ArticleIntensive care medicine2004
Increased diffusion of soluble adhesion molecules in meningitis, severe sepsis and systemic inflammatory response without neurological infection is associated with intrathecal shedding in cases of meningitis.
Article in Intensive care medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Clinical utility of biomarkers of endothelial activation in sepsis--a systematic review.Critical care (London, England) · 2012Pooled it
- The Biological Changes of Synaptic Plasticity in the Pathological Process of Sepsis-associated Encephalopathy.Current neuropharmacology · 2025Review
- ICAM1 and VCAM1 are associated with outcome in patients with sepsis: A systematic review and meta-analysis.Heliyon · 2024Article
- Brain Barrier Breakdown as a Cause and Consequence of Neuroinflammation in Sepsis.Molecular neurobiology · 2018Review
- Review
- Serum intercellular adhesion molecule 1 variations in young children with acute otitis media.Clinical and vaccine immunology : CVI · 2010Article
- Adhesion molecule levels in serum and cerebrospinal fluid in children with bacterial meningitis and sepsis.Journal of pediatric neurosciences · 2009Article
- Association of plasminogen activators and matrix metalloproteinase-9 proteolytic cascade with blood-CNS barrier damage of angiostrongyliasis.International journal of experimental pathology · 2006Article
- Accuracy of clinical presentation for differentiating bacterial from viral meningitis in adults: a multivariate approach.Intensive care medicine · 2005Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveSepsis and systemic inflammatory response syndrome (SIRS) result in the release in plasma of inflammatory cytokines and soluble forms of adhesion molecules in relation to endothelial activation. This study was designed to compare cerebrospinal fluid (CSF) concentrations of adhesion molecules in meningitis and SIRS without neurological infection and to evaluate in meningitis whether they originate from passive diffusion through damaged blood-CSF barrier or from local production.
designProspective observational study.
settingUniversity hospital medical intensive care unit. PATIENTS: Nineteen patients with meningitis and 41 patients with sepsis or SIRS without cerebrospinal infection consecutively admitted to the critical care unit over an 18-month period.
interventionsSoluble forms of adhesion molecules (ICAM-1, VCAM-1, E-selectin) and cytokines (interleukin (IL)-1beta and TNF-alpha) were measured in paired CSF and blood samples.
resultsSerum concentrations of soluble adhesion molecules and cytokines were increased in the two groups, without significant differences. The CSF concentrations were elevated in both cases, whereas patients with meningitis demonstrated significantly higher CSF concentrations of soluble ICAM-1, VCAM-1, E-selectin, and TNF-alpha ( p<0.001), with higher corresponding CSF/serum ratios. Correlations between CSF and serum concentrations were found only in meningitis. These correlations were strong for soluble ICAM-1 (r(2)=0.7, p<0.001) and E-selectin (r(2)=0.9, p<0.001), but weaker for VCAM-1. VCAM-1 CSF/serum ratios were increased, in comparison with ICAM-1 and E-selectin CSF/serum ratios, despite similar molecular weights. Serum and CSF levels of cytokines and adhesion molecules were not predictive of death for the whole population, except concentrations of ICAM-1 significantly increased in non-surviving patients ( p<0.05).
conclusionsThe CSF soluble adhesion molecules are increased in sepsis, SIRS and meningitis. In meningitis, the correlation between CSF and serum concentrations of adhesion molecules and the presence of a discrepancy of CSF/serum ratios for molecules of the same molecular weight may suggest intrathecal shedding in addition to diffusion through blood-CSF barrier.
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