenia were present. One patient was admitted twice with two different causes for thrombocytopenia (sepsis and ITP). Review of the peripheral smear is both necessary and mandatory. All three patients with APL were initially diagnosed with ITP, and the diagnosis of APL was not made until the smear was assessed. Smear review confirmed or made the diagnosis of TTP. Platelet clumping could not be made without reviewing the peripheral smear. Primary hematologic diagnoses (ITP, HIT, clumping, TTP, MDS, APL, AML, APLS) were present in 33 patients. Secondary causes for thrombocytopenia were present in the majority of patients. In summary thrmobocytopenia a frequent cause for hematologic consultation, and most patients will not have a primary hematologic etiology for the thrombocytopenia. Advanced liver disease is an underappreciated cause for thrombocytopenia and was never considered to be the cause for the thrombocytopenia by the referring physician. Despite exhaustive testing the cause for thrombocytopenia could not be made in 13 patients. However in these patients the platelet count rarely was below 100,000. The importance of reviewing the peripheral smear cannot be overemphasized. Disclosures: No relevant conflicts of interest to declare.
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Ye, Ji-bin, Chuan-Song Hu, Tai-Sheng Li, and Li Fang. "View Point on Severe Fever with Thrombocytopenia Syndrome." Infection International 2, no. 3 (September 1, 2013): 141–44. http://dx.doi.org/10.1515/ii-2017-0056.
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Abstract Severe fever with thrombocytopenia syndrome (SFTS), a new disease of zoonotic natural foci has been increasing in recent years. In this review, the disease of human granulocytic anaplasmosis infection due to tickborne and new Bunia virus infection, have similar clinical symptoms. Total of 11 articles were retrieved. The emergence, etiology, nomenclature and pathogenic mechanisms, clinical diagnosis and genotyping of SFTS were summarized, and the current situation of treatment was also evaluated. In conclusion, early detection, identification and treatment are the key points to SFTS, but how to reduce the mortality of critically ill patients is still the focus in the future.
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Pinnamaneni, Pawankalyan, Rakesh Devabhakthuni, and Ravikumar Chodavarapu. "Clinical epidemiology of paediatric febrile and afebrile in-patients and their association with thrombocytopenia." International Journal of Contemporary Pediatrics 7, no. 5 (April 24, 2020): 972. http://dx.doi.org/10.18203/2349-3291.ijcp20201491.
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Background: Fever is one of the commonest and thrombocytopenia is one of the common clinical problems in children. The current study was done with the aim to identify the frequency and the etiology of thrombocytopenia in febrile children. This study was planned to identify epidemiological observations associated with pediatric fever and with febrile thrombocytopenia children, in this area among hospitalized children.Methods: A sample of 530 children of age 6 months to 18 years were studied. Febrile children were taken as cases (n=268) and afebrile children as controls (n=262). Demographic, clinical and laboratory characteristics were measured and compared between the cases and controls.Results: Significant proportion of 1-3 years age group of children belong to febrile group compared to afebrile group. There is no significant difference in the gender, region, WFH or BMI, WFA, HFA between febrile and afebrile children. No significant difference in pulse rate, respiratory rate; TLC, ALC, ANC, Hb; Widal test or CRP was noted between pyrexial and apyrexial children. The median platelet count, in the pyrexial group is significantly lower than that of apyrexial group. Prevalence of thrombocytopenia in pyrexial group is significantly more than that observed in apyrexial group. The commonest illness in pyrexial group is non-bacterial-probable viral illness (59.7%). In the apyrexial group the common diseases are neurological (36.6%) disorders.Conclusions: Prevalence of thrombocytopenia is 11.45% in febrile children and in afebrile children it is 2.38%. In this study, viral infections and neurological disorders are the commonest etiology in febrile group and afebrile children respectively.