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Departments of Anesthesia and Neurosurgery, University of Pennsylvania, Philadelphia, PA, andrew.kofke{at}uphs.upenn.edu
In Response:
Dr. Grocott’s insights that factors other than neurologic injury could provide alternative explanations for the observed increase in S100ß levels in patients with the ApoE4 genotype undergoing cardiac operations are helpful and appreciated. This certainly underscores the need for ongoing research to find a reliable plasma biomarker for brain injury (1) and raises important issues about our interpretations. Despite the limitations of using S100ß, with the older assay, as a biomarker for brain injury, the potential neurologic implications of the study cannot be completely discounted.
We reported an observation of a postcardiac surgery association between S100ß and the ApoE4 genotype. The possible causes for this, as we suggested, include (but do not prove) neurologic injury. Nonetheless, the possibility of a neurologic contribution to our findings cannot be totally discounted, as this notion is supported by: a) previous observations of worse cognitive outcome after cardiac surgery in ApoE4 positive patients (2), b) observations that postoperative levels of S100ß correlate with cognitive outcome after cardiac surgery (3), c) correlating increases in neuron-specific enolase and S100ß reported in our study and in previous work (4), and d) increases in neuron-specific enolase and S100ß from effluent blood of retrograde-perfused brains of patients undergoing deep hypothermic arrest (4).
Dr. Grocott’s alternative hypothesis that the increased S100ß and neuron-specific enolase may have been caused by inflammatory responses to surgery and extracorporeal circulation and that patients with the ApoE4 genotype may exhibit exaggerated inflammatory responses is reasonable and novel. This explanation may also be interpreted as consistent with our conclusion because neurologic injury is often associated with, or pathophysiologically related to, inflammatory processes. Thus, as Dr. Grocott correctly suggests, all of these biomarker correlations really may be nothing more than epiphenomena for more fundamental processes like inflammation or increased bleeding. We hope future work will provide the answer.
References
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