Elevated serum levels of S-100β protein and neuron-specific enolase are associated with brain injury in patients with severe sepsis and septic shock*

Nguyen, Duc Nam; Spapen, Herbert; Su, Fuhong; Schiettecatte, Johan; Shi, Lin; Hachimi-Idrissi, Saı̈d; Huyghens, Luc

doi:10.1097/01.ccm.0000217218.51381.49

Cited by 184 publications

(152 citation statements)

References 39 publications

Supporting

Mentioning

130

Contrasting

Unclassified

Order By: Relevance

“…S100B (S100 A1B and S100 BB) and NSE were measured with an automated, noncompetitive, electrochemiluminescent immunoassay on a Cobas e411 (Roche Diagnostics) following the manufacturer's instructions. 42 …”

Section: Blood Measurementsmentioning

confidence: 99%

“…42 We investigated whether neuronal damage occurs concomitantly with astrocyte loss in ODS and whether NSE could serve as a marker of injury. We performed IHC for the neuronal marker microtubule-associated protein 2, and we did not find any apparent neuronal loss in the region of astrocyte death (Supplemental Figure S4A).…”

Section: Astrocyte Death Occurs Without Neuronal Damage In Odsmentioning

confidence: 99%

See 1 more Smart Citation

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

Kengne

Nicaise²,

Soupart³

et al. 2011

Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

Abrupt osmotic changes during rapid correction of chronic hyponatremia result in demyelinative brain lesions, but the sequence of events linking rapid osmotic changes to myelin loss is not yet understood. Here, in a rat model of osmotic demyelination syndrome, we found that massive astrocyte death occurred after rapid correction of hyponatremia, delineating the regions of future myelin loss. Astrocyte death caused a disruption of the astrocyte-oligodendrocyte network, rapidly upregulated inflammatory cytokines genes, and increased serum S100B, which predicted clinical manifestations and outcome of osmotic demyelination. These results support a model for the pathophysiology of osmotic brain injury in which rapid correction of hyponatremia triggers apoptosis in astrocytes followed by a loss of trophic communication between astrocytes and oligodendrocytes, secondary inflammation, microglial activation, and finally demyelination.

show abstract

Section: Blood Measurementsmentioning

confidence: 99%

Section: Astrocyte Death Occurs Without Neuronal Damage In Odsmentioning

confidence: 99%

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

Kengne

Nicaise²,

Soupart³

et al. 2011

Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

show abstract

“…W rozpoznaniu SAD stosuje się skale majaczenia dedykowane dla intensywnej terapii, które mogą wskazywać na patologię w zakresie OUN jeszcze przed rozpoznaniem sepsy [16,17].…”

Section: Biomarkeryunclassified

Encefalopatia septyczna a majaczenie stanu ciężkiego

Kotfis

2018

Pomeranian J Life Sci

View full text Add to dashboard Cite

Introduction: Sepsis-associated encephalopathy is an acute dysfunction of the central nervous system (CNS) that arises as a consequence of generalized systemic infection, yet without brain infection. The aim of this review is to introduce septic encephalopathy as a disease, with all of the epidemiology data, diagnostic opportunities, pathophysiology and possible treatment. Sepsis-associated encephalopathy is a medical condition characterized by a broad spectrum of disturbances of consciousness, from delirium to coma, with possible seizures or focal neurological signs. Many pathophysiological mechanisms lie at the basis of septic encephalopathy, including inflammation or dysfunction of cerebral perfusion. Another important mechanism includes interactions between inflammatory cytokines and acetylcholine that lead to abnormal cholinergic transmission and neuronal death. Moreover, interaction between acetylcholine and inflammatory cytokines may induce immunosuppression. Sepsis-associated encephalopathy diagnosis is strictly clinical, based on neurological examination and the exclusion of other causes, because there are no definite biochemical tests or radiological studies specific for this disease. The use of ICU delirium screening tools, such as CAM-ICU (Confusion Assessment Method for the Intensive Care Unit) enables earlier detection of brain dysfunction. Neuroimaging studies (computed tomography, magnetic resonance imaging), as well as electroencephalograhy may be helpful in the assessment of the severity of dysfunction. The most important element is early diagnosis of sepsis, especially with the use of the QuickSOFA scale, and early initiation of multidirectional treatment according to Surviving Sepsis Campaign guidelines: early source identification and source control, initiation of optimal antibiotic therapy, adequate fluid therapy and supportive treatment for major organs. In order to prevent CNS dysfunction in the ICU, deep sedation and benzodiazepines should be avoided and dexmedetomidine and propofol introduced instead. Pharmacological treatment of ICU delirium is based on the use of typical (haloperidol) and atypical (i.e. quetiapine) antipsychotics. Non-pharmacological methods include early mobilization, ensuring day and night cycles, the minimalization of noctural factors (light, sounds, interventions), and family engagement. Conclusion: Sepsis-associated encephalopathy is a serious illness associated with severe consequences, including increased mortality, long-term cognitive dysfunction, and immunosuppression. The co-dependence between septic encephalopathy and the immune system should be underlined in the approach towards sepsis treatment. Keywords: sepsis associated encephalopathy; sepsis; ICU delirium; CAM-ICU; cognitive dysfunction. ABSTRAKT Wstęp:Encefalopatia septyczna (sepsis-associated encephalopathy -SAE) jest ostrym zaburzeniem funkcjonowania ośrodko-wego układu nerwowego (OUN), które pojawia się w następstwie infekcji ogólnoustrojowej, jednak bez infekcji samego mózgu. Celem ninie...

show abstract

“…(30) NSE also increases and associates with brain injury in patients with severe sepsis and septic shock. (31) Tumor cells in APUDomas, neuroblastomas and small cell lung carcinomas are able to produce NSE and increase serum levels of this protein, That is why, serum dosage of NSE has been considered as a diagnostic and prognostic serum marker in the clinical management of these neoplasms. (32) High serum concentrations of NSE are found in TBI correlating with injury severity.…”

Section: S100bmentioning

confidence: 99%