Hematological findings in SARS patients and possible mechanisms (review).
Identifieur interne : 005327 ( Main/Exploration ); précédent : 005326; suivant : 005328Hematological findings in SARS patients and possible mechanisms (review).
Auteurs : Mo Yang [Hong Kong] ; Chi Kong Li ; Karen Li ; K L E. Hon ; M H L. Ng ; Paul K S. Chan ; Tai Fai FokSource :
- International journal of molecular medicine [ 1107-3756 ] ; 2004.
Descripteurs français
- KwdFr :
- Antigènes CD (biosynthèse), Antigènes CD34 (biosynthèse), Antigènes de différenciation (biosynthèse), Autoanticorps (), Cellules de la moelle osseuse (métabolisme), Facteurs temps, Humains, Lymphocytes T CD4+ (virologie), Lymphocytes T CD8+ (virologie), Lymphomes (étiologie), Molécules d'adhérence cellulaire, Numération formule sanguine, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (physiopathologie), Syndrome respiratoire aigu sévère (sang), Thrombopénie (étiologie), Virus du SRAS (métabolisme).
- MESH :
- biosynthèse : Antigènes CD, Antigènes CD34, Antigènes de différenciation.
- métabolisme : Cellules de la moelle osseuse, Virus du SRAS.
- physiopathologie : Syndrome respiratoire aigu sévère.
- sang : Syndrome respiratoire aigu sévère.
- virologie : Lymphocytes T CD4+, Lymphocytes T CD8+.
- étiologie : Lymphomes, Thrombopénie.
- Autoanticorps, Facteurs temps, Humains, Molécules d'adhérence cellulaire, Numération formule sanguine, Syndrome respiratoire aigu sévère.
English descriptors
- KwdEn :
- Antigens, CD (biosynthesis), Antigens, CD34 (biosynthesis), Antigens, Differentiation (biosynthesis), Autoantibodies (chemistry), Blood Cell Count, Bone Marrow Cells (metabolism), CD13 Antigens (biosynthesis), CD4-Positive T-Lymphocytes (virology), CD8-Positive T-Lymphocytes (virology), Cell Adhesion Molecules, Humans, Lymphoma (etiology), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (blood), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (physiopathology), Thrombocytopenia (etiology), Time Factors.
- MESH :
- chemical , biosynthesis : Antigens, CD, Antigens, CD34, Antigens, Differentiation, CD13 Antigens.
- chemical , chemistry : Autoantibodies.
- blood : Severe Acute Respiratory Syndrome.
- complications : Severe Acute Respiratory Syndrome.
- etiology : Lymphoma, Thrombocytopenia.
- metabolism : Bone Marrow Cells, SARS Virus.
- physiopathology : Severe Acute Respiratory Syndrome.
- virology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes.
- Blood Cell Count, Cell Adhesion Molecules, Humans, Time Factors.
Abstract
Severe acute respiratory syndrome (SARS) is a new human infectious disease. The causative agent of SARS is a novel coronavirus (SARS-CoV). This report summarizes the hematological findings in SARS patients and proposes the possible mechanisms of SARS-CoV related abnormal hematopoiesis. Hematological changes in patients with SARS are common and include lymphopenia, thrombocytopenia and occasionally leukopenia. A significant decrease was also observed in peripheral CD4+ and CD8+ T lymphocyte subsets and it was related to onset of SARS. A number of potential mechanisms may be involved. The development of auto-immune antibodies or immune complexes triggered by viral infection may play a major role in inducing lymphopenia and thrombocytopenia. Moreover, SARS-CoV may also directly infect hematopoietic stem/progenitor cells via CD13 or CD66a inducing their growth inhibition and apoptosis. The receptor for group I and III CoV is aminopeptidase N (CD13). CD13 has been identified in human bone marrow CD34+ cells, platelets, megakaryocytes, myeloid cells, and erythroid cells, but not in lymphocytes. The common receptor for group II CoV is CEACAM1a (CD66a). CD66a is an adhesion molecule expressed on bone marrow CD34+ cells, platelets, granulocytes and activated lymphocytes. In addition, glucocorticoids could induce lymphopenia and the use of steroids may account for the decrease of lymphocytes in some SARS patients. The increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative but often overlooked mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions.
PubMed: 15254784
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 002C61
- to stream PubMed, to step Curation: 002C61
- to stream PubMed, to step Checkpoint: 002C83
- to stream Ncbi, to step Merge: 000951
- to stream Ncbi, to step Curation: 000951
- to stream Ncbi, to step Checkpoint: 000951
- to stream Main, to step Merge: 005743
- to stream Main, to step Curation: 005327
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Hematological findings in SARS patients and possible mechanisms (review).</title><author><name sortKey="Yang, Mo" sort="Yang, Mo" uniqKey="Yang M" first="Mo" last="Yang">Mo Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Paediatrics, The Chinese University of Hong Kong, Shatin, Hong Kong, P.R. China. yang1091@cuhk.edu.hk</nlm:affiliation><country wicri:rule="url">Hong Kong</country></affiliation></author><author><name sortKey="Li, Chi Kong" sort="Li, Chi Kong" uniqKey="Li C" first="Chi Kong" last="Li">Chi Kong Li</name></author><author><name sortKey="Li, Karen" sort="Li, Karen" uniqKey="Li K" first="Karen" last="Li">Karen Li</name></author><author><name sortKey="Hon, K L E" sort="Hon, K L E" uniqKey="Hon K" first="K L E" last="Hon">K L E. Hon</name></author><author><name sortKey="Ng, M H L" sort="Ng, M H L" uniqKey="Ng M" first="M H L" last="Ng">M H L. Ng</name></author><author><name sortKey="Chan, Paul K S" sort="Chan, Paul K S" uniqKey="Chan P" first="Paul K S" last="Chan">Paul K S. Chan</name></author><author><name sortKey="Fok, Tai Fai" sort="Fok, Tai Fai" uniqKey="Fok T" first="Tai Fai" last="Fok">Tai Fai Fok</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2004">2004</date><idno type="RBID">pubmed:15254784</idno><idno type="pmid">15254784</idno><idno type="wicri:Area/PubMed/Corpus">002C61</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002C61</idno><idno type="wicri:Area/PubMed/Curation">002C61</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002C61</idno><idno type="wicri:Area/PubMed/Checkpoint">002C83</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">002C83</idno><idno type="wicri:Area/Ncbi/Merge">000951</idno><idno type="wicri:Area/Ncbi/Curation">000951</idno><idno type="wicri:Area/Ncbi/Checkpoint">000951</idno><idno type="wicri:doubleKey">1107-3756:2004:Yang M:hematological:findings:in</idno><idno type="wicri:Area/Main/Merge">005743</idno><idno type="wicri:Area/Main/Curation">005327</idno><idno type="wicri:Area/Main/Exploration">005327</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Hematological findings in SARS patients and possible mechanisms (review).</title><author><name sortKey="Yang, Mo" sort="Yang, Mo" uniqKey="Yang M" first="Mo" last="Yang">Mo Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Paediatrics, The Chinese University of Hong Kong, Shatin, Hong Kong, P.R. China. yang1091@cuhk.edu.hk</nlm:affiliation><country wicri:rule="url">Hong Kong</country></affiliation></author><author><name sortKey="Li, Chi Kong" sort="Li, Chi Kong" uniqKey="Li C" first="Chi Kong" last="Li">Chi Kong Li</name></author><author><name sortKey="Li, Karen" sort="Li, Karen" uniqKey="Li K" first="Karen" last="Li">Karen Li</name></author><author><name sortKey="Hon, K L E" sort="Hon, K L E" uniqKey="Hon K" first="K L E" last="Hon">K L E. Hon</name></author><author><name sortKey="Ng, M H L" sort="Ng, M H L" uniqKey="Ng M" first="M H L" last="Ng">M H L. Ng</name></author><author><name sortKey="Chan, Paul K S" sort="Chan, Paul K S" uniqKey="Chan P" first="Paul K S" last="Chan">Paul K S. Chan</name></author><author><name sortKey="Fok, Tai Fai" sort="Fok, Tai Fai" uniqKey="Fok T" first="Tai Fai" last="Fok">Tai Fai Fok</name></author></analytic><series><title level="j">International journal of molecular medicine</title><idno type="ISSN">1107-3756</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigens, CD (biosynthesis)</term><term>Antigens, CD34 (biosynthesis)</term><term>Antigens, Differentiation (biosynthesis)</term><term>Autoantibodies (chemistry)</term><term>Blood Cell Count</term><term>Bone Marrow Cells (metabolism)</term><term>CD13 Antigens (biosynthesis)</term><term>CD4-Positive T-Lymphocytes (virology)</term><term>CD8-Positive T-Lymphocytes (virology)</term><term>Cell Adhesion Molecules</term><term>Humans</term><term>Lymphoma (etiology)</term><term>SARS Virus (metabolism)</term><term>Severe Acute Respiratory Syndrome (blood)</term><term>Severe Acute Respiratory Syndrome (complications)</term><term>Severe Acute Respiratory Syndrome (physiopathology)</term><term>Thrombocytopenia (etiology)</term><term>Time Factors</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antigènes CD (biosynthèse)</term><term>Antigènes CD34 (biosynthèse)</term><term>Antigènes de différenciation (biosynthèse)</term><term>Autoanticorps ()</term><term>Cellules de la moelle osseuse (métabolisme)</term><term>Facteurs temps</term><term>Humains</term><term>Lymphocytes T CD4+ (virologie)</term><term>Lymphocytes T CD8+ (virologie)</term><term>Lymphomes (étiologie)</term><term>Molécules d'adhérence cellulaire</term><term>Numération formule sanguine</term><term>Syndrome respiratoire aigu sévère ()</term><term>Syndrome respiratoire aigu sévère (physiopathologie)</term><term>Syndrome respiratoire aigu sévère (sang)</term><term>Thrombopénie (étiologie)</term><term>Virus du SRAS (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Antigens, CD</term><term>Antigens, CD34</term><term>Antigens, Differentiation</term><term>CD13 Antigens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Autoantibodies</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Antigènes CD</term><term>Antigènes CD34</term><term>Antigènes de différenciation</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphoma</term><term>Thrombocytopenia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bone Marrow Cells</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules de la moelle osseuse</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Lymphocytes T CD4+</term><term>Lymphocytes T CD8+</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Lymphomes</term><term>Thrombopénie</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blood Cell Count</term><term>Cell Adhesion Molecules</term><term>Humans</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autoanticorps</term><term>Facteurs temps</term><term>Humains</term><term>Molécules d'adhérence cellulaire</term><term>Numération formule sanguine</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a new human infectious disease. The causative agent of SARS is a novel coronavirus (SARS-CoV). This report summarizes the hematological findings in SARS patients and proposes the possible mechanisms of SARS-CoV related abnormal hematopoiesis. Hematological changes in patients with SARS are common and include lymphopenia, thrombocytopenia and occasionally leukopenia. A significant decrease was also observed in peripheral CD4+ and CD8+ T lymphocyte subsets and it was related to onset of SARS. A number of potential mechanisms may be involved. The development of auto-immune antibodies or immune complexes triggered by viral infection may play a major role in inducing lymphopenia and thrombocytopenia. Moreover, SARS-CoV may also directly infect hematopoietic stem/progenitor cells via CD13 or CD66a inducing their growth inhibition and apoptosis. The receptor for group I and III CoV is aminopeptidase N (CD13). CD13 has been identified in human bone marrow CD34+ cells, platelets, megakaryocytes, myeloid cells, and erythroid cells, but not in lymphocytes. The common receptor for group II CoV is CEACAM1a (CD66a). CD66a is an adhesion molecule expressed on bone marrow CD34+ cells, platelets, granulocytes and activated lymphocytes. In addition, glucocorticoids could induce lymphopenia and the use of steroids may account for the decrease of lymphocytes in some SARS patients. The increased consumption of platelets and/or the decreased production of platelets in the damaged lungs are a potential alternative but often overlooked mechanism that can contribute to thrombocytopenia in severe critical pulmonary conditions.</div></front></TEI><affiliations><list><country><li>Hong Kong</li></country></list><tree><noCountry><name sortKey="Chan, Paul K S" sort="Chan, Paul K S" uniqKey="Chan P" first="Paul K S" last="Chan">Paul K S. Chan</name><name sortKey="Fok, Tai Fai" sort="Fok, Tai Fai" uniqKey="Fok T" first="Tai Fai" last="Fok">Tai Fai Fok</name><name sortKey="Hon, K L E" sort="Hon, K L E" uniqKey="Hon K" first="K L E" last="Hon">K L E. Hon</name><name sortKey="Li, Chi Kong" sort="Li, Chi Kong" uniqKey="Li C" first="Chi Kong" last="Li">Chi Kong Li</name><name sortKey="Li, Karen" sort="Li, Karen" uniqKey="Li K" first="Karen" last="Li">Karen Li</name><name sortKey="Ng, M H L" sort="Ng, M H L" uniqKey="Ng M" first="M H L" last="Ng">M H L. 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)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SrasV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 005327 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 005327 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= SrasV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:15254784
|texte= Hematological findings in SARS patients and possible mechanisms (review).
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:15254784" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a SrasV1
| This area was generated with Dilib version V0.6.33. |  |