Kinetics of indium-111-labelled platelets in HIV-infected patients with and without associated thrombocytopaenia.
Identifieur interne : 003C15 ( Main/Exploration ); précédent : 003C14; suivant : 003C16Kinetics of indium-111-labelled platelets in HIV-infected patients with and without associated thrombocytopaenia.
Auteurs : RBID : pubmed:10359062English descriptors
- KwdEn :
- Adult, Blood Platelets (pathology), Blood Platelets (physiology), Female, HIV Infections (blood), HIV Infections (complications), HIV Infections (physiopathology), HIV-1, Half-Life, Humans, Indium Radioisotopes, Kinetics, Male, Thrombocytopenia (blood), Thrombocytopenia (etiology), Thrombocytopenia (pathology), Thrombocytopenia (physiopathology).
- MESH :
- chemical : Indium Radioisotopes.
- blood : HIV Infections, Thrombocytopenia.
- complications : HIV Infections.
- etiology : Thrombocytopenia.
- pathology : Blood Platelets, Thrombocytopenia.
- physiology : Blood Platelets.
- physiopathology : HIV Infections, Thrombocytopenia.
- Adult, Female, HIV-1, Half-Life, Humans, Kinetics, Male.
Abstract
Seven to 12% of HIV-infected patients have thrombocytopaenia. The pathophysiology of the thrombocytopaenia is not clear. It has been variously suggested that it may be caused by an increased peripheral platelet destruction, a defect in platelet production, or by a combination of these. The aim of the study was to elucidate the pathogenesis of HIV-associated thrombocytopaenia. We determined the mean platelet life span (MPLS) and calculated the turnover of autologous indium-111-labelled platelets in 17 HIV-positive patients, seven with thrombocytopaenia. The sites of sequestration of labelled platelets were quantified. The thrombocytopaenic patients had a very short MPLS (3.0+/-3.8 h) and a marked increase in platelet production (18.2+/-12.6x10(9)/l/h). The majority of these patients (5 of 7) had excessive sequestration of platelets in the spleen. Five of the patients with a normal blood platelet count had a shortened MPLS (109+/-23 h) and increased platelet turnover (3.8+/-1.2x10(9)/l/h), i.e. the increased peripheral platelet destruction was compensated for by increased platelet production. The other five patients with a normal platelet count had normal MPLS (195+/-11 h) and slightly increased platelet production (2.5+/-0.6x10(9)/l/h). We conclude that patients with HIV-associated thrombocytopaenia have increased peripheral platelet destruction. Platelet production is elevated but is insufficient to maintain a normal peripheral platelet count. In these patients platelets are predominantly sequestrated in the spleen. Patients with HIV infection and a normal blood platelet count may also have increased platelet production. This may be an early subclinical phase in the development of full-blown HIV-associated thrombocytopaenia.
PubMed: 10359062
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The pathophysiology of the thrombocytopaenia is not clear. It has been variously suggested that it may be caused by an increased peripheral platelet destruction, a defect in platelet production, or by a combination of these. The aim of the study was to elucidate the pathogenesis of HIV-associated thrombocytopaenia. We determined the mean platelet life span (MPLS) and calculated the turnover of autologous indium-111-labelled platelets in 17 HIV-positive patients, seven with thrombocytopaenia. The sites of sequestration of labelled platelets were quantified. The thrombocytopaenic patients had a very short MPLS (3.0+/-3.8 h) and a marked increase in platelet production (18.2+/-12.6x10(9)/l/h). The majority of these patients (5 of 7) had excessive sequestration of platelets in the spleen. Five of the patients with a normal blood platelet count had a shortened MPLS (109+/-23 h) and increased platelet turnover (3.8+/-1.2x10(9)/l/h), i.e. the increased peripheral platelet destruction was compensated for by increased platelet production. The other five patients with a normal platelet count had normal MPLS (195+/-11 h) and slightly increased platelet production (2.5+/-0.6x10(9)/l/h). We conclude that patients with HIV-associated thrombocytopaenia have increased peripheral platelet destruction. Platelet production is elevated but is insufficient to maintain a normal peripheral platelet count. In these patients platelets are predominantly sequestrated in the spleen. Patients with HIV infection and a normal blood platelet count may also have increased platelet production. This may be an early subclinical phase in the development of full-blown HIV-associated thrombocytopaenia.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">10359062</PMID><DateCreated><Year>1999</Year><Month>06</Month><Day>23</Day></DateCreated><DateCompleted><Year>1999</Year><Month>06</Month><Day>23</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0902-4441</ISSN><JournalIssue CitedMedium="Print"><Volume>62</Volume><Issue>5</Issue><PubDate><Year>1999</Year><Month>May</Month></PubDate></JournalIssue><Title>European journal of haematology</Title><ISOAbbreviation>Eur. J. Haematol.</ISOAbbreviation></Journal><ArticleTitle>Kinetics of indium-111-labelled platelets in HIV-infected patients with and without associated thrombocytopaenia.</ArticleTitle><Pagination><MedlinePgn>332-5</MedlinePgn></Pagination><Abstract><AbstractText>Seven to 12% of HIV-infected patients have thrombocytopaenia. The pathophysiology of the thrombocytopaenia is not clear. It has been variously suggested that it may be caused by an increased peripheral platelet destruction, a defect in platelet production, or by a combination of these. The aim of the study was to elucidate the pathogenesis of HIV-associated thrombocytopaenia. We determined the mean platelet life span (MPLS) and calculated the turnover of autologous indium-111-labelled platelets in 17 HIV-positive patients, seven with thrombocytopaenia. The sites of sequestration of labelled platelets were quantified. The thrombocytopaenic patients had a very short MPLS (3.0+/-3.8 h) and a marked increase in platelet production (18.2+/-12.6x10(9)/l/h). The majority of these patients (5 of 7) had excessive sequestration of platelets in the spleen. Five of the patients with a normal blood platelet count had a shortened MPLS (109+/-23 h) and increased platelet turnover (3.8+/-1.2x10(9)/l/h), i.e. the increased peripheral platelet destruction was compensated for by increased platelet production. The other five patients with a normal platelet count had normal MPLS (195+/-11 h) and slightly increased platelet production (2.5+/-0.6x10(9)/l/h). We conclude that patients with HIV-associated thrombocytopaenia have increased peripheral platelet destruction. Platelet production is elevated but is insufficient to maintain a normal peripheral platelet count. In these patients platelets are predominantly sequestrated in the spleen. Patients with HIV infection and a normal blood platelet count may also have increased platelet production. This may be an early subclinical phase in the development of full-blown HIV-associated thrombocytopaenia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Van Wyk</LastName><ForeName>V</ForeName><Initials>V</Initials><Affiliation>Department of Haematology and Cell Biology, University of the Orange Free State, Bloemfontein, South Africa.</Affiliation></Author><Author ValidYN="Y"><LastName>Kotzé</LastName><ForeName>H F</ForeName><Initials>HF</Initials></Author><Author ValidYN="Y"><LastName>Heyns</LastName><ForeName>A P</ForeName><Initials>AP</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType>Journal Article</PublicationType><PublicationType>Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>DENMARK</Country><MedlineTA>Eur J Haematol</MedlineTA><NlmUniqueID>8703985</NlmUniqueID><ISSNLinking>0902-4441</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance>Indium Radioisotopes</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CitationSubset>X</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Blood Platelets</DescriptorName><QualifierName MajorTopicYN="N">pathology</QualifierName><QualifierName MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">HIV Infections</DescriptorName><QualifierName MajorTopicYN="N">blood</QualifierName><QualifierName MajorTopicYN="N">complications</QualifierName><QualifierName MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y">HIV-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Half-Life</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Indium Radioisotopes</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N">Thrombocytopenia</DescriptorName><QualifierName MajorTopicYN="N">blood</QualifierName><QualifierName MajorTopicYN="N">etiology</QualifierName><QualifierName MajorTopicYN="N">pathology</QualifierName><QualifierName MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>6</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1999</Year><Month>6</Month><Day>8</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1999</Year><Month>6</Month><Day>8</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10359062</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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