Temporal Profile of Release of Neurobiochemical Markers of Brain Damage After Traumatic Brain Injury Is Associated With Intracranial Pathology as Demonstrated in Cranial Computerized Tomography

Herrmann, Manfred; Jost, Stefan; Kutz, Susanne; Ebert, Anne; Kratz, Torsten; Wunderlich, Michael T.; Synowitz, Hans

doi:10.1089/neu.2000.17.113

Cited by 165 publications

(113 citation statements)

References 39 publications

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“…Interestingly, the initial, highly elevated S-100B values in subgroup 1 of 2.60 ng/mL (1.52-5.89 ng/mL) were within the data ranges recently demonstrated for patients with out-of-hospital car- diac arrest or severe traumatic brain injury (21,33). Furthermore, median S-100B serum levels in subgroup 2 decreased to 0.05 ng/mL (0.02-0.18 ng/mL) at PM13, and were still elevated compared to the value for healthy controls of 0.04 ng/mL (0.01-0.08 ng/mL) (17).…”

Section: Sofa Score Il-8 Serum and Pmn Elastase Plasma Levels Dependsupporting

confidence: 85%

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Effect of stress doses of hydrocortisone on S-100B vs. interleukin-8 and polymorphonuclear elastase levels in human septic shock

Mussack¹,

Briegel²,

Schelling³

et al. 2005

Clinical Chemistry and Laboratory Medicine (CCLM)

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Stress doses of hydrocortisone are known to have immunomodulatory effects in patients with hyperdynamic septic shock. The prognosis correlates with the presence and severity of septic encephalopathy. However, neurological evaluation is influenced by the use of analgesia sedation during artificial ventilation. The objective of this study was to demonstrate the effect of stress doses of hydrocortisone during the initial phase of human septic shock on the serum values of the neurospecific protein S-100B in comparison to the inflammation markers interleukin (IL)-8 in serum and polymorphonuclear (PMN) elastase in plasma. A total of 24 consecutive patients, who met the American College of Chest Physicians/Society of Critical Care Medicine criteria for septic shock, were enrolled in this prospective, randomized, double-blind, singlecenter trial. The severity of illness at recruitment was graded using the Acute Physiology and Chronic Health Evaluation II and the Simplified Acute Physiology Score II scoring systems. Multi-organ dysfunction syndrome was described by the Sepsis-related Organ Failure Assessment (SOFA) score. All patients were prospectively randomized to receive either stress doses of hydrocortisone or placebo. Hydrocortisone was started in 12 patients with a loading dose of 100 mg and followed by a continuous infusion of 0.18 mg/kg/h for 6 days. Median S-100B serum levels of the hydrocortisone group decreased from 0.32 ng/mL at study entry to 0.07 ng/mL 6 days later without significant differences compared to the placebo group. Initial IL-8 serum levels were significantly higher in the hydrocortisone group up to 12 h after study entry, and significantly decreased from 715 to 17 pg/mL at the end of the observation period. Median PMN elastase plasma levels were not affected by hydrocortisone infusion. Patients with initial S-100B *Corresponding author: Thomas Mussack, MD, Department of Surgery Innenstadt, Klinikum der Universitä t Mü nchen, Nussbaumstraße 20, 80336 Mü nchen, Germany Phone: q49-89-5160-2638, Fax: q49-89-5160-4489, E-mail: thomas.mussack@med.uni-muenchen.de serum levels )0.50 ng/mL revealed significantly higher SOFA scores up to 30 h, IL-8 serum levels up to 12 h, and PMN elastase plasma levels up to 36 h after study entry than those patients with F0.50 ng/mL. These effects were independent of the amount of fluid correction for hemodilution. Starting S-100B, IL-8 and PMN elastase values of the hydrocortisone group were within the ranges already known in patients with out-of-hospital cardiac arrest or severe traumatic brain injury. Stress doses of hydrocortisone resulted in a significant reduction in IL-8 serum, but not in S-100B serum and PMN elastase plasma concentrations in patients with hyperdynamic septic shock. For the first time, a similar extent of S-100B increase in serum of septic patients at the time of diagnosis was shown as reported for cardiac arrest or severe traumatic brain injury.

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Section: Sofa Score Il-8 Serum and Pmn Elastase Plasma Levels Dependsupporting

confidence: 85%

“…Biochemical data for septic patients were compared to those reported for patients with out-ofhospital cardiac arrest or isolated severe traumatic brain injury (GCS score F8 points), and healthy volunteers without a history of brain or cardiac damage (17,21,33). Blood sampling of the control groups was carried out after informed consent.…”

Section: Discussionmentioning

confidence: 99%

Effect of stress doses of hydrocortisone on S-100B vs. interleukin-8 and polymorphonuclear elastase levels in human septic shock

Mussack¹,

Briegel²,

Schelling³

et al. 2005

Clinical Chemistry and Laboratory Medicine (CCLM)

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“…1,[44][45][46] Because newly acquired anti-GFAP antibody response usually takes about 5 days to manifest, 26,47,48 it is unlikely that the acute post-TBI autoantibody levels we report here were from a de novo response to current TBI, but rather to a sustained increase because of previous head injuries. At present, however, we cannot rule out whether the acute TBI event might serve to be an antigen-boosting event for those with pre-existing anti-GFAP antibody titers.…”

Section: Discussionmentioning

confidence: 89%

Plasma Anti-Glial Fibrillary Acidic Protein Autoantibody Levels during the Acute and Chronic Phases of Traumatic Brain Injury: A Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot Study

Wang

Yang

Yue

et al. 2016

Journal of Neurotrauma

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We described recently a subacute serum autoantibody response toward glial fibrillary acidic protein (GFAP) and its breakdown products 5-10 days after severe traumatic brain injury (TBI). Here, we expanded our anti-GFAP autoantibody (AutoAb[GFAP]) investigation to the multicenter observational study Transforming Research and Clinical Knowledge in TBI Pilot (TRACK-TBI Pilot) to cover the full spectrum of TBI (Glasgow Coma Scale 3-15) by using acute (<24 h) plasma samples from 196 patients with acute TBI admitted to three Level I trauma centers, and a second cohort of 21 participants with chronic TBI admitted to inpatient TBI rehabilitation. We find that acute patients self-reporting previous TBI with loss of consciousness (LOC) (n = 43) had higher day 1 AutoAb[GFAP] (mean -standard error: 9.11 -1.42; n = 43) than healthy controls (2.90 -0.92; n = 16; p = 0.032) and acute patients reporting no previous TBI (2.97 -0.37; n = 106; p < 0.001), but not acute patients reporting previous TBI without LOC (8.01 -1.80; n = 47; p = 0.906). These data suggest that while exposure to TBI may trigger the AutoAb[GFAP] response, circulating antibodies are elevated specifically in acute TBI patients with a history of TBI. AutoAb[GFAP] levels for participants with chronic TBI (average post-TBI time 176 days or 6.21 months) were also significantly higher (15.08 -2.82; n = 21) than healthy controls ( p < 0.001). These data suggest a persistent upregulation of the autoimmune response to specific brain antigen(s) in the subacute to chronic phase after TBI, as well as after repeated TBI insults. Hence, AutoAb[GFAP] may be a sensitive assay to study the dynamic interactions between postinjury brain and patient-specific autoimmune responses across acute and chronic settings after TBI.

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“…The serum level for NSE (normally Ͻ12.5 ng/mL) has been reported to increase after TBI, the levels of which have been correlated with the severity of the injury. [25][26][27] At serum levels Ͼ21.7 ng/mL, NSE has been demonstrated to be a sensitive indicator of mortality (85% sensitivity) and poor outcome (80% sensitivity). However, inadequate sensitivity and specificity have limited the use of NSE regarding the neuropsychological outcome (55% sensitivity; 77.8% specificity) and predicting the presence of intracranial lesions (77% sensitivity; 52% specificity).…”

Section: Neuron-specific Enolasementioning

confidence: 99%

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

et al. 2010

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Temporal Profile of Release of Neurobiochemical Markers of Brain Damage After Traumatic Brain Injury Is Associated With Intracranial Pathology as Demonstrated in Cranial Computerized Tomography

Cited by 165 publications

References 39 publications

Effect of stress doses of hydrocortisone on S-100B vs. interleukin-8 and polymorphonuclear elastase levels in human septic shock

Effect of stress doses of hydrocortisone on S-100B vs. interleukin-8 and polymorphonuclear elastase levels in human septic shock

Plasma Anti-Glial Fibrillary Acidic Protein Autoantibody Levels during the Acute and Chronic Phases of Traumatic Brain Injury: A Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot Study

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

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