Coagulant and fibrinolytic status in tuberculous meningitis

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dc.contributor.authorSchoeman J.
dc.contributor.authorMansvelt E.
dc.contributor.authorSpringer P.
dc.contributor.authorVan Rensburg A.J.
dc.contributor.authorCarlini S.
dc.contributor.authorFourie E.
dc.date.accessioned2011-05-15T16:00:06Z
dc.date.available2011-05-15T16:00:06Z
dc.date.issued2007
dc.description.abstractBACKGROUND: The long-term neurologic sequelae of childhood tuberculous meningitis (TBM) mainly result from ischemia owing to cerebral vasculitis. Deep vein thrombosis occurs in adults with pulmonary tuberculosis owing to hypercoaguability. The present study aimed to investigate coagulation status during acute childhood TBM. METHODS: Coagulation status, including the natural anticoagulants, antithrombin, protein C and protein S; procoagulant FVIII; fibrinolytic factors, tissue plasminogen activator and plasminogen activator inhibitor-1 (PAI-1) as well as anticardiolipin antibodies (ACA), was determined in 16 children with TBM before and during treatment. RESULTS: A prothrombotic profile was found as expressed by a decrease of anticoagulant (protein S) and increase of the procoagulant (factor VIII) activity. Raised PAI-1 and normal tissue plasminogen activator values indicated deficient fibrinolysis. This hypercoagulable state was more pronounced in stage 3 patients than in stage 2 patients. The bleeding time on admission ranged from 1.2 to 10 minutes [mean 4.2 minutes]. The mean platelet count on admission was 577.9 ± 188.6 × 10/L and increased further during the course of the treatment. CONCLUSIONS: The hypercoagulable state in childhood TBM is comparable to that described in adults with pulmonary tuberculosis and may further increase the risk for infarction. Therapeutic measures that reduce the risk for thrombosis could therefore be potentially beneficial in childhood TBM. © 2007 Lippincott Williams & Wilkins, Inc.
dc.description.versionArticle
dc.identifier.citationPediatric Infectious Disease Journal
dc.identifier.citation26
dc.identifier.citation5
dc.identifier.issn8913668
dc.identifier.other10.1097/01.inf.0000261126.60283.cf
dc.identifier.urihttp://hdl.handle.net/10019.1/11531
dc.subjectanticoagulant agent
dc.subjectantithrombin
dc.subjectblood clotting factor 8
dc.subjectcardiolipin antibody
dc.subjectethionamide
dc.subjectfibrinolytic factor
dc.subjectisoniazid
dc.subjectplasminogen activator inhibitor 1
dc.subjectprednisone
dc.subjectprotein C
dc.subjectprotein S
dc.subjectpyrazinamide
dc.subjectrifampicin
dc.subjecttissue plasminogen activator
dc.subjectacute disease
dc.subjectadulthood
dc.subjectarticle
dc.subjectbleeding time
dc.subjectblood clotting
dc.subjectblood clotting test
dc.subjectcardiovascular risk
dc.subjectchild
dc.subjectchildhood disease
dc.subjectcontrolled study
dc.subjectdisease severity
dc.subjectfibrinolysis
dc.subjectheart infarction
dc.subjecthuman
dc.subjecthypercoagulability
dc.subjectinfant
dc.subjectlung tuberculosis
dc.subjectmajor clinical study
dc.subjectpriority journal
dc.subjectrisk factor
dc.subjectthrombocyte count
dc.subjecttreatment outcome
dc.subjecttuberculous meningitis
dc.subjectAspirin
dc.subjectBlood Coagulation
dc.subjectChild
dc.subjectChild, Preschool
dc.subjectFibrinolysis
dc.subjectHumans
dc.subjectInfant
dc.subjectPlatelet Count
dc.subjectThrombolytic Therapy
dc.subjectTuberculosis, Meningeal
dc.titleCoagulant and fibrinolytic status in tuberculous meningitis
dc.typeArticle
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