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(Stroke. 2003;34:1869.)
© 2003 American Heart Association, Inc.
Original Contributions |
Neurological Section, SMDN-Center for Cardiovascular Medicine and Cerebrovascular Disease Prevention, Sulmona, LAquila, Italy
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In this issue of the Stroke, Acalovschi and colleagues1 furnish new evidence on the hot topic of inflammatory response after stroke and its regulatory mechanisms, pointing our attention to the interleukin-6 (IL-6) genetic polymorphisms. In the last years, part of this picture has been discovered, but many issues remain to be explored. It is very clear that ischemic stroke is a multifactorial and dynamic process.2 However, not all questions are answered. We should search for the origin of the acute-phase response after stroke; so far, no hypothesis on the source of inflammation has been proved. We should search for the reasons for a strong association between inflammatory markers and prognosis.3 We should search for anti-inflammatory therapies; these therapies, if effective, could prove definitely the pathogenic role of inflammation in acute ischemic stroke.4 These points represent a rich task for future exploration, but will answering these questions shed light on all problems? For example, why do some patients have a marked inflammatory response after stroke and others do not? The degree of inflammatory response to ischemic stroke is variable:
25% of patients with ischemic stroke have normal levels of inflammatory markers after stroke, implying that ischemic stroke itself does not induce a full-blown acute-phase response.3,5
To respond to these questions, Acalovschi et al1 analyze the IL-6 system and the acute-phase response after stroke, showing that there is a genetically determined difference in the degree of IL-6 response to stroke between individuals. The immune haplotype A-G-8/12-C was associated with lower levels
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