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Thrombocytopenia Causes

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1. Peripheral serotonin causes dengue-induced thrombocytopenia through 5HT<sub>2</sub> receptors. (PubMed)

Peripheral serotonin causes dengue-induced thrombocytopenia through 5HT2 receptors. Dengue virus (DENV) is the most prevalent vector-borne viral pathogen, infecting millions of patients annually. Thrombocytopenia, a reduction in circulating platelet counts, is the most consistent sign of DENV-induced disease, independent of disease severity. However, the mechanisms leading to DENV-induced thrombocytopenia are unknown. Here, we show that thrombocytopenia is caused by serotonin (...) , derived from mast cells (MCs), which are immune cells that are present in the perivascular space and a major peripheral source of serotonin. We show that during DENV infection, MCs release serotonin, which prompts platelet activation, aggregation and enhanced phagocytosis, dependent on 5HT2A receptors. MC-deficiency in mice or pharmacological inhibition of MCs reversed thrombocytopenia. Furthermore, reconstitution of MC-deficient mice with wild-type MCs, but not MCs lacking serotonin synthesis due

2019 Blood

2. TUBB1 dysfunction in inherited thrombocytopenia causes genome instability. (PubMed)

TUBB1 dysfunction in inherited thrombocytopenia causes genome instability. Inherited thrombocytopenia is a genetically heterogeneous disease characterized by varying degrees of thrombocytopenia and risk of haematological malignancy, and the genetic cause of many cases remains unknown. We performed whole-exome sequencing of a family with thrombocytopenia and myeloid malignancy and identified a novel TUBB1 variant, T149P. Screening of other thrombocytopenia pedigrees identified another TUBB1

2019 British journal of haematology

3. Immune thrombocytopenia

Immune thrombocytopenia Immune thrombocytopenia - Symptoms, diagnosis and treatment | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Immune thrombocytopenia Last reviewed: February 2019 Last updated: March 2019 Summary Immune thrombocytopenia (ITP), also known as immune thrombocytopenic purpura, is defined as an autoimmune haematological disorder characterised by isolated thrombocytopenia in the absence of an identifiable cause. Typically found (...) immune thrombocytopenia (ITP) is a haematological disorder characterised by isolated thrombocytopenia (platelet count <100 × 10⁹/L [<100 × 10³/microlitre]) in the absence of an identifiable cause. Rodeghiero F, Stasi R, Gernsheimer T, et al. Standardization of terminology, definitions and outcome criteria in immune thrombocytopenic purpura of adults and children: report from an international working group. Blood. 2009 Mar 12;113(11):2386-93. http://bloodjournal.hematologylibrary.org/cgi/content/full

2019 BMJ Best Practice

4. Lusutrombopag - to prevent excessive bleeding in adults with thrombocytopenia due to long-standing liver disease

EMEA/H/C/004720 Lusutrombopag Shionogi (lusutrombopag) An overview of Lusutrombopag Shionogi and why it is authorised in the EU What is Lusutrombopag Shionogi and what is it used for? Lusutrombopag Shionogi is a medicine used to prevent excessive bleeding in adults with thrombocytopenia due to long-standing liver disease. Patients with thrombocytopenia have reduced number of platelets (components in the blood that help it to clot), which can cause excessive bleeding. The medicine is for use (...) Lusutrombopag - to prevent excessive bleeding in adults with thrombocytopenia due to long-standing liver disease Official address Domenico Scarlattilaan 6 ? 1083 HS Amsterdam ? The Netherlands An agency of the European Union Address for visits and deliveries Refer to www.ema.europa.eu/how-to-find-us Send us a question Go to www.ema.europa.eu/contact Telephone +31 (0)88 781 6000 © European Medicines Agency, 2019. Reproduction is authorised provided the source is acknowledged. EMA/889817/2018

2019 European Medicines Agency - EPARs

5. Prenatal Management of Pregnancies at Risk of Fetal Neonatal Alloimmune Thrombocytopenia (FNAIT)

access Please review our and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Shareable Link Use the link below to share a full-text version of this article with your friends and colleagues. Copy URL Share a link - FNAIT is suspected in a neonate with thrombocytopenia for which there is no other medical cause identified. In mild to moderately affected neonates, FNAIT typically resolves in the first week of life without (...) Prenatal Management of Pregnancies at Risk of Fetal Neonatal Alloimmune Thrombocytopenia (FNAIT) Prenatal Management of Pregnancies at Risk of Fetal Neonatal Alloimmune Thrombocytopenia (FNAIT) - Regan - - BJOG: An International Journal of Obstetrics & Gynaecology - Wiley Online Library By continuing to browse this site, you agree to its use of cookies as described in our . Search within Search term Search term RCOG Scientific Impact Paper Free Access Prenatal Management of Pregnancies

2019 Royal College of Obstetricians and Gynaecologists

6. Assessment of thrombocytopenia

a reduced production of platelets in the bone marrow, increased clearance, or sequestering of platelets in the spleen. Epidemiology The causes of thrombocytopenia are diverse, making epidemiological generalisations difficult. However, immune thrombocytopenia (ITP) is typically an illness of young women. Provan D, Stasi R, Newland AC, et al. International consensus report on the investigation and management of primary immune thrombocytopenia. Blood. 2010;115:168-186. http (...) Assessment of thrombocytopenia Assessment of thrombocytopenia - Differential diagnosis of symptoms | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Assessment of thrombocytopenia Last reviewed: February 2019 Last updated: June 2018 Summary Thrombocytopenia is defined as a low circulating platelet count (<150,000 per microlitre). Platelet life span is normally approximately 5 days, with continual renewal. True thrombocytopenia results from either

2018 BMJ Best Practice

7. Heparin-induced thrombocytopenia

and medications that cause thrombocytopenia history of recent surgery or trauma features consistent with recent venous or arterial thromboembolic event (e.g., PE, DVT, stroke, MI) necrosis at heparin injection site(s) absence of bleeding signs of adrenal haemorrhagic necrosis acute systemic reaction signs of venous limb gangrene recent heparin exposure (within past 100 days) recent orthopaedic or cardiovascular surgery female sex Diagnostic investigations FBC Warkentin (4Ts) Probability Scale HIT antigen (...) Heparin-induced thrombocytopenia Heparin-induced thrombocytopenia - Symptoms, diagnosis and treatment | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Heparin-induced thrombocytopenia Last reviewed: February 2019 Last updated: May 2018 Summary A severe drug reaction to heparin that can lead to life- and limb-threatening venous and/or arterial thromboembolism. Diagnosis requires the combination of a compatible clinical picture and laboratory confirmation

2018 BMJ Best Practice

8. Use of platelet transfusions prior to lumbar punctures or epidural anaesthesia for the prevention of complications in people with thrombocytopenia. (PubMed)

Use of platelet transfusions prior to lumbar punctures or epidural anaesthesia for the prevention of complications in people with thrombocytopenia. People with a low platelet count (thrombocytopenia) often require lumbar punctures or an epidural anaesthetic. Lumbar punctures can be diagnostic (haematological malignancies, subarachnoid haematoma, meningitis) or therapeutic (spinal anaesthetic, administration of chemotherapy). Epidural catheters are placed for administration of epidural (...) anaesthetic. Current practice in many countries is to correct thrombocytopenia with platelet transfusions prior to lumbar punctures and epidural anaesthesia, in order to mitigate the risk of serious procedure-related bleeding. However, the platelet count threshold recommended prior to these procedures varies significantly from country to country. This indicates significant uncertainty among clinicians regarding the correct management of these patients. The risk of bleeding appears to be low

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2018 Cochrane

9. Sphingolipid dysregulation due to lack of functional KDSR impairs proplatelet formation causing thrombocytopenia. (PubMed)

Sphingolipid dysregulation due to lack of functional KDSR impairs proplatelet formation causing thrombocytopenia. Sphingolipids are fundamental to membrane trafficking, apoptosis and cell differentiation and proliferation. KDSR or 3-keto-dihydrosphingosine reductase is an essential enzyme for de novo sphingolipid synthesis, and pathogenic mutations in KDSR result in the severe skin disorder erythrokeratodermia variabilis et progressiva-4. Four of the eight reported cases also had (...) thrombocytopenia but the underlying mechanism has remained unexplored. Here we expand upon the phenotypic spectrum of KDSR deficiency with studies in two siblings with novel compound heterozygous variants associated with thrombocytopenia, anemia and minimal skin involvement. We report a novel phenotype of progressive juvenile myelofibrosis in the propositus, with spontaneous recovery of anemia and thrombocytopenia in the first decade of life. Examination of bone marrow biopsies showed megakaryocyte

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2018 Haematologica

10. Author Correction: Variants in exons 5 and 6 of ACTB cause syndromic thrombocytopenia (PubMed)

Author Correction: Variants in exons 5 and 6 of ACTB cause syndromic thrombocytopenia The original version of this Article contained an error in Figure 4. In panel i, the lower CYA and α-SMA images were inadvertently inverted. This has been corrected in both the PDF and HTML versions of the Article.

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2018 Nature communications

11. Variants in exons 5 and 6 of ACTB cause syndromic thrombocytopenia (PubMed)

Variants in exons 5 and 6 of ACTB cause syndromic thrombocytopenia Germline mutations in the ubiquitously expressed ACTB, which encodes β-cytoplasmic actin (CYA), are almost exclusively associated with Baraitser-Winter Cerebrofrontofacial syndrome (BWCFF). Here, we report six patients with previously undescribed heterozygous variants clustered in the 3'-coding region of ACTB. Patients present with clinical features distinct from BWCFF, including mild developmental disability, microcephaly (...) , and thrombocytopenia with platelet anisotropy. Using patient-derived fibroblasts, we demonstrate cohort specific changes to β-CYA filament populations, which include the enhanced recruitment of thrombocytopenia-associated actin binding proteins (ABPs). These perturbed interactions are supported by in silico modeling and are validated in disease-relevant thrombocytes. Co-examination of actin and microtubule cytoskeleton constituents in patient-derived megakaryocytes and thrombocytes indicates that these β-CYA

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2018 Nature communications

12. Ovarian teratoma: yet another cause of immune thrombocytopenia (PubMed)

Ovarian teratoma: yet another cause of immune thrombocytopenia A hematologic disorder occurred simultaneously with an ovarian cystic teratoma in a young woman. The blood disorder was a severe thrombocytopenia, with no spontaneous remission, or improvement after steroids tapering. To date, this is the second report in literature of immune thrombocytopenia associated with an ovarian teratoma, completely resolving following surgical excision of the ovarian teratoma. This case may suggest

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2018 International journal of women's health

13. A novel CYCS mutation in the α-helix of the CYCS C-terminal domain causes non-syndromic thrombocytopenia. (PubMed)

A novel CYCS mutation in the α-helix of the CYCS C-terminal domain causes non-syndromic thrombocytopenia. We report a patient with thrombocytopenia from a Japanese family with hemophilia A spanning four generations. Various etiologies of thrombocytopenia, including genetic, immunological, and hematopoietic abnormalities, determine the prognosis for this disease. In this study, we identified a novel heterozygous mutation in a gene encoding cytochrome c, somatic (CYCS, MIM123970) using whole (...) expression and functional defects in the mitochondrial respiratory chain, indicating that the loss of function of cytochrome c underlies thrombocytopenia. The clinical features of known CYCS variants have been reported to be confined to mild or asymptomatic thrombocytopenia, as was observed for the patient in our study. This study clearly demonstrates that thrombocytopenia can result from CYCS loss-of-function variants.© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

2018 Clinical Genetics

14. Successful use of ofatumumab in two cases of early-onset juvenile SLE with thrombocytopenia caused by a mutation in protein kinase C δ. (PubMed)

Successful use of ofatumumab in two cases of early-onset juvenile SLE with thrombocytopenia caused by a mutation in protein kinase C δ. We previously described an endogamous Pakistani kindred in whom we identified a novel homozygous missense mutation in the PRKCD gene encoding for protein kinase C δ (PKCδ) as a cause of monogenic systemic lupus erythematosus (SLE). PKCδ has a role in the negative regulation of B cells. Given the nature of the disease, a logical targeted therapeutic approach (...) in these patients is B cell depletion. Indeed, the 3 siblings all had a marked clinical response and resolution of symptoms with rituximab, although 2 of the siblings had severe reactions to rituximab thus precluding further treatment with this. We therefore describe the first successful use of ofatumumab for this rare form of monogenic SLE.All three affected siblings presented with SLE before the age of 3-years with lethargy, intermittent fever, thrombocytopenia, cutaneous involvement, alopecia

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2018 Pediatric Rheumatology

15. T-448, a specific inhibitor of LSD1 enzyme activity, improves learning function without causing thrombocytopenia in mice. (PubMed)

T-448, a specific inhibitor of LSD1 enzyme activity, improves learning function without causing thrombocytopenia in mice. Dysregulation of histone H3 lysine 4 (H3K4) methylation has been implicated in the pathogenesis of several neurodevelopmental disorders. Targeting lysine-specific demethylase 1 (LSD1), an H3K4 demethylase, is therefore a promising approach to treat these disorders. However, LSD1 forms complexes with cofactors including growth factor independent 1B (GFI1B), a critical (...) regulator of hematopoietic differentiation. Known tranylcypromine-based irreversible LSD1 inhibitors bind to coenzyme flavin adenine dinucleotide (FAD) and disrupt the LSD1-GFI1B complex, which is associated with hematotoxicity such as thrombocytopenia, representing a major hurdle in the development of LSD1 inhibitors as therapeutic agents. To discover LSD1 inhibitors with potent epigenetic modulation and lower risk of hematotoxicity, we screened small molecules that enhance H3K4 methylation

2018 Neuropsychopharmacology

16. A new form of inherited thrombocytopenia caused by loss-of-function mutations in <i>PTPRJ</i>. (PubMed)

A new form of inherited thrombocytopenia caused by loss-of-function mutations in PTPRJ. Inherited thrombocytopenias (ITs) are a heterogeneous group of disorders characterized by low platelet count that may result in bleeding tendency. Despite progress being made in defining the genetic causes of ITs, nearly 50% of patients with familial thrombocytopenia are affected with forms of unknown origin. Here, through exome sequencing of two siblings with autosomal recessive thrombocytopenia, we (...) PTPRJ) in zebrafish, which induced a significantly decreased number of CD41+ thrombocytes in vivo. Moreover, megakaryocytes of our patients showed impaired maturation and profound defects in SDF1-driven migration and formation of proplatelets in vitro. Silencing of PTPRJ in a human megakaryocytic cell line reproduced the functional defects observed in patients' megakaryocytes. The disorder caused by PTPRJ mutations presented as a non-syndromic thrombocytopenia characterized by spontaneous bleeding

2018 Blood

17. Thrombopoietin receptor agonists for prevention and treatment of chemotherapy-induced thrombocytopenia in patients with solid tumours. (PubMed)

Thrombopoietin receptor agonists for prevention and treatment of chemotherapy-induced thrombocytopenia in patients with solid tumours. Chemotherapy-induced thrombocytopenia (CIT) is defined as a peripheral platelet count less than 100×109/L, with or without bleeding in cancer patients receiving myelosuppressive chemotherapy. CIT is a significant medical problem during chemotherapy, and it carries the risk of sub-optimal overall survival and bleeding. Alternative interventions to platelet (...) transfusion are limited. Different stages of preclinical and clinical studies have examined the thrombopoietin receptor agonists (TPO-RAs) for CIT in patients with solid tumours.To assess the effects of TPO-RAs to prevent and treat CIT in patients with solid tumours:(1) to prevent CIT in patients without thrombocytopenia before chemotherapy, (2) to prevent recurrence of CIT, and (3) to treat CIT in patients with thrombocytopenia during chemotherapy.We searched the Cochrane Central Register of Controlled

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2017 Cochrane

18. An α<sub>II</sub><sub>b</sub> β<sub>3</sub> antagonist prevents thrombosis without causing FcγRIIa-mediated thrombocytopenia. (PubMed)

An αIIb β3 antagonist prevents thrombosis without causing FcγRIIa-mediated thrombocytopenia. Essentials FcγRIIa-mediated thrombocytopenia is associated with drug-dependent antibodies (DDAbs). We investigated the correlation between αIIb β3 binding epitopes and induction of DDAbs. An FcγRIIa-transgenic mouse model was used to evaluate thrombocytopenia among anti-thrombotics. An antithrombotic with binding motif toward αIIb β-propeller domain has less bleeding (...) caused a conformational change of αIIb β3 as identified with the ligand-induced binding site mAb AP5. In contrast to eptifibatide and TMV-2, cotreatment of TMV-7 with AP2 did not induce FcγRIIa-mediated platelet aggregation and the downstream activation cascade. Both TMV-2 and TMV-7 efficaciously prevented occlusive thrombosis in vivo. Notably, both eptifibatide and TMV-2 caused severe thrombocytopenia mediated by FcγRIIa, prolonged tail bleeding time in vivo, and repressed human whole blood

2017 Journal of Thrombosis and Haemostasis

19. A Cluster of Symptomatic and Asymptomatic Infections of Severe Fever with Thrombocytopenia Syndrome Caused by Person-to-Person Transmission. (PubMed)

A Cluster of Symptomatic and Asymptomatic Infections of Severe Fever with Thrombocytopenia Syndrome Caused by Person-to-Person Transmission. Severe fever with thrombocytopenia syndrome virus (SFTSV) is a novel phlebovirus that was identified to be the etiological pathogen of the emerging infectious disease, severe fever with thrombocytopenia syndrome (SFTS). SFTSV could be transmitted through tick bite. Transmission of SFTSV among humans has also been reported mainly through direct blood (...) contact. In July 2014, a cluster of six suspected SFTS cases occurred in Shandong Province, China. In this cluster, both symptomatic and asymptomatic persons were included. By analyzing the clinical data and results of laboratory tests, and conducting the epidemiological interviews with the cases and their families, risk factors responsible for the transmission were evaluated. The findings suggested that SFTSV transmission among humans may cause asymptomatic infection via personal contact without

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2017 American Journal of Tropical Medicine & Hygiene

20. Inherited thrombocytopenia caused by ANKRD26 mutations misdiagnosed and treated as myelodysplastic syndrome: report on two cases. (PubMed)

Inherited thrombocytopenia caused by ANKRD26 mutations misdiagnosed and treated as myelodysplastic syndrome: report on two cases. Essentials Thrombocytopenia 2 (THC2) is an inherited thrombocytopenia (IT) with dysmegakaryopoiesis. Physicians often do not suspect the genetic origin of thrombocytopenia in patients with THC2. We report two THC2 patients misdiagnosed with myelodysplasia and treated with chemotherapy. IT should be always considered in patients with isolated thrombocytopenia (...) and dysmegakaryopoiesis.Thrombocytopenia 2 (THC2) is an autosomal-dominant disorder caused by point substitutions in the 5'UTR of the ANKRD26 gene. Patients have congenital thrombocytopenia, normal platelet morphology and function, and dysmegakaryopoiesis. Thrombocytopenia is frequently discovered only in adulthood and physicians often do not suspect its genetic origin. We describe two unrelated patients referred to two different institutions for investigation of thrombocytopenia. Based on the finding of dysmegakaryopoiesis at bone

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2017 Journal of Thrombosis and Haemostasis

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