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Stroke. 2003;34:1869-1870
Published online before print July 3, 2003, doi: 10.1161/01.STR.0000079816.60008.73
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(Stroke. 2003;34:1869.)
© 2003 American Heart Association, Inc.


Original Contributions

Editorial Comment—How to Search for the Role of Genetic Polymorphisms in Stroke: Theory Versus Practice

Mario Di Napoli, MD, Guest Editor

Neurological Section, SMDN-Center for Cardiovascular Medicine and Cerebrovascular Disease Prevention, Sulmona, L’Aquila, 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: {approx}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 . . . [Full Text of this Article]




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R. B. Ramoni, B. E. Himes, M. M. Sale, K. L. Furie, and M. F. Ramoni
Predictive Genomics of Cardioembolic Stroke
Stroke, March 1, 2009; 40(3_suppl_1): S67 - S70.
[Abstract] [Full Text] [PDF]