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Effect of our therapeutic interventions in real time. Despite these promising advances, it remains difficult to precisely measure the extent of neurological injury in patients affected by stroke, trauma, or cardiac arrest. In the intensive care unit, where neurological deterioration is often obscured by encephalopathy or sedative medications, determination of the extent of primary and secondary injury often eludes clinicians, making prognostication imprecise and difficult. For decades, researchers have sought clinically useful biomarkers of nervous system injury, and these efforts have intensified in the past few years. Early candidates for brain injury biomarkers included lactate dehydrogenase and creatinine kinase enzyme subtypes in the serum andOHCA = out-of-hospital cardiac arrest.Page 1 of(page number not for citation purposes)Critical CareVol 13 NoMayer and Linareshypothermic and normothermic patients. It is our view that this should not be interpreted as lack of efficacy of hypothermia, an intervention that has been shown to improve survival and recovery after OHCA in large randomized control trials [2-5]. The lack of randomized treatment allocation makes it hard to reach any definitive conclusions regarding the effect of therapeutic hypothermia. It also remains possible that S-100B is not a useful surrogate marker for the efficacy of delayed therapeutic interventions such as hypothermia for OHCA. This may reflect the fact that most of the damage measured by S-100B elevation is related to the primary global hypoxic-ischemic insult, rather than temperaturemodifiable reperfusion injury. By contrast, this paper does suggest that S-100B may have utility as a prognostic indicator after OHCA. S-100B levels were significantly lower in patients with a favorable outcome, but only among those treated with hypothermia. It may be that the uniformly poor RRx-001 outcomes among those treated with normothermic supportive care reduced the ability of S-100B to discriminate between poor and favorable outcomes. From a clinical perspective, however, the most important finding of this study is that S-100B levels were consistently the highest on admission, with a progressive decline over the next several days. These findings suggest that elevation of S100B reflects the severity of the primary hypoxic-ischemic insult, rather than the effects of the cooling intervention. Neuron specific enolase has been recognized in recent guidelines developed by the American Academy of Neurology as a useful prognostic indicator in comatose patients with global hypoxic-ischemic brain injury [6]. Derwall and colleagues now present data suggesting that admission S-100B levels may also be useful in this setting. The obvious challenges now are to determine whether panels of multiple biomarkers provide greater prognostic accuracy than any single measure, and to better understand how hypothermia influences the relationship between S-100B elevation, the severity of the initial insult, and long-term outcome.5. 6.Bernard S: Therapeutic hypothermia after cardiac arrest. Neurol Clin 2006, 24:61-71. Wijdicks EFM, Hijdra A, Young GB, Bassetti CL, Wiebe S: Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation. Neurology 2006, 67:203210.Competing interestsThe authors declare that they have no competing interests.
Faria-Oliveira et al. BMC Microbiology 2014, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/7500280 14:244 http://www.biomedcentral.com/1471-2180/14/METHODOLOGY ARTICLEOpen AccessMethodologie.