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Vascular endothelial growth factor and blood-brain barrier disruption in tuberculous meningitis

dc.contributor.authorVan Der Flier M.
dc.contributor.authorHoppenreijs S.
dc.contributor.authorVan Rensburg A.J.
dc.contributor.authorRuyken M.
dc.contributor.authorKolk A.H.J.
dc.contributor.authorSpringer P.
dc.contributor.authorHoepelman A.I.M.
dc.contributor.authorGeelen S.P.M.
dc.contributor.authorKimpen J.L.L.
dc.contributor.authorSchoeman J.F.
dc.date.accessioned2011-05-15T16:17:38Z
dc.date.available2011-05-15T16:17:38Z
dc.date.issued2004
dc.identifier.citationPediatric Infectious Disease Journal
dc.identifier.citation23
dc.identifier.citation7
dc.identifier.issn08913668
dc.identifier.other10.1097/01.inf.0000131634.57368.45
dc.identifier.urihttp://hdl.handle.net/10019.1/14302
dc.description.abstractBackground: Tuberculous meningitis (TBM) is characterized by disruption of the blood-brain barrier (BBB), cerebral edema and increased intracranial pressure (ICP). Vascular endothelial growth factor (VEGF) is a potent vascular permeability factor and a mediator of brain edema. Aims: To investigate whether in children with TBM disruption of the BBB relates to VEGF production and to assess the effect of corticosteroids on Mycobacterium tuberculosis-induced VEGF production by mononuclear leukocytes. Methods: Blood and CSF samples were collected from 26 children with stage 2-3 TBM and 20 controls. All patients received antituberculous and adjuvant corticosteroid therapy. Children were evaluated by ICP recording, computerized tomography scanning and outcome assessment at 6 months follow-up. BBB disruption was quantified by cerebrospinal fluid (CSF)-serum albumin ratios. VEGF concentrations were measured by enzyme-linked immunosorbent assay. In vitro human monocytic THP-1 cells were stimulated with M. tuberculosis sonicate or culture supernatant, and VEGF production was measured in the presence or absence of corticosteroids. Results: CSF VEGF concentrations were significantly higher in TBM patients than in the controls and correlated with mononuclear cell counts (r = 0.64; P = 0.001) and CSF-serum albumin ratio (r = 0.49; P = 0.015). CSF VEGF did not significantly correlate with elevated ICP. In vitro induction of VEGF production by M. tuberculosis sonicate or culture supernatant could be completely abrogated by corticosteroid treatment. Conclusions: Inflammatory cells secrete VEGF during TBM. CSF VEGF correlates with BBB disruption. Inhibition of VEGF may explain part of the clinical effect of adjuvant corticosteroid therapy in TBM.
dc.subjectacetazolamide
dc.subjectcorticosteroid
dc.subjectdexamethasone
dc.subjectethionamide
dc.subjectfurosemide
dc.subjectisoniazid
dc.subjectprednisone
dc.subjectpyrazinamide
dc.subjectrifampicin
dc.subjectserum albumin
dc.subjecttuberculostatic agent
dc.subjecttumor necrosis factor alpha
dc.subjectvasculotropin
dc.subjectadolescent
dc.subjectarticle
dc.subjectblood brain barrier
dc.subjectblood sampling
dc.subjectbrain edema
dc.subjectcerebrospinal fluid analysis
dc.subjectchild
dc.subjectclinical article
dc.subjectcomputer assisted tomography
dc.subjectcontrolled study
dc.subjectcorticosteroid therapy
dc.subjectenzyme linked immunosorbent assay
dc.subjectfemale
dc.subjectfollow up
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthydrocephalus
dc.subjectinfant
dc.subjectintracranial hypertension
dc.subjectLimulus lysate test
dc.subjectmale
dc.subjectmononuclear cell
dc.subjectMycobacterium tuberculosis
dc.subjectpriority journal
dc.subjecttuberculous meningitis
dc.subjectAlbumins
dc.subjectAntitubercular Agents
dc.subjectBlood-Brain Barrier
dc.subjectBrain Edema
dc.subjectChild
dc.subjectChild, Preschool
dc.subjectDrug Therapy, Combination
dc.subjectFemale
dc.subjectHumans
dc.subjectHydrocephalus
dc.subjectInfant
dc.subjectIntracranial Pressure
dc.subjectMale
dc.subjectPrednisone
dc.subjectSeverity of Illness Index
dc.subjectTuberculosis, Meningeal
dc.subjectVascular Endothelial Growth Factors
dc.titleVascular endothelial growth factor and blood-brain barrier disruption in tuberculous meningitis
dc.typeArticle
dc.description.versionArticle


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