Thrombocytopenia in patients with severe acute respiratory syndrome (review).
Identifieur interne : 001058 ( Ncbi/Merge ); précédent : 001057; suivant : 001059Thrombocytopenia in patients with severe acute respiratory syndrome (review).
Auteurs : Mo Yang [Hong Kong] ; Margaret H L. Ng ; Chi Kong LiSource :
- Hematology (Amsterdam, Netherlands) [ 1024-5332 ] ; 2005.
Descripteurs français
- KwdFr :
- Cellules souches hématopoïétiques (immunologie), Cellules souches hématopoïétiques (virologie), Humains, Lymphopénie (immunologie), Lymphopénie (virologie), Lymphopénie (étiologie), Numération des lymphocytes, Purpura thrombopénique idiopathique (immunologie), Purpura thrombopénique idiopathique (virologie), Purpura thrombopénique idiopathique (étiologie), Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS (immunologie).
- MESH :
- immunologie : Cellules souches hématopoïétiques, Lymphopénie, Purpura thrombopénique idiopathique, Syndrome respiratoire aigu sévère, Virus du SRAS.
- virologie : Cellules souches hématopoïétiques, Lymphopénie, Purpura thrombopénique idiopathique.
- étiologie : Lymphopénie, Purpura thrombopénique idiopathique.
- Humains, Numération des lymphocytes, Syndrome respiratoire aigu sévère.
English descriptors
- KwdEn :
- Hematopoietic Stem Cells (immunology), Hematopoietic Stem Cells (virology), Humans, Lymphocyte Count, Lymphopenia (etiology), Lymphopenia (immunology), Lymphopenia (virology), Purpura, Thrombocytopenic, Idiopathic (etiology), Purpura, Thrombocytopenic, Idiopathic (immunology), Purpura, Thrombocytopenic, Idiopathic (virology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (immunology).
- MESH :
- complications : Severe Acute Respiratory Syndrome.
- etiology : Lymphopenia, Purpura, Thrombocytopenic, Idiopathic.
- immunology : Hematopoietic Stem Cells, Lymphopenia, Purpura, Thrombocytopenic, Idiopathic, SARS Virus, Severe Acute Respiratory Syndrome.
- virology : Hematopoietic Stem Cells, Lymphopenia, Purpura, Thrombocytopenic, Idiopathic.
- Humans, Lymphocyte Count.
Abstract
Severe Acute Respiratory Syndrome (SARS) has been recognized as a new human infectious disease caused by a novel coronavirus (SARS-CoV). Hematological changes in patients with SARS were common, including notably lymphopenia and thrombocytopenia. While the former is the result of decreases in CD4+ or CD8+ T-lymphocytes related to the onset of disease or use of glucocorticoids, the latter may involve a number of potential mechanisms. Although the development of autoimmune antibodies or immune complexes triggered by viral infection may play a significant role in inducing thrombocytopenia, SARS-CoV may also directly infect hematopoietic stem/progenitor cells, megakaryocytes and platelets inducing their growth inhibition and apoptosis. Moreover, the increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions, which has been rarely revealed and will be discussed.
DOI: 10.1080/10245330400026170
PubMed: 16019455
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Hematological changes in patients with SARS were common, including notably lymphopenia and thrombocytopenia. While the former is the result of decreases in CD4+ or CD8+ T-lymphocytes related to the onset of disease or use of glucocorticoids, the latter may involve a number of potential mechanisms. Although the development of autoimmune antibodies or immune complexes triggered by viral infection may play a significant role in inducing thrombocytopenia, SARS-CoV may also directly infect hematopoietic stem/progenitor cells, megakaryocytes and platelets inducing their growth inhibition and apoptosis. Moreover, the increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions, which has been rarely revealed and will be discussed.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16019455</PMID><DateCompleted><Year>2005</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1024-5332</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><Issue>2</Issue><PubDate><Year>2005</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Hematology (Amsterdam, Netherlands)</Title><ISOAbbreviation>Hematology</ISOAbbreviation></Journal><ArticleTitle>Thrombocytopenia in patients with severe acute respiratory syndrome (review).</ArticleTitle><Pagination><MedlinePgn>101-5</MedlinePgn></Pagination><Abstract><AbstractText>Severe Acute Respiratory Syndrome (SARS) has been recognized as a new human infectious disease caused by a novel coronavirus (SARS-CoV). Hematological changes in patients with SARS were common, including notably lymphopenia and thrombocytopenia. While the former is the result of decreases in CD4+ or CD8+ T-lymphocytes related to the onset of disease or use of glucocorticoids, the latter may involve a number of potential mechanisms. Although the development of autoimmune antibodies or immune complexes triggered by viral infection may play a significant role in inducing thrombocytopenia, SARS-CoV may also directly infect hematopoietic stem/progenitor cells, megakaryocytes and platelets inducing their growth inhibition and apoptosis. 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Ng</name></noCountry><country name="Hong Kong"><noRegion><name sortKey="Yang, Mo" sort="Yang, Mo" uniqKey="Yang M" first="Mo" last="Yang">Mo Yang</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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