Published online before print December 29, 2004, doi: 10.1161/01.STR.0000155197.88944.ac
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(Stroke. 2005;36:228-a.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
Correlation of Systemic Inflammatory Response With Infarct Volume in Acute Ischemic Stroke Patients
Division of Neuroscience, University of Liverpool, The Walton Centre for Neurology & Neurosurgery, Liverpool, United Kingdom
University of Manchester Hope Hospital, Salford, United Kingdom
Stroke Medicine (Neurosciences), Hope Hospital, Salford, United Kingdom
Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom
Injury Research, Hope Hospital, Salford, United Kingdom
To the Editor:
In the September 2004 issue of Stroke, Audebert and colleagues1 commented on a study conducted by our group "in a small number of acute stroke patients."2 Contrary to the authors’ assertion that "[T]here are no reports so far on the association between lesion size and elevated CRP in the acute phase of ischemic stroke," the relationship between C-reactive protein (CRP) and both infarct volume and clinical outcome in this study was subsequently reported in January 2004.3 In fact, despite the smaller size of our study, a notable difference between the studies is that whereas Audebert et al suggest the correlations with CRP are quite weak,1 our own data indicated rather higher correlations across a range of measures, although they were not as high as for interleukin-6, which is a more direct measure of tissue inflammation. A possible explanation lies in the measurements of CRP used in the German study. Their lower cutoff for CRP was 0.5 mg/dL, which does not approach the normal range, and our own data suggest they may have used a cutoff value of 0.4 mg/dL for approximately half the data points. That this is the case is supported by the data in Figure 2, in which the error, or range, for day 1 CRP is indicated as a negative value, which is clearly not possible. Their large number of ties at 0.4 mg/dL could then result in spuriously low correlations in the analyses.
References
1. Audebert HJ, Rott MM, Eck T, Haberl RL. Systemic inflammatory response depends on initial stroke severity but is attenuated by successful thrombolysis. Stroke. 2004; 35: 2128–2133.
2. Emsley HCA, Smith CJ, Gavin CM, et al. An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis. J Neuroimmunol. 2003; 139: 93–101.[CrossRef][Medline] [Order article via Infotrieve]
3. Smith CJ, Emsley HCA, Gavin CM, et al. Peak plasma interleukin-6 and other peripheral markers of inflammation in the first week of ischaemic stroke correlate with brain infarct volume, stroke severity and long-term outcome. BMC Neurol. 2004; 4: 2–9.[CrossRef][Medline] [Order article via Infotrieve]
Response
Department of Neurology, University of Munich, Munich, Germany
We thank Dr Emsley for his critical comment on our article. In fact, their analysis of January 2004 resulted in a relationship between infarct volume and C-reactive protein (CRP) in the acute phase of ischemic stroke. However, it was published just at the time when our paper was submitted the first time to Stroke. We agree that the relatively weak correlation between CRP and lesion size on the first day after admission may be caused by the lower cutoff level of CRP (0.5 mg/dL) in our study. This cutoff was introduced for clinical use to exclude nontherapy relevant elevations of CRP. The reduced sensitivity in lower CRP ranges is less relevant in the subsequent days, when CRP increases, especially in patients with large infarcts. However, the peak plasma CRP levels (measurements within 5 to 7days) as used in the publication of Emsley et al are a different method and cannot be compared directly to our results with particular correlations for each day.
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