To see the other types of publications on this topic, follow the link: Thrombocytopenia.
Journal articles on the topic 'Thrombocytopenia'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Thrombocytopenia.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Browning, James, and David James. "Immune thrombocytopenia in pregnancy." Fetal and Maternal Medicine Review 2, no. 2 (July 1990): 143–57. http://dx.doi.org/10.1017/s0965539500000334.
Full textAbstract:
Autoimmune thrombocytopenia (ITP)1) The risks to mother and fetus have previously been overstated.2) There is no maternal test which will accurately determine fetal thrombocytopenia.3) The only reliable test for fetal thrombocytopenia is cordocentesis – this carries a higher morbidity than that of fetal intracerebral haemorrhage from ITP.4) Contrary to received wisdom, there is no evidence that, even for the most severely thrombocytopenic infant, abdominal delivery protects against intracranial haemorrhage.5) Management therefore involves keeping the maternal platelet count above 50 × 1091 and choosing the route of delivery on normal obstetric grounds.Alloimmune thrombocytopenia1) Alloimmune thrombocytopenia is commoner than hitherto believed (0.15% all neonates).2) The fetal risks are considerable: intracranial haemorrhage occurs in 4% of cases antenatally and in 10% in labour. The risks are virtually confined to those with a platelet count of less than 30 × 109l−1.3) Cordocentesis is justified for the ‘at risk’ fetus; fetal immunoglobulin or platelet therapy can be given.4) When the fetal platelet count is below 50 × 109l−1, abdominal delivery should be planned.5) A maternal screening test for neonatal alloimmune thrombocytopenia exists (lack of P1A1 antigen).
2
Gouin-Thibault, Isabelle, Bruno Cassinat, Christine Chomienne, Jean-Didier Rain, Yves Najean, and Marie-Hélène Schlageter. "Is the Thrombopoietin Assay Useful for Differential Diagnosis of Thrombocytopenia? Analysis of a Cohort of 160 Patients with Thrombocytopenia and Defined Platelet Life Span." Clinical Chemistry 47, no. 9 (September 1, 2001): 1660–65. http://dx.doi.org/10.1093/clinchem/47.9.1660.
Full textAbstract:
Abstract Background: Thrombopoietin (TPO), the major hormone controlling platelet production, has been measured in thrombocytopenias with discordant results. The aim of our work was to assess the value of the TPO assay for differential diagnosis of thrombocytopenias in a large cohort of patients classified according to the results of their platelet isotopic study. Methods: We measured TPO (R&D Systems) in serum of 160 thrombocytopenic patients referred to our department for platelet life span isotopic studies. We classified patients as follows: (a) idiopathic or autoimmune thrombocytopenia group (ITP; patients with increased platelet destruction and shortened platelet life span; n = 67); (b) pure genetic thrombocytopenia group (patients with decreased platelet production, normal platelet life span, and without bone marrow aplasia; n = 55); (c) bone marrow aplasia group (BM; patients with decreased platelet production, normal platelet life span, and bone marrow aplasia; n = 13). Results: In patients with pure genetic thrombocytopenia, TPO (median, 55 ng/L) was not different from TPO in patients with ITP (median, 58 ng/L) or controls (n = 54; median, 51 ng/L). Only in patients with bone marrow aplasia was TPO significantly higher (median, 155 ng/L) and negatively correlated to the platelet count (r2 = 0.5014). Conclusions: Although the median serum TPO is increased in thrombocytopenia with decreased platelet production from bone marrow aplasia, it does not differentiate patients with pure genetic thrombocytopenia from those with ITP.
3
Weimann, Andreas, Andreas Lun, Gerhard Gaedicke, and Malte Cremer. "Immature Platelet Fraction (IPF) as Novel Laboratory Parameter for Managing Early Onset Thrombocytopenia in Very Low Birth Weight Infants." Blood 112, no. 11 (November 16, 2008): 4552. http://dx.doi.org/10.1182/blood.v112.11.4552.4552.
Full textAbstract:
Abstract Thrombocytopenia (platelet count <150/nl) is one of the most common hematologic problems in preterm and term neonates and affects 18 to 35% of all patients admitted to neonatal intensive care units (NICU). Thrombocytopenia is more than twice common in extremely low birth weight infants (ELBW; <1000g) as reported among the general NICU population. Among thrombocytopenic ELBW infants almost 40% suffer from severe thrombocytopenia as defined by a platelet count <50nl. The risk for hemorrhage, which may cause acute life-threatening complications and/or life-long disability in more than 15%, is difficult to assess, because it is closely related to the gestational and postnatal age of the neonate as well as the cause of the thrombocytopenia and the severity of concurrent conditions. From routine full blood counts of premature (birth weight <1500g) and full term babies we additionally determined platelet counts, IPF, MPV, NRBC and reticulocyte counts. On the basis of individual IPF and platelet counts we were able to predict the platelet counts of the following day. In non-thrombocytopenic preterm and term neonates no significant changes in IPF values were found during the first week of life. In the first week, thrombocytopenic neonates displayed higher IPF values than neonates with normal plaletet counts. We hypothesize that IPF is higher in neonates with chronic hypoxia as leading cause for thrombocytopenia and lower in case of perinatal infections. IPF could be a novel parameter in routine diagnostics available at a 24/7 basis in VLBW infants and may be valuable in identifying the underlying pathomechanism of various thrombocytopenias and in clinical decision making on platelet transfusions.
4
Skupski, Daniel W., and James B. Bussel. "Antenatal treatment of fetal immune thrombocytopenias." Fetal and Maternal Medicine Review 10, no. 1 (February 1998): 1–19. http://dx.doi.org/10.1017/s0965539598000114.
Full textAbstract:
Advances in both imaging techniques and in treatments for immune thrombocytopenias affecting the fetus have allowed for more accurate antenatal predictions of severe disease and effective antenatal treatments for those fetuses who are at risk of sequelae. This article will review current knowledge of the diagnosis and treatment of affected fetuses in alloimmune thrombocytopenia and in immune thrombocytopenic purpura.
5
Lee, S. H., S. Looareesuwan, J. Chan, P. Wilairatana, S. Vanijanonta, S. M. Chong, and B. H. Chong. "Plasma Macrophage Colony-Stimulating Factor and P-Selectin Levels in Malaria-Associated Thrombocytopenia." Thrombosis and Haemostasis 77, no. 02 (1997): 289–93. http://dx.doi.org/10.1055/s-0038-1655955.
Full textAbstract:
SummaryThrombocytopenia is a common finding in malaria. In clinical trials, recombinant macrophage colony-stimulating factor (M-CSF) causes a reversible, dose-dependent thrombocytopenia, and high M-CSF has been reported in autoimmune thrombocytopenias. P-selectin, which is secreted into the plasma following platelet/endothelial activation or damage, is elevated in certain consumptive thrombocytopenic disorders. The relationships between thrombocytopenia, M-CSF and P-selectin were analysed in 63 patients with severe (n = 13) or uncomplicated (n = 26) P. falciparum (PF) or P. vivax (PV) malaria (n = 24). On admission, 69% of PF patients and 75% of PV patients were thrombocytopenic (platelets < 150 X 109/1). M-CSF was elevated in PF (3021 ± 1844 pg/ml) and PV (2602 ± 1668 pg/ml) patients, compared to controls (589 ± 200 pg/ml). The platelet count was inversely correlated with M-CSF in PF (r = -0.681), and in PV malaria (r = -0.548). Elevated P-selectin was found in severe PF malaria, but not in PV malaria. Severe PF malaria was associated with marked thrombocytopenia, very high M-CSF, elevated P-selectin and compelling evidence of disseminated intravascular coagulopathy (DIC). Platelet counts, M-CSF and P-selectin returned to control values in 7-14 days. These data suggest that elevated M-CSF in malaria, by enhancing macrophage activity, may result in increased macrophage-mediated platelet destruction. Further, platelet/endothelial activation or damage, as measured by P-selectin, or DIC could intensify thrombocytopenia in severe PF malaria, but does not appear to contribute to thrombocytopenia in uncomplicated PF or PV malaria.
6
Ellahi, Ayesha, Muhammad Wasiullah Khan, Samra Shahid, Javaid Usman, Hassan Ikran, and Safoora Naveed. "Thrombocytopenia in Pregnancy: A Cross-Sectional Study in Northern Pakistan." Pakistan Armed Forces Medical Journal 72, no. 3 (June 26, 2022): 1013–17. http://dx.doi.org/10.51253/pafmj.v72i3.7048.
Full textAbstract:
Objective: To determine the association of thrombocytopenia (mild, moderate & severe) with pregnancy-related disorders.
Study Design: Cross-sectional study.
Place and Duration of Study: Department of Haematology of Pakistan Railway Hospital, Rawalpindi Pakistan, in collaboration with the Departments of Obstetrics and Gynecology of Pak Emirates Military Hospital and Fuji Foundation Hospital, Rawalpindi Pakistan, from Oct 2018 to Oct 2019.
Methodology: Seventy-five pregnant females with platelet count <150x109/l were included. Blood samples were taken and analyzed for complete blood count, peripheral blood smear, manual count by Neubauer chamber, uric acid, urinary proteins, liver function tests (bilirubin & aspartate aminotransferase), lactate dehydrogenase, coagulation profile and viral serology (Hepatitis B & C).
Results: Out of a total of 75 thrombocytopenic pregnant females, gestational thrombocytopenia was most common (74.7%), followed by preeclampsia (17.3%), HELLP syndrome (4%), immune thrombocytopenic purpura (4%) respectively. Mild thrombocytopenia was frequently observed in patients of G.T. (62.5%), while moderate thrombocytopenia (84.6%) was generally detected in preeclampsia patients. Severe thrombocytopenia was mostly identified in patients with HELLP syndrome (66.7%) and immune thrombocytopenic purpura (66.7%).
Conclusion: Mild thrombocytopenia is mostly presented in gestational thrombocytopenia. Moderate thrombocytopenia was frequent in patients with preeclampsia, and severe thrombocytopenia was usually diagnosed in patients with HELLP syndrome and immune thrombocytopenic purpura, which require apposite and judicious management for the safety of mother and fetus.
7
Komatsu, Norio. "1. Immune Thrombocytopenic Purpura (Immune Thrombocytopenia)." Nihon Naika Gakkai Zasshi 103, no. 7 (2014): 1593–98. http://dx.doi.org/10.2169/naika.103.1593.
Full text
8
Özsoylu, Sinasi, Janine Campbell, and Christina Mitchell. "Autoimmune thrombocytopenia versus idiopathic thrombocytopenic purpura." European Journal of Haematology 53, no. 1 (April 24, 2009): 54–55. http://dx.doi.org/10.1111/j.1600-0609.1994.tb00181.x.
Full text
9
Arnott, J., P. Horsewood, and JG Kelton. "Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia." Blood 69, no. 5 (May 1, 1987): 1294–99. http://dx.doi.org/10.1182/blood.v69.5.1294.1294.
Full textAbstract:
Abstract Platelet-associated IgG (PAIgG) is elevated in idiopathic thrombocytopenic purpura (ITP), but it also is elevated in other thrombocytopenic disorders traditionally considered to be nonimmune. Consequently it is possible that elevated PAIgG is a nonspecific finding secondary to thrombocytopenia. To study this issue we developed a rabbit model of immune and nonimmune mediated thrombocytopenia. The mechanism of the thrombocytopenia was validated by platelet survival studies. Immune thrombocytopenia was produced by injection of antirabbit platelet serum that was raised in guinea pigs. Nonimmune aregenerative thrombocytopenia was produced by irradiation of the animals; nonimmune consumptive thrombocytopenia was produced by injection of adenosine diphosphate (ADP). PAIgG was measured in a direct binding assay using 125I-labeled staphylococcal protein A (SpA). Washed platelets from normal, nonthrombocytopenic rabbits bound an average of 81 molecules of SpA per platelet (81 +/- 168, mean +/- 2 SD, n = 39). Infusion of the antiplatelet antiserum produced thrombocytopenia with a rise in PAIgG that was closely correlated with the level of PAIgG (r = 0.86, n = 12). The thrombocytopenia was consumptive, as shown by a very short platelet life span using 111In- labeled platelets. In contrast, both nonimmune thrombocytopenic states resulted in an equal or greater drop in the platelet count but no change in the level of PAIgG. The animals with aregenerative thrombocytopenia had normal or only moderately reduced platelet life spans; however, in every animal the level of PAIgG was not different from the nonthrombocytopenic controls, irrespective of the platelet count. Similarly, the level of PAIgG was unchanged in those rabbits with nonimmune consumptive thrombocytopenia following infusion of ADP (82 +/- 55 molecules of SpA per platelet, mean +/- SD, n = 6). These studies indicate that elevated PAIgG is a specific finding of immune thrombocytopenia and is not secondary to thrombocytopenia itself. Indirectly these results support our hypothesis that immune mechanisms contribute to more thrombocytopenic disorders than was once thought likely.
10
Arnott, J., P. Horsewood, and JG Kelton. "Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia." Blood 69, no. 5 (May 1, 1987): 1294–99. http://dx.doi.org/10.1182/blood.v69.5.1294.bloodjournal6951294.
Full textAbstract:
Platelet-associated IgG (PAIgG) is elevated in idiopathic thrombocytopenic purpura (ITP), but it also is elevated in other thrombocytopenic disorders traditionally considered to be nonimmune. Consequently it is possible that elevated PAIgG is a nonspecific finding secondary to thrombocytopenia. To study this issue we developed a rabbit model of immune and nonimmune mediated thrombocytopenia. The mechanism of the thrombocytopenia was validated by platelet survival studies. Immune thrombocytopenia was produced by injection of antirabbit platelet serum that was raised in guinea pigs. Nonimmune aregenerative thrombocytopenia was produced by irradiation of the animals; nonimmune consumptive thrombocytopenia was produced by injection of adenosine diphosphate (ADP). PAIgG was measured in a direct binding assay using 125I-labeled staphylococcal protein A (SpA). Washed platelets from normal, nonthrombocytopenic rabbits bound an average of 81 molecules of SpA per platelet (81 +/- 168, mean +/- 2 SD, n = 39). Infusion of the antiplatelet antiserum produced thrombocytopenia with a rise in PAIgG that was closely correlated with the level of PAIgG (r = 0.86, n = 12). The thrombocytopenia was consumptive, as shown by a very short platelet life span using 111In- labeled platelets. In contrast, both nonimmune thrombocytopenic states resulted in an equal or greater drop in the platelet count but no change in the level of PAIgG. The animals with aregenerative thrombocytopenia had normal or only moderately reduced platelet life spans; however, in every animal the level of PAIgG was not different from the nonthrombocytopenic controls, irrespective of the platelet count. Similarly, the level of PAIgG was unchanged in those rabbits with nonimmune consumptive thrombocytopenia following infusion of ADP (82 +/- 55 molecules of SpA per platelet, mean +/- SD, n = 6). These studies indicate that elevated PAIgG is a specific finding of immune thrombocytopenia and is not secondary to thrombocytopenia itself. Indirectly these results support our hypothesis that immune mechanisms contribute to more thrombocytopenic disorders than was once thought likely.
11
Saha, Sarbari, Debabrata Roy, Ismat Jahan, Mohammad Kamrul Hassan Shabuj, Sadeka Choudhury, MA Mannan, Mohammod Shahidullah, and Sanjoy Kumer Dey. "Frequency and outcome of thrombocytopenia in neonates who are at risk of developing thrombocytopenia - a prospective observational study." Bangabandhu Sheikh Mujib Medical University Journal 15, no. 2 (January 16, 2023): 115–20. http://dx.doi.org/10.3329/bsmmuj.v15i2.60866.
Full textAbstract:
Thrombocytopenia is the commonest hematological abnormality encountered in the neonatal intensive care unit (NICU). This prospective, observational study was conducted among 78 consecutive at-risk neonates admitted in NICU, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka from September 2016 to August 2017. Platelet count was measured in all at risk neonates at enrollment and less than 1,50,000/cmm was consiered as the cut off point for determining thrombocytopenia. Platelet count was measured every alternate day till discharge or normalisation of platelet count if the initial platelet count was low. If initial platelet count revealed normal, then the babies were followed up clinically if they develop any further risk condition for developing thrombocytopenia. During the period from enrollment to discharge, if any baby develops thrombocytopenia at any time then baby was defined as thrombocytopenic. Overall 39.7%patients found to be thrombocytopenic among 78 at-risk neonates. Pregnancy induced hypertension (PIH), neonatal sepsis and small for gestational age (SGA), intra uterine growth restriction(IUGR), prematurity, necrotizing enterocolitis (NEC) were significantly associated with thrombocytopenia. Sepsis and NEC were found to be independent risk factor for thrombocytopenia. Regarding outcome, length of hospital stay was significantly more in thrombocytopenic patients than non-thrombocytopenic patients. Death rate was also higher in thrombocytopenic patients in comparison to non-thrombocytopenic patients. BSMMU J 2022; 15(2): 115-120
12
Baldeo, Cherisse, Karan Seegobin, and Lara Zuberi. "Immune Thrombocytopenia as a Consequence of Rocky Mountain Spotted Fever." Case Reports in Oncology 10, no. 3 (October 23, 2017): 945–47. http://dx.doi.org/10.1159/000481617.
Full textAbstract:
Primary immune thrombocytopenia (ITP) – also called idiopathic thrombocytopenic purpura or immune thrombocytopenic purpura – is an acquired thrombocytopenia caused by autoantibodies against platelet antigens. It is one of the more common causes of thrombocytopenia in otherwise asymptomatic adults. Rocky Mountain spotted fever (RMSF) is a potentially lethal, but curable, tick-borne disease. We present a case of ITP that was triggered by RMSF.
13
Pishko, Allyson M., and Ariela L. Marshall. "Thrombocytopenia in pregnancy." Hematology 2022, no. 1 (December 9, 2022): 303–11. http://dx.doi.org/10.1182/hematology.2022000375.
Full textAbstract:
Abstract Hematologists are often consulted for thrombocytopenia in pregnancy, especially when there is a concern for a non-pregnancy-specific etiology or an insufficient platelet count for the hemostatic challenges of delivery. The severity of thrombocytopenia and trimester of onset can help guide the differential diagnosis. Hematologists need to be aware of the typical signs of preeclampsia with severe features and other hypertensive disorders of pregnancy to help distinguish these conditions, which typically resolve with delivery, from other thrombotic microangiopathies (TMAs) (eg, thrombotic thrombocytopenic purpura or complement-mediated TMA). Patients with chronic thrombocytopenic conditions, such as immune thrombocytopenia, should receive counseling on the safety and efficacy of various medications during pregnancy. The management of pregnant patients with chronic immune thrombocytopenia who are refractory to first-line treatments is an area that warrants further research. This review uses a case-based approach to discuss recent updates in diagnosing and managing thrombocytopenia in pregnancy.
14
McCrae, Keith R. "Thrombocytopenia in Pregnancy." Hematology 2010, no. 1 (December 4, 2010): 397–402. http://dx.doi.org/10.1182/asheducation-2010.1.397.
Full textAbstract:
Abstract Thrombocytopenia occurs commonly during pregnancy, and may result from diverse etiologies. Awareness of these many causes facilitates proper diagnosis and management of thrombocytopenia in the pregnant setting. Some causes of thrombocytopenia are unique to pregnancy and may not be familiar to hematologists. In the review, we will discuss the differential diagnosis of thrombocytopenia in pregnancy, and the pathogenesis of selected thrombocytopenic disorders. Considerations for optimal management of the pregnant patient with thrombocytopenia will also be described.
15
Nagalla, Srikanth, and Ravindra Sarode. "Recent advances in understanding and management of acquired thrombocytopenia." F1000Research 7 (January 17, 2018): 68. http://dx.doi.org/10.12688/f1000research.12309.1.
Full textAbstract:
There are numerous congenital and acquired causes of thrombocytopenia. Thrombocytopenia could be a result of decreased bone marrow production, increased consumption, increased destruction, splenic sequestration or a combination of these causes. In this review, we have focused on some of the serious acquired causes of thrombocytopenia. There have been some significant advances in our understanding of the pathophysiology, diagnostic testing, and treatment of immune thrombocytopenia, heparin-induced thrombocytopenia, thrombotic thrombocytopenic purpura, and atypical hemolytic uremic syndrome over the past five years. These advances have resulted in a significant decrease in mortality and morbidity of patients with these disorders. Despite these advances, we are still faced with numerous unanswered questions in the pathophysiology and management of these complex thrombocytopenic disorders.
16
Sojitra, Manthan, Sushma R. Shah, Ami V. Mehta, Payal P. Panchal, and Ronak Bhankhar. "Maternal outcome in pregnancy with thrombocytopenia." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 9, no. 7 (June 25, 2020): 2895. http://dx.doi.org/10.18203/2320-1770.ijrcog20202729.
Full textAbstract:
Background: Thrombocytopenia is second most common haematological abnormality in pregnancy after anemia. The aim of this study was to find out the prevalence, causative factor of thrombocytopenia and to observe the obstetrics outcome of pregnancies complicated with thrombocytopenia.Methods: This is prospective study of maternal outcome in pregnancy with thrombocytopenia carried out at tertiary care center from February 2019 to January 2020. Out of 350 antenatal screened women, 25 women who were diagnosed with thrombocytopenia, were included in the study.Results: The incidence of maternal thrombocytopenia in this study was 7.1%. 60% of the women had mild thrombocytopenia while 24% and 16% of women were moderate and severe thrombocytopenic respectively. Amongst 25 thrombocytopenic women 68% had gestational thrombocytopenia, 24% had gestational hypertensive disorder,4% had HELLP syndrome, 4% had immune thrombocytopenic purpura. 60% were delivered vaginally and 40% were delivered by LSCS. The most common indication of LSCS was acute fetal distress (40%) followed by failed induction (30%), breech (10%), and the rest (20%) for other obstetrical indications. The most common indication for induction was pre-eclampsia followed by IUGR, and post-date.Conclusions: In pregnancy with thrombocytopenia, gestational thrombocytopenia is the commonest and benign condition which does not alter the obstetrical management. Still a vigil 4 should be kept on maternal platelet count in antenatal period to prevent unfavorable outcome in serious conditions that may require specific and urgent management (HELLP syndrome, severe pre-eclampsia, ITP).
17
Cines, Douglas B., James B. Bussel, Robert B. McMillan, and James L. Zehnder. "Congenital and Acquired Thrombocytopenia." Hematology 2004, no. 1 (January 1, 2004): 390–406. http://dx.doi.org/10.1182/asheducation-2004.1.390.
Full textAbstract:
Abstract The diagnosis and management of thrombocytopenia is a growing component in the practice of hematology. The frequency with which hematologists are called in consultation for thrombocytopenia continues to increase with the advent of routine automated platelet determinations and the introduction of new medications. For most patients, such as those with inherited and auto-immune thrombocytopenia, emphasis is focused on efforts to treat or forestall bleeding without excess drug-induced toxicity or burden to the patient. However, in disorders such as heparin-induced thrombocytopenia (HIT), avoidance of thrombotic complications is the key to management. In this chapter, we provide the pediatric and adult hematologist with new insights into the pathogenesis and recognition of congenital inherited thrombocytopenias (CTP), a hitherto difficult to comprehend constellation of clinical entities. We also highlight new approaches to the diagnosis and treatment of two of the more common thrombocytopenic conditions encountered in practice, autoimmune or idiopathic thrombocytopenic purpura (ITP) and HIT. In Section I, Dr. James Bussel discusses CTPs and their distinction from childhood ITP. He emphasizes the clinical features that enable the pediatrician and hematologist to suspect the diagnosis of CTP and those that are of use to subcategorize the various entities, where possible. He also emphasizes newer molecular markers that afford definitive diagnosis in some cases and provide insight into platelet production. This section highlights the characteristic associated findings and differences in the natural history and approaches to management of the various entities. In Section II, Dr. Robert McMillan discusses adult chronic ITP. He revisits the utility of platelet antibody determination in diagnosis and review new insights into pathogenesis. The role of Helicobacter pylori infection and the timing of splenectomy in the management of acute and emergent ITP are examined. New insights into the natural history of ITP post-splenectomy and management strategies for patients with severe, chronic, refractory ITP are discussed. In Section III, Dr. James Zehnder updates us on HIT. He emphasizes new insights into the clinical presentation and pathogenesis of this condition. He critically reviews the utility of laboratory testing for heparin-dependent antibodies. Recent studies on the use of direct thrombin inhibitors are examined and the management of cardiopulmonary bypass surgery in patients with HIT is discussed.
18
Patel, Saumil M., Kinjal Patel, Karan Patel, and Rekha Thaddanee. "Comparison of outcomes of thrombocytopenic and non-thrombocytopenic culture proven neonatal sepsis." International Journal of Contemporary Pediatrics 8, no. 3 (February 23, 2021): 512. http://dx.doi.org/10.18203/2349-3291.ijcp20210656.
Full textAbstract:
Background: Due to high incidence of sepsis as a main cause of neonatal mortality, early detection and proper treatment are important in reducing neonatal mortality. Thrombocytopenia is a common hematological problem encountered during neonatal period, particularly in neonatal sepsis. This study was done to know the incidence of thrombocytopenia in neonatal sepsis and to compare clinical outcome in patients with thrombocytopenic and non-thrombocytopenic neonatal sepsis.Methods: This was a prospective study carried out at neonatal intensive care unit of a tertiary care teaching hospital of western Gujarat, India, from October 2018 to August 2020. 2739 neonates were admitted with probable sepsis during study period. 299 neonates with positive blood cultures were recruited for the study. They were divided into two groups; group-1 had patients with thrombocytopenia, while group-2 included patients without thrombocytopenia. Severity of thrombocytopenia was assessed in group-1. Micro-organisms isolated and outcome of sepsis were compared in both the groups. Results: There were 208 neonates in group-1 (thrombocytopenic) and 91 in group-2 (non-thrombocytopenic). There was no significant difference in demographic profiles of neonates in both groups. Klebsiella pneumonia was the most common organism isolated from 79 patients of group-1 and 19 patients of group-2 (p=0.033). Coagulase negative Staphylococci and Candida were the second and third most common micro-organisms isolated from 30.2% and 15.1% of blood cultures respectively. In group-1, 85 (40.8%), 72 (34.6%) and 51 (24.5%) neonates had severe, moderate and mild thrombocytopenia respectively. Klebsiella pneumoniae (45.9%) was the commonest organism isolated in severe thrombocytopenic neonates, followed by Candia (22.4%) and Enterococcus (14.1%).Conclusions: Thrombocytopenia is a specific marker of neonatal sepsis. The platelet count is a simple test that facilitates diagnostic orientation and the establishment of an early empirical treatment. Klebsiella pneumoniae was the commonest organism isolated in severe thrombocytopenic neonates.
19
Ajzenberg, Nadine, Marie Dreyfus, Cécile Kaplan, Jeannine Yvart, Bernard Weill, and Gil Tchernia. "Pregnancy-Associated Thrombocytopenia Revisited: Assessment and Follow-Up of 50 Cases." Blood 92, no. 12 (December 15, 1998): 4573–80. http://dx.doi.org/10.1182/blood.v92.12.4573.
Full textAbstract:
Abstract Thrombocytopenia detected during pregnancy addresses the issue of its mechanism and of the possible occurrence of neonatal thrombocytopenia. To further investigate these issues, 50 women referred to us because of thrombocytopenia detected during pregnancy (platelet count, <150 × 109/L), were extensively studied, as well as their offspring. Among these thrombocytopenic women, we used the threshold of 70 × 109/L to differentiate between mild and severe thrombocytopenia. Whatever the severity of thrombocytopenia, we found biological features of an autoimmune disorder in 48% of the women, and chronic thrombocytopenia in 55%. A familial thrombocytopenia was evidenced in 1 case. These 50 women gave birth to 63 neonates, among whom 24 were thrombocytopenic, either at birth or during the first week of life. Neonatal thrombocytopenia could only be predicted in multiparous women, on the basis of previous neonatal thrombocytopenia in older siblings, and/or when maternal platelet life span study, performed before pregnancy, had evidenced an autoimmune thrombocytopenia (AITP)-like profile. These results suggest that, in case of pregnancy-associated thrombocytopenia, familial and immunological studies, combined with postdelivery iterative platelet counts, should be performed to properly characterize the thrombocytopenia. Moreover, the platelet count of the neonate should be carefully assessed at birth and during the following days, a platelet life span study should be performed after delivery in the mother, because these two parameters are likely to bring valuable information regarding the forthcoming pregnancies and the risk of neonatal thrombocytopenia.
20
Ajzenberg, Nadine, Marie Dreyfus, Cécile Kaplan, Jeannine Yvart, Bernard Weill, and Gil Tchernia. "Pregnancy-Associated Thrombocytopenia Revisited: Assessment and Follow-Up of 50 Cases." Blood 92, no. 12 (December 15, 1998): 4573–80. http://dx.doi.org/10.1182/blood.v92.12.4573.424k25_4573_4580.
Full textAbstract:
Thrombocytopenia detected during pregnancy addresses the issue of its mechanism and of the possible occurrence of neonatal thrombocytopenia. To further investigate these issues, 50 women referred to us because of thrombocytopenia detected during pregnancy (platelet count, <150 × 109/L), were extensively studied, as well as their offspring. Among these thrombocytopenic women, we used the threshold of 70 × 109/L to differentiate between mild and severe thrombocytopenia. Whatever the severity of thrombocytopenia, we found biological features of an autoimmune disorder in 48% of the women, and chronic thrombocytopenia in 55%. A familial thrombocytopenia was evidenced in 1 case. These 50 women gave birth to 63 neonates, among whom 24 were thrombocytopenic, either at birth or during the first week of life. Neonatal thrombocytopenia could only be predicted in multiparous women, on the basis of previous neonatal thrombocytopenia in older siblings, and/or when maternal platelet life span study, performed before pregnancy, had evidenced an autoimmune thrombocytopenia (AITP)-like profile. These results suggest that, in case of pregnancy-associated thrombocytopenia, familial and immunological studies, combined with postdelivery iterative platelet counts, should be performed to properly characterize the thrombocytopenia. Moreover, the platelet count of the neonate should be carefully assessed at birth and during the following days, a platelet life span study should be performed after delivery in the mother, because these two parameters are likely to bring valuable information regarding the forthcoming pregnancies and the risk of neonatal thrombocytopenia.
21
Court, WS, JM Bozeman, SJ Soong, MN Saleh, DR Shaw, and AF LoBuglio. "Platelet surface-bound IgG in patients with immune and nonimmune thrombocytopenia." Blood 69, no. 1 (January 1, 1987): 278–83. http://dx.doi.org/10.1182/blood.v69.1.278.278.
Full textAbstract:
Abstract We quantitated the amount of platelet surface-bound IgG using an 125I monoclonal anti-IgG assay in 149 patients with thrombocytopenia and 260 normal donors. The normal subjects had 122 +/- 5 molecules of IgG/platelet (mean +/- SE). Fifty-five patients with nonimmune thrombocytopenia had 338 +/- 37 molecules of IgG/platelet, whereas 67 patients with immune thrombocytopenia studied at the time of their initial evaluation had 4,120 +/- 494 molecules of IgG/platelet. An analysis of the distribution of values in these two groups indicated that 90% of the patients with immune thrombocytopenia had greater than 800 molecules of IgG/platelet, whereas only 7% of patients with nonimmune thrombocytopenia exceeded this amount. The immune thrombocytopenia patients included 39 idiopathic, 14 secondary, and 14 drug-induced disorders, and they did not significantly differ in their distribution of values for platelet IgG. The nonimmune thrombocytopenic patients included 12 cases with a platelet destructive mechanism; their platelet-bound IgG was similar to that of the other nonimmune patients. Twenty-seven patients with treatment resistant immune thrombocytopenia were also studied they had 2,100 +/- 670 molecules of IgG/platelet. Their values were significantly greater than those of the nonimmune thrombocytopenic patients and not significantly different from those of immune thrombocytopenic group. Their distribution of values was much broader, however, with 33% of patients having less than 800 molecules of IgG/platelet, suggesting possible alternate mechanisms in their thrombocytopenia. Thus, patients with immune thrombocytopenia have a high frequency of elevated IgG on the platelet surface which reflects the pathophysiology of this disorder. Quantitation of platelet-bound IgG provides a useful laboratory tool in the differential between immune and nonimmune thrombocytopenia.
22
Court, WS, JM Bozeman, SJ Soong, MN Saleh, DR Shaw, and AF LoBuglio. "Platelet surface-bound IgG in patients with immune and nonimmune thrombocytopenia." Blood 69, no. 1 (January 1, 1987): 278–83. http://dx.doi.org/10.1182/blood.v69.1.278.bloodjournal691278.
Full textAbstract:
We quantitated the amount of platelet surface-bound IgG using an 125I monoclonal anti-IgG assay in 149 patients with thrombocytopenia and 260 normal donors. The normal subjects had 122 +/- 5 molecules of IgG/platelet (mean +/- SE). Fifty-five patients with nonimmune thrombocytopenia had 338 +/- 37 molecules of IgG/platelet, whereas 67 patients with immune thrombocytopenia studied at the time of their initial evaluation had 4,120 +/- 494 molecules of IgG/platelet. An analysis of the distribution of values in these two groups indicated that 90% of the patients with immune thrombocytopenia had greater than 800 molecules of IgG/platelet, whereas only 7% of patients with nonimmune thrombocytopenia exceeded this amount. The immune thrombocytopenia patients included 39 idiopathic, 14 secondary, and 14 drug-induced disorders, and they did not significantly differ in their distribution of values for platelet IgG. The nonimmune thrombocytopenic patients included 12 cases with a platelet destructive mechanism; their platelet-bound IgG was similar to that of the other nonimmune patients. Twenty-seven patients with treatment resistant immune thrombocytopenia were also studied they had 2,100 +/- 670 molecules of IgG/platelet. Their values were significantly greater than those of the nonimmune thrombocytopenic patients and not significantly different from those of immune thrombocytopenic group. Their distribution of values was much broader, however, with 33% of patients having less than 800 molecules of IgG/platelet, suggesting possible alternate mechanisms in their thrombocytopenia. Thus, patients with immune thrombocytopenia have a high frequency of elevated IgG on the platelet surface which reflects the pathophysiology of this disorder. Quantitation of platelet-bound IgG provides a useful laboratory tool in the differential between immune and nonimmune thrombocytopenia.
23
Tavares, FL, ME Peichoto, JR Marcelino, KC Barbaro, MC Cirillo, ML Santoro, and IS Sano-Martins. "Platelet participation in the pathogenesis of dermonecrosis induced by Loxosceles gaucho venom." Human & Experimental Toxicology 35, no. 6 (August 6, 2015): 666–76. http://dx.doi.org/10.1177/0960327115597983.
Full textAbstract:
Loxosceles gaucho spider venom induces in vitro platelet activation and marked thrombocytopenia in rabbits. Herein, we investigated the involvement of platelets in the development of the dermonecrosis induced by L. gaucho venom, using thrombocytopenic rabbits as a model. L. gaucho venom evoked a drop in platelet and neutrophil counts 4 h after venom injection. Ecchymotic areas at the site of venom inoculation were noticed as soon as 4 h in thrombocytopenic animals but not in animals with initial normal platelet counts. After 5 days, areas of scars in thrombocytopenic animals were also larger, evidencing the marked development of lesions in the condition of thrombocytopenia. Histologically, local hemorrhage, collagen fiber disorganization, and edema were more severe in thrombocytopenic animals. Leukocyte infiltration, predominantly due to polymorphonuclears, was observed in the presence or not of thrombocytopenia. Thrombus formation was demonstrated by immunohistochemistry at the microvasculature, and it occurred even under marked thrombocytopenia. Taken together, platelets have an important role in minimizing not only the hemorrhagic phenomena but also the inflammatory and wound-healing processes, suggesting that cutaneous loxoscelism may be aggravated under thrombocytopenic conditions.
24
Akbayram, Sinan, Murat Dogan, Cihangir Akgun, Erdal Peker, Mehmet Parlak, and Ahmet Faik Oner. "An Analysis of Children With Brucellosis Associated With Isolated Thrombocytopenia." Clinical and Applied Thrombosis/Hemostasis 17, no. 6 (September 9, 2010): E36—E38. http://dx.doi.org/10.1177/1076029610382104.
Full textAbstract:
Hematologic abnormalities of mild anemia and leucopenia have been frequently associated with acute brucellosis, but thrombocytopenia are less frequently seen. In the present study, we documented 5 (2.6%) isolated thrombocytopenic patients with the manifestations of brucellosis observed during the course of active infection. Five (2.6%) patients, 4 boys and 1 girl, with ages ranging from 2 to 14 years, had isolated thrombocytopenic at diagnosis. In 5 (2.6%) patients, platelet counts ranged from 39 000 to 120 000/mm3. Tube agglutination tests for brucellosis were positive for all patients (1/160-1/1280). All patients recovered completely, and their thrombocytopenia returned to normal by 2 to 4 weeks after antibiotic treatment of brucellosis. In our study, we present 5 patients with Brucella-induced thrombocytopenia mimicking idiopathic thrombocytopenic purpura to emphasize the isolated thrombocytopenia and the resolution of thrombocyte counts following treatment of brucellosis.
25
Zaher, Galila F., and Maha A. Badawi. "Heparin-Induced Thrombocytopenia Complicating Thrombotic Thrombocytopenic Purpura." Journal of King Abdulaziz University - Medical Sciences 24, no. 1 (March 31, 2017): 43–48. http://dx.doi.org/10.4197/med.24-1.5.
Full textAbstract:
Since the introduction of therapeutic plasma exchange for the management of thrombotic thrombocytopenic purpura, the prognosis of this disease improved signifi cantly. Some patients suffer from refractory disease and adjunctive therapy needs to be considered. In addition, alternative explanations for thrombocytopenia may bepresent. In this report we discuss a patient who presented with typical fi ndings of thrombotic thrombocytopenic purpura and responded initially to therapeutic plasma exchange and steroids. Shortlyafterwards, his platelet count deteriorated and he was found to have acute pulmonary embolism. Prior to the pulmonary embolism, the patient had received venous thromboembolism prophylaxis in the form of low molecular weight heparin and had a history of previous exposure to unfractionated heparin. Testing for heparin-induced thrombocytopenia antibodies was positive and the patient was started on an alternative anticoagulant. Despite these early interventions the patient did not survive. It is essential that physicians be aware of such possible associations to request appropriate investigations and start appropriate management, accordingly.
26
Albagshi, MuneerHassan, AbbasM Al Omran, and HebaA Elhakeem. "Congenital thrombotic thrombocytopenic purpura simulating alloimmune thrombocytopenia." Journal of Clinical Neonatology 11, no. 4 (2022): 224. http://dx.doi.org/10.4103/jcn.jcn_63_22.
Full text
27
Generali, Joyce A., and Dennis J. Cada. "Rituximab: Primary Immune Thrombocytopenia (Idiopathic Thrombocytopenic Purpura)." Hospital Pharmacy 46, no. 4 (April 2011): 251–53. http://dx.doi.org/10.1310/hpj4604-251.
Full text
28
Zimmer, Jacques, François Hentges, and Emmanuel Andres. "Borderline Thrombocytopenia or Mild Idiopathic Thrombocytopenic Purpura?" PLoS Medicine 3, no. 8 (August 29, 2006): e362. http://dx.doi.org/10.1371/journal.pmed.0030362.
Full text
29
Schwartz, Kenneth A. "GESTATIONAL THROMBOCYTOPENIA AND IMMUNE THROMBOCYTOPENIAS IN PREGNANCY." Hematology/Oncology Clinics of North America 14, no. 5 (October 2000): 1101–16. http://dx.doi.org/10.1016/s0889-8588(05)70173-8.
Full text
30
Eissa, Adil Abozaid. "COVID-19 Disease and Associated Thrombocytopenia: Pathogenesis and a Clue to the Etiology." Diagnostics 12, no. 5 (April 20, 2022): 1038. http://dx.doi.org/10.3390/diagnostics12051038.
Full textAbstract:
(1) Background: Hospital mortality in patients suffering from SARS-CoV-2 infection has been associated with thrombocytopenia. The present study was conducted to establish the correlation of thrombocytopenia and the severity of infection. The impact of IL-1Ra gene polymorphism on the incidence and severity of thrombocytopenia was also studied. (2) Methods: Various biochemical parameters measured in all the 1200 enrolled patients included full blood counts, renal and liver function tests, iron study, inflammatory markers, and coagulation assays. A further 70 patients each were selected from the severe thrombocytopenic and non-thrombocytopenic patient groups to study the IL-1Ra gene polymorphism by RCR. (3) Results: Out of 1200 patients, 436 (36.3%) had thrombocytopenia. Among these patients, 118 (27.1%), 75 (17.2%), and 42 (9.6%) had mild, moderate, severe, and very severe thrombocytopenia, respectively. Severe cases mostly resulted from peripheral consumption (73.5%), hemo-phagocytosis (15.4%), and bone marrow suppression (11.11%). A statistically significant correlation was found between the occurrence and severity of thrombocytopenia with perturbated levels of inflammatory markers and the presence of comorbidities. The IL-1Ra∗3 variant was found to be significantly associated with thrombocytopenia. The IL-1Ra∗2 variant was significantly seen among controls. (4) Conclusions: The present study revealed a significant correlation between thrombocytopenia and the severity of COVID-19 disease. Moreover, the IL-1Ra∗3 variant of IL-1Ra gene was associated with thrombocytopenia.
31
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.
Full textAbstract:
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.
32
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.
Full textAbstract:
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.
33
Marques, Marisa B. "Thrombotic Thrombocytopenic Purpura and Heparin-Induced Thrombocytopenia: Two Unique Causes of Life-Threatening Thrombocytopenia." Clinics in Laboratory Medicine 29, no. 2 (June 2009): 321–38. http://dx.doi.org/10.1016/j.cll.2009.03.003.
Full text
34
Maskey, R., R. Sharma, B. Sharma, S. Upadhaya, and SS Dhakal. "Thyroid disease in patients with idiopathic thrombocytopenic purpura." Health Renaissance 10, no. 3 (November 13, 2012): 254–55. http://dx.doi.org/10.3126/hren.v10i3.7058.
Full textAbstract:
Idiopathic thrombocytopenia (ITP) is an autoimmune disorder characterized by a reduced platelet count with otherwise normal blood cell counts. Autoimmune thyroid disease is not considered a cause of thrombocytopenia. We report a case of autoimmune thrombocytopenic purpura associated with hyperthyroidism in which the patient's thrombocytopenia and thyrotoxicosis resolved concomitantly. We recommend testing for hyperthyroidism in all patients with unexplained thrombocytopenia and that family members of patients be evaluated, screened, and observed for thrombocytopenia and hyperthyroidism. Health Renaissance; September-December 2012; Vol 10 (No.3);254-255DOI: http://dx.doi.org/10.3126/hren.v10i3.7058
35
Sah, Vijay Kumar, Arun Giri, Milan KC, and Niraj Niraula. "Association of Thrombocytopenia and Mortality in Critically ill Children Admitted to PICU in Tertiary Hospital In Biratnagar." Birat Journal of Health Sciences 4, no. 1 (May 3, 2019): 649–53. http://dx.doi.org/10.3126/bjhs.v4i1.23940.
Full textAbstract:
Introduction: Thrombocytopenia is a clinical condition characterized by decrease in number of platelets below the normal range. It is associated with bleeding tendency, hemodynamic instability, impaired inflammatory process and thus affecting host defence mechanism. There has been only few studies published till date in pediatric intensive care units suggesting thrombocytopenia is associated with increased mortality.
Objectives: To determine the prevalence of thrombocytopenia in the critically ill children and its relationship with mortality in Pediatric intensive care unit (PICU) admitted children.
Methodology: A prospective observational study was performed over a period of 12 months on 102 critically ill children admitted in PICU who fulfilled the criteria. Two patients left the study due to financial problems and as outcome could not be assessed on them, they were excluded from the study. Platelet count was noted at the time of admission and consecutively for the initial four days at PICU. Thrombocytopenia was defined as platelet count less than 150/nL. Mortality in PICU was recorded as primary outcome.
Results: The prevalence of thrombocytopenia during consecutive 4 days was 34% (n=34) and at the time of admission in PICU was 16% (n=16) among 100 children analysed in the study. The mortality in the PICU was 27% (n=27). Mortality among thrombocytopenic children was 61.7% (n=21) as compared to 7.6% (n=5) in non-thrombocytopenic children (p=<0.001). Mortality was 18 times more for those who were thrombocytopenic at the time of admission as compared to those who subsequently developed thrombocytopenia during course of stay in PICU.
Conclusion: Thrombocytopenia has significant association with increased mortality. Thrombocytopenic children at the time of admission have more likelihood of mortality than nonthrombocytopenic children in intensive care units.
36
Singh, Shivraj, Avyact Agrawal, Uthara Mohan, and Sukarn Awasthi. "Prevalence of thrombocytopenia in neonates admitted in NICU with culture proven sepsis." International Journal of Contemporary Pediatrics 5, no. 3 (April 20, 2018): 743. http://dx.doi.org/10.18203/2349-3291.ijcp20181461.
Full textAbstract:
Background: Thrombocytopenia is a common haematological problem encountered during neonatal period, particularly in the sick, premature neonates admitted in the NICU, and usually indicate an underlying disease process. Thrombocytopenia may be considered as an important and early tool in diagnosis of septicaemia in neonates.Methods: It is a hospital based cross sectional study. A total 105 neonates with blood and/CSF culture positive sepsis and associated thrombocytopenia admitted in NICU. This study was conducted to find the prevalence of thrombocytopenia in neonates admitted in NICU with culture proven sepsis and to observe the outcome of thrombocytopenia and sepsis.Results: Out of 105 culture positive neonates K. pneumoniae 47/105 (44.8%) was the commonest micro-organism isolated, followed by Pseudomonas 26/105 (24.8%), E. coli 14/105 (13.3%), Staphylococcus 11/105 (10.5%), Candida 2/105 (1.9%) in decreasing order. Thrombocytopenia was present in 100/105 (95.2%). Among thrombocytopenic neonates 38/100 (38%), 36/100 (36%) and 26/100 (26%) having severe, moderate and mild thrombocytopenia respectively. 38 (38%) newborns of severe thrombocytopenia among them K. pneumoniae (50.0%) was commonest organism, followed by Pseudomonas. (23.7%) and Staphylococcus (15.8%) in the decreasing order. 36 (36%) newborns of moderate thrombocytopenia among them K. pneumoniae (47.2%) again commonest organism associated, followed by Pseudomonas. (25.0%), and E- coli (11.1%). In severe thrombocytopenic newborns both GI and pulmonary (60.50%) haemorrhage was the most common bleeding manifestation. Mortality rate (37.1%) was high in newborns having sepsis.Conclusions: Bacterial sepsis is significantly complicated by thrombocytopenia. Severe thrombocytopenia in a suspected case of bacterial sepsis might predict Klebsiella sepsis and hence it may be rational to start empirical antibiotics covering the same.
37
Siddiqui, Sadia Niaz, Mushtaq Ali Memon, Ghulam Hussain Baloch, Hamid Nawaz Ali Memon, Suneel Arwani, and Syed Zulfiquar Ali Shah. "LIVER CIRRHOSIS." Professional Medical Journal 22, no. 04 (April 10, 2015): 426–31. http://dx.doi.org/10.29309/tpmj/2015.22.04.1319.
Full textAbstract:
Objectives: To determine the frequency and severity of thrombocytopenia inpatients with liver cirrhosis. Study Deisgn: Cross sectional study. Period: 01-03-2013 to 31-08-2013. Setting: Liaquat University Hospital, Hyderabad. Methods: The cirrhotic patients wereassessed for thrombocytopenia and its severity. The data was analyzed in SPSS version 11.00and frequency and percentage was computed. The chi-square test was applied and p -value≤0.05 was considered as statistically significant. Results: Total one hundred patients wereevaluated for thrombocytopenia, 70% males and 30% females. The mean ± SD for age incirrhotic subjects was 41.16±14.24 whereas the mean ±SD for age in male and female cirrhoticpatients was 42.81±10.96 and 40.63±9.85. The thrombocytopenia was detected in 68%, ofwhich 43(63.2%) were males and 25(36.8%) were females. Mean±SD for platelet in all subjectswas 130.85±8.33 whereas it was 68.82±6.52 in thrombocytopenic cirrhotic patients. Mean±SDplatelet count in male and female thrombocytopenic patients was 70.94±7.42 and 64.72±5.84.Out of sixty eight thrombocytopenic cirrhotic subjects 23 had mild thrombocytopenia, 25had moderate thrombocytopenia and 20 had severe thrombocytopenia while in relation toChild-Pugh class B (p<0.01) predominant. Regarding the duration of the liver cirrhosis, thethrombocytopenia was predominant in patients between 6-12 months. The common presentingfeature observed in relation to gender were malaise 21%, fatigue 17, nausea / vomiting 14%and combine feature in 21 cirrhotic patients (p=0.04). Conclusions: The thrombocytopeniawas detected in patients with liver cirrhosis, therefore frequent platelet assessment is one of themost important step to monitor platelet count and reduce severe and life threatening episodesof bleeding.
38
De Jesus Henriques, Leidy, Katherine Rosales Pereira, Diana De Oliveira-Gomes, Rocío Iglesias Fortes, and Erick Dávila Alcalá. "Púrpura trombocitopénica trombótica versus síndrome HELLP: reto diagnóstico en el embarazo." Revista de Obstetricia y Ginecología de Venezuela 81, no. 03 (September 25, 2021): 292–96. http://dx.doi.org/10.51288/00810313.
Full textAbstract:
Worldwide, thrombocytopenia is one of the first causes of hematological alterations in pregnancy, affecting up to 10% of them. Despite the fact that all clinical entities with thrombocytopenia in pregnancy have a similar clinical spectrum, the distinction between them is vital to establish the appropriate treatment and thus reduce maternal-fetal morbidity and mortality. Purpura thrombotic thrombocytopenic is an infrequent disease, which despite not being linked to pregnancy, is not exempt from occurring in it, compared to HELLP syndrome, which is a multisystemic complication that occurs during pregnancy. The following is the case of a pregnant woman with microangiopathic thrombocytopenic anemia where the clinical similarity of both pathologies is evidenced, representing a diagnostic challenge. Keywords: Thrombocytopenia, Pregnancy, HELLP Syndrome, Purpura thrombotic thrombocytopenic, Anemia.
39
Kobayashi, Takayuki, Ayako Shigeta, Jiro Terada, Nobuhiro Tanabe, Toshihiko Sugiura, Seiichiro Sakao, Kohei Taniguchi, Takahiro Oto, and Koichiro Tatsumi. "Severe thrombocytopenia in patients with idiopathic pulmonary arterial hypertension provided several strategies for lung transplantation." Pulmonary Circulation 10, no. 4 (October 2020): 204589402096910. http://dx.doi.org/10.1177/2045894020969103.
Full textAbstract:
While the prognosis of idiopathic pulmonary arterial hypertension has improved significantly due to newer medications, lung transplantation remains a critical therapeutic option for severe pulmonary arterial hypertension. Hence, it is essential for patients awaiting lung transplantation to avoid complications, including thrombocytopenia, which may affect their surgical outcomes. Herein we present the case of a 21-year-old woman diagnosed with idiopathic pulmonary arterial hypertension at the age of 15. She developed thrombocytopenia while awaiting lung transplantation. Her medication was switched from epoprostenol to treprostinil, suspecting possible drug-induced thrombocytopenia. Furthermore, she was administered thrombopoietin receptor agonists in view of the possibility of idiopathic thrombocytopenic purpura, along with maximum support for right heart failure. Subsequently, her platelet count increased to >70,000/µL, enabling her to successfully undergo bilateral lung transplantation. Post-bilateral lung transplantation, pulmonary arterial hypertension as well as thrombocytopenia appeared to have resolved. In this case, we suspected that thrombocytopenia could have resulted owing to a combination of pulmonary arterial hypertension, right heart failure, drug interactions, and idiopathic thrombocytopenic purpura. Thrombocytopenia is a very critical condition in patients with pulmonary arterial hypertension, especially those awaiting lung transplantation. Several approaches are known to improve intractable thrombocytopenia in patients with pulmonary arterial hypertension.
40
Kam, Teresa, and Maurice Alexander. "Drug-Induced Immune Thrombocytopenia." Journal of Pharmacy Practice 27, no. 5 (August 17, 2014): 430–39. http://dx.doi.org/10.1177/0897190014546099.
Full textAbstract:
Thrombocytopenia is commonly seen in laboratory findings, especially in critically ill patients. Although the incidence is rare, drug-induced immune thrombocytopenia (DITP) is a serious complication that is often overlooked as a cause of thrombocytopenia. Over the last century, extensive research and data collection have been done in an attempt to better characterize DITP. Heparin-induced thrombocytopenia is the most common DITP and has distinct pathogenesis, diagnosis, and treatment options. However, other offending medications are less well known and have triggered many questions and constant search for answers. This review will discuss both drug-induced immune-mediated and nonimmune-mediated thrombocytopenias, with a focus on immune-mediated processes. Thrombocytopenia caused by chemotherapy will not be discussed in this article.
41
Yan, Matthew, Ann K. Malinowski, and Nadine Shehata. "Thrombocytopenic syndromes in pregnancy." Obstetric Medicine 9, no. 1 (September 21, 2015): 15–20. http://dx.doi.org/10.1177/1753495x15601937.
Full textAbstract:
The physiological changes in pregnancy result in platelet counts that are lower than in nonpregnant women. Consequently, thrombocytopenia is a common finding occurring in 7–12% of pregnant women. Gestational thrombocytopenia, the most common cause of low platelet counts, tends to be mild in most women and does not affect maternal, fetal or neonatal outcomes. Gestational thrombocytopenia needs to be distinguished from other less common causes of isolated thrombocytopenia, such as immune thrombocytopenia, which affects approximately 3% of thrombocytopenic pregnant women and can lead to neonatal thrombocytopenia. Hypertensive disorders of pregnancy and thrombotic microangiopathies are both associated with thrombocytopenia. They share a considerable number of similar characteristics and are associated with significant maternal and neonatal morbidity and rarely mortality. Accurate identification of the aetiology of thrombocytopenia and appropriate management are integral to optimizing the pregnancy, delivery and neonatal outcomes of this population. Clinical cases are described to illustrate the various aetiologies of thrombocytopenia in pregnancy and their treatment.
42
Gowri, Vaidyanathan, Miriam George fenn, Al Muhanad Al Abri, and Lubna Al Hashmi. "Prevalence of Thrombocytopenia and Platelet Dysfunction in Women Delivering at a Tertiary Care Hospital and Prevalence of Platelet Abnormalities in their Neonates with Perinatal Outcomes: A Retrospective Study." International Journal of Innovative Research in Medical Science 7, no. 11 (November 19, 2022): 634–40. http://dx.doi.org/10.23958/ijirms/vol07-i11/1548.
Full textAbstract:
Objective: To study the etiology and severity of platelet disorders, clinical manifestations, mode of delivery and neonatal outcome in pregnant women with thrombocytopenia and platelet dysfunction delivering in a tertiary care center in the Middle east. Methods: A retrospective cohort study was done on pregnant women admitted to Sultan Qaboos University Hospital (SQUH) from January 2011 to December 2020 with platelet abnormalities as per the registry were included. Thrombocytopenia associated with drugs, viral infection, pre-eclampsia, and HELLP syndrome were excluded. Results: Total number of deliveries were 39,522 during the study period. Of these 220 patients had thrombocytopenia and platelet abnormalities according to our inclusion criteria. The incidence of platelet abnormalities was 0.56% The mean gestational age at delivery was age 37.53 weeks. The mean platelet count was 90.41cells/dl. The highest two etiologies in this study were gestational thrombocytopenia (GT) (24.6%) and immune thrombocytopenic purpura (ITP) (22.6%). Out of 220, 9.5% were treated with prednisolone. There was a significant correlation between maternal platelet counts and medical treatment was received. No significant correlation between maternal platelet counts and mode of delivery was obtained. Nine neonates had platelet abnormalities, of which 44.4% were born to mothers with immune thrombocytopenic purpura (ITP). Mild to moderate neonatal thrombocytopenia was present in 66.6% of the neonates. 33.3% of the thrombocytopenic neonates had experienced hemorrhagic manifestations with good clinical outcome. Conclusion: The incidence of platelet abnormalities was 0.56% according to our study. ITP was more associated with severe thrombocytopenia and premature delivery.
43
Guerra, João Carlos de Campos, Ruth Hissae Kanayama, Sonia Tsukasa Nozawa, Márcia Regina Ioshida, Irina Yoko Takiri, Robson José Lazaro, Nelson Hamerschlak, Luiz Gastão Mange Rosenfeld, Celso Carlos de Campos Guerra, and Nydia Strachman Bacal. "Thrombocytopenia: diagnosis with flow cytometry and antiplatelet antibodies." Einstein (São Paulo) 9, no. 2 (June 2011): 130–34. http://dx.doi.org/10.1590/s1679-45082011ao1846.
Full textAbstract:
Objective: To identify antiplatelet antibodies by flow cytometry (direct method) in patients with thrombocytopenia. Methods: Between January 1997 and March 2004 a total of 15100 patients were referred to the Centro de Hematologia de São Paulo for hematological investigation of several diagnoses (anemia, leukopenia, thrombocytopenia, coagulation abnormalities, adenomegaly, leukemia and others). Of those, 1057 were referred because of thrombocytopenia and were divided into two groups: Group Idiopathic thrombocytopenic purpura, with no identifiable cause; and Group Other thrombocytopenia, which included low normal platelet counts cause to be established, hepatitis C and HIV infection, hypersplenism, EDTA-induced artifacts, laboratory error, and other causes. Flow cytometry immunophenotyping was done in 115 cases to identify platelet autoantibodies (direct method). Results: Of the total number of patients, 1057 (7%) presented low platelet counts, 670 were females (63.4%) and age range of one to 75 years. Of the 115 cases (9.7%) submitted to immunophenotyping, the results were positive in 40% and the test was inconclusive in 5%. Idiopathic thrombocytopenic purpura was found in 52% of patients, more often in women. Hepatitis C virus infection was found in 7% and HIV infection in 1%. Low normal platelet counts were found in 17%, laboratory errors in 6%, and laboratory artifacts in 1% of cases. Platelet autoantibodies were found in 76.9% of all idiopathic thrombocytopenic purpura cases. It was negative in 83.3% of the low normal counts. Conclusion: antiplatelet autoantibodies when present help to diagnose idiopathic thrombocytopenic purpura. When absent, suggest other causes of thrombocytopenia.
44
Musson, E. Nuttall, O. Lomas, and MF Murphy. "Acute thrombocytopenia: picking a way through a paucity of platelets." British Journal of Hospital Medicine 80, no. 9 (September 2, 2019): 507–12. http://dx.doi.org/10.12968/hmed.2019.80.9.507.
Full textAbstract:
Thrombocytopenia is defined as a platelet count under 150x109/litre. It may be found as a bystander to other pathology or directly related to an underlying haematological condition. Apart from laboratory artefact, it should be treated seriously as it often reflects serious underlying disease. This review uses short case histories to illustrate how to approach thrombocytopenia during the initial presentation of an adult patient to hospital. This article guides the general hospital physician through the narrow but potentially confusing differential diagnoses related to thrombocytopenia, with particular focus on immune thrombocytopenia, disseminated intravascular coagulation and thrombotic thrombocytopenic purpura. Thrombocytopenia in pregnancy deserves special consideration and will not be discussed in this article.
45
Aponte Barrios, Nelson Hernando, Adriana Linares Ballesteros, Isabel Cristina Sarmiento Urbina, and Gloria Inés Uribe Botero. "Evaluation of the diagnostic performance of platelet-derived indices for the differential diagnosis of thrombocytopenia in pediatrics." Revista de la Facultad de Medicina 62, no. 4 (May 7, 2015): 547–52. http://dx.doi.org/10.15446/revfacmed.v62n4.43754.
Full textAbstract:
<p>Background. Platelet-derived indices have a well-established correlation with the differential diagnosis of thrombocytopenia in adult-based research. These indices include mean platelet volume, platelet distribution width, and platelet-large cell ratio.</p><p>Objective. To determine the values of platelet-derived indices in a pediatric population with diagnoses of thrombocytopenia and their etiologic correlation.</p><p>Materials and methods. Analytic observational diagnostictest study. The population for this analytical study was pediatric patients between 6 months and 18 years of age who had thrombocytopenia (<100x109/L). The study period was 18 months long.</p><p>Results. Of 54 subjects, 18 (33.3%) were diagnosed with idiopathic thrombocytopenic purpura, and 36 (66.7%) were diagnosed with acute leukemia. Mean age was 7.4 years and 6.8 years for immune thrombocytopenic purpura and acute leukemia, respectively. Mean platelet distribution width values for immune thrombocytopenic purpura and acute leukemia were 15.08 fL and 10.73, respectively. Mean MPV for immune thrombocytopenic purpura and acute leukemia was 11.7 fL and 9.8 fL, respectively. Mean platelet-large cell ratio was 38.26% and 24.97% for idiopathic thrombocytopenic purpura and acute leukemia, respectively. Differences in these three distinct platelet indices between idiopathic thrombocytopenic purpura and acute leukemia were statistically significant (p=0.00). The area under the ROC curve for platelet-derived indices showed that they were adequate for defining the causes of thrombocytopenia. MPV and platelet-large cell ratio had an area under the curve of 0.89 and 0.88, respectively, while platelet size deviation width had an area under the curve of 0.903.</p><p>Conclusions. Platelet-derived indices could be useful in the initial approach for the differential diagnosis of pediatric patients with thrombocytopenia.</p>
46
First, LR, BR Smith, J. Lipton, DG Nathan, R. Parkman, and JM Rappeport. "Isolated thrombocytopenia after allogeneic bone marrow transplantation: existence of transient and chronic thrombocytopenic syndromes." Blood 65, no. 2 (February 1, 1985): 368–74. http://dx.doi.org/10.1182/blood.v65.2.368.368.
Full textAbstract:
Abstract Isolated thrombocytopenia after bone marrow transplantation was investigated in 65 fully engrafted patients surviving at least 60 days posttransplant. Twenty-four patients (37%) developed this complication, which occurred most frequently in patients receiving pretransplant preparation with total body irradiation or busulfan. Two distinct thrombocytopenic syndromes were identified: (1) transient thrombocytopenia (nine patients), in which a normal platelet count (greater than 100,000/microL) was initially established by day +40 but then diminished to less than 10,000 to 45,000/microL on day +40 to +70, with subsequent resolution of the thrombocytopenia by day +90; (2) chronic thrombocytopenia (15 patients), in which a platelet count greater than 100,000/microL was not achieved at any time during the first four months posttransplant, despite the simultaneous presence of normal granulocyte and reticulocyte counts. Although the transient syndrome did not adversely affect prognosis, the chronic syndrome carried a high mortality (21% actuarial survival at 1,000 days posttransplant compared with 67% survival for all patients, P less than .01) and had a high association with both severe (grades 3 to 4) acute graft-versus-host disease (GVHD) and chronic GVHD. In three of nine patients with transient thrombocytopenia, a temporal association with trimethoprim-sulfamethoxazole administration was observed, whereas in all other patients, no drug association could be found. Bone marrow biopsies in those patients with drug-associated thrombocytopenia showed decreased numbers of megakaryocytes, whereas biopsies in the remainder of the transiently thrombocytopenic patients demonstrated adequate numbers of platelet precursors, suggesting peripheral platelet destruction or ineffective thrombopoiesis. Biopsies in the chronic thrombocytopenic patients included those with and without adequate numbers of platelet precursors, although the association with chronic GVHD was strongest in patients demonstrating normal numbers of megakaryocytes. We conclude that isolated thrombocytopenia represents a significant complication of bone marrow transplantation, particularly in patients receiving hematopoietic ablative preparatory regimens, and that it is the chronic, not the transient, thrombocytopenic syndrome that is associated with an adverse patient prognosis.
47
First, LR, BR Smith, J. Lipton, DG Nathan, R. Parkman, and JM Rappeport. "Isolated thrombocytopenia after allogeneic bone marrow transplantation: existence of transient and chronic thrombocytopenic syndromes." Blood 65, no. 2 (February 1, 1985): 368–74. http://dx.doi.org/10.1182/blood.v65.2.368.bloodjournal652368.
Full textAbstract:
Isolated thrombocytopenia after bone marrow transplantation was investigated in 65 fully engrafted patients surviving at least 60 days posttransplant. Twenty-four patients (37%) developed this complication, which occurred most frequently in patients receiving pretransplant preparation with total body irradiation or busulfan. Two distinct thrombocytopenic syndromes were identified: (1) transient thrombocytopenia (nine patients), in which a normal platelet count (greater than 100,000/microL) was initially established by day +40 but then diminished to less than 10,000 to 45,000/microL on day +40 to +70, with subsequent resolution of the thrombocytopenia by day +90; (2) chronic thrombocytopenia (15 patients), in which a platelet count greater than 100,000/microL was not achieved at any time during the first four months posttransplant, despite the simultaneous presence of normal granulocyte and reticulocyte counts. Although the transient syndrome did not adversely affect prognosis, the chronic syndrome carried a high mortality (21% actuarial survival at 1,000 days posttransplant compared with 67% survival for all patients, P less than .01) and had a high association with both severe (grades 3 to 4) acute graft-versus-host disease (GVHD) and chronic GVHD. In three of nine patients with transient thrombocytopenia, a temporal association with trimethoprim-sulfamethoxazole administration was observed, whereas in all other patients, no drug association could be found. Bone marrow biopsies in those patients with drug-associated thrombocytopenia showed decreased numbers of megakaryocytes, whereas biopsies in the remainder of the transiently thrombocytopenic patients demonstrated adequate numbers of platelet precursors, suggesting peripheral platelet destruction or ineffective thrombopoiesis. Biopsies in the chronic thrombocytopenic patients included those with and without adequate numbers of platelet precursors, although the association with chronic GVHD was strongest in patients demonstrating normal numbers of megakaryocytes. We conclude that isolated thrombocytopenia represents a significant complication of bone marrow transplantation, particularly in patients receiving hematopoietic ablative preparatory regimens, and that it is the chronic, not the transient, thrombocytopenic syndrome that is associated with an adverse patient prognosis.
48
Mazurov, A. V., S. G. Khaspekova, and S. A. Vasiliev. "Diagnostics of thrombocytopenias." Terapevticheskii arkhiv 90, no. 7 (July 15, 2018): 4–13. http://dx.doi.org/10.26442/terarkh20189074-13.
Full textAbstract:
Laboratory methods used for the diagnostics of thrombocytopenias are reviewed. Differential diagnosis is usually carried out between immune and hypoproductive forms of thrombocytopenia. Immune thrombocytopenias are caused by appearance in blood of antiplatelet abtibodies and accelerated destruction of platelets sensibilized by those antibodies, and hypoproductive thrombocytopenias - by impaired platelet production in the bone marrow. Main directions of the laboratory diagnostics of thrombocytopenias - analysis of auto - and alloautoantibodies and evaluation of platelet production and turnover in the blood stream. The following methods are used for the investigation of antiplatelet antibodies: 1) measurement of platelet associated immunoglobulins; 2) determination of circulating antibodies reacting with platelets; 3) determination of antibodies using antigen specific methods - by their reactivity with isolated platelet antigens (glycoproteins). Efficacy of platelet production could be assessed by measuring in blood the amount of “young” (reticulated) platelets. One more method for the evaluation of platelet production as well as the rate of platelet turnover - measurement of plasma soluble glycocalicin, glycoprotein Ib fragment shed from the surface of platelets upon their destruction in spleen and liver. In patients with immune thrombocytopenia autoantibodies are evaluated in all cases, the percentage of reticulated platelets is significantly increased and the amount of plasma glycocalicin is within the normal range or increased. In patients with hypoproductive thrombocytopenia autoantibodies are not detected or detected at low level, the percentage of reticulated platelets is within the normal range or slightly increased and the amount of plasma glycocalicin is lowered. Diagnostics of hapten forms of immune thromocytopenias (heparin-induced thrombocytopenia and others) and of alloimmune thrombocytopenias (neonatal alloimmune thrombocytopenia in particular) are considered in the separate sections of this review.
49
Corash, L., HY Chen, J. Levin, G. Baker, H. Lu, and Y. Mok. "Regulation of thrombopoiesis: effects of the degree of thrombocytopenia on megakaryocyte ploidy and platelet volume." Blood 70, no. 1 (July 1, 1987): 177–85. http://dx.doi.org/10.1182/blood.v70.1.177.177.
Full textAbstract:
Abstract We have established a murine model and techniques with which to serially study thrombocytopoiesis after induction of experimental immune thrombocytopenia of variable severity and duration. Bone marrow megakaryocyte ploidy distribution was determined by using unfractionated bone marrow, a polyclonal megakaryocyte-specific probe, and two-color, fluorescence-activated flow cytometry. With these techniques, the modal megakaryocyte ploidy class in normal murine bone marrow was 16N. Serial studies of bone marrow megakaryocyte ploidy after the induction of acute, severe thrombocytopenia (platelet count, less than 0.05 X 10(6) microL) demonstrated no detectable change in the ploidy distribution at 12, 24, and 36 hours after the onset of thrombocytopenia. At 48 hours, the modal ploidy class shifted from 16N to 32N, and the 64N class increased significantly (P less than .001). The ploidy distribution returned to normal 120 hours after the onset of thrombocytopenia. A lesser degree of thrombocytopenia (platelet count reduction to 0.100 to 0.200 X 10(6)/microL) delayed the modal ploidy class shift from 16N to 32N until 72 hours after the onset of thrombocytopenia. Chronic, severe thrombocytopenia (platelet count, less than 0.05 X 10(6)/microL for seven days) resulted in a modal ploidy class shift from 16N to 32N during the thrombocytopenic phase and an enhanced increase in the 64N megakaryocyte class during the recovery phase. Mean platelet volume (MPV) was simultaneously measured on isolated total platelet populations after induction of thrombocytopenia. MPV was significantly increased (P less than .001) as early as eight hours after the onset of acute, severe thrombocytopenia, 40 hours before a shift in the ploidy distribution. Mild thrombocytopenia (platelet count reduction to 0.400 X 10(6)/microL) was not associated with a ploidy shift but did result in a significantly increased MPV (P less than .001). These studies demonstrate that the temporal relationship and magnitude of the effects of thrombocytopenia upon megakaryocyte ploidy distribution are dependent upon the degree and the duration of the thrombocytopenic stimulus and that the effects of experimental thrombocytopenia on platelet volume and megakaryocyte ploidy are dissociated.
50
Corash, L., HY Chen, J. Levin, G. Baker, H. Lu, and Y. Mok. "Regulation of thrombopoiesis: effects of the degree of thrombocytopenia on megakaryocyte ploidy and platelet volume." Blood 70, no. 1 (July 1, 1987): 177–85. http://dx.doi.org/10.1182/blood.v70.1.177.bloodjournal701177.
Full textAbstract:
We have established a murine model and techniques with which to serially study thrombocytopoiesis after induction of experimental immune thrombocytopenia of variable severity and duration. Bone marrow megakaryocyte ploidy distribution was determined by using unfractionated bone marrow, a polyclonal megakaryocyte-specific probe, and two-color, fluorescence-activated flow cytometry. With these techniques, the modal megakaryocyte ploidy class in normal murine bone marrow was 16N. Serial studies of bone marrow megakaryocyte ploidy after the induction of acute, severe thrombocytopenia (platelet count, less than 0.05 X 10(6) microL) demonstrated no detectable change in the ploidy distribution at 12, 24, and 36 hours after the onset of thrombocytopenia. At 48 hours, the modal ploidy class shifted from 16N to 32N, and the 64N class increased significantly (P less than .001). The ploidy distribution returned to normal 120 hours after the onset of thrombocytopenia. A lesser degree of thrombocytopenia (platelet count reduction to 0.100 to 0.200 X 10(6)/microL) delayed the modal ploidy class shift from 16N to 32N until 72 hours after the onset of thrombocytopenia. Chronic, severe thrombocytopenia (platelet count, less than 0.05 X 10(6)/microL for seven days) resulted in a modal ploidy class shift from 16N to 32N during the thrombocytopenic phase and an enhanced increase in the 64N megakaryocyte class during the recovery phase. Mean platelet volume (MPV) was simultaneously measured on isolated total platelet populations after induction of thrombocytopenia. MPV was significantly increased (P less than .001) as early as eight hours after the onset of acute, severe thrombocytopenia, 40 hours before a shift in the ploidy distribution. Mild thrombocytopenia (platelet count reduction to 0.400 X 10(6)/microL) was not associated with a ploidy shift but did result in a significantly increased MPV (P less than .001). These studies demonstrate that the temporal relationship and magnitude of the effects of thrombocytopenia upon megakaryocyte ploidy distribution are dependent upon the degree and the duration of the thrombocytopenic stimulus and that the effects of experimental thrombocytopenia on platelet volume and megakaryocyte ploidy are dissociated.