(Stroke. 2001;32:1443-a.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Department of Neurology and Neurorehabilitation, Casa di Cura Villa Pini dAbruzzo, Chieti, Italy
To the Editor:
Activation of the complement system has been reported in a variety of inflammatory diseases and neurodegenerative processes of the central nervous system, and recent evidence indicates that complement proteins and receptors are synthesized on or by glial cells and, surprisingly, neurons.1
In their study, Xi and colleagues2 furnish new indirect data on the activation of complement system after intracerebral hemorrhage (ICH) in rats and suggest a possible pharmacological manipulation preventing complement activation to reduce the brain edema in ICH. However, despite the large number of therapeutic interventions that decrease damage in experimental animals, many negative results have been produced in the history of therapy in cerebrovascular disease when the same agent is tested in clinical trials. Experimental studies are conducted on healthy, young animals under rigorously controlled laboratory conditions. However, the typical stroke patient is elderly with numerous risk factors and complicating disease (for example, diabetes, arterial hypertension, and heart disease). Therefore, we must have more strong data on complement activation in stroke patients from observational epidemiological studies before suggesting a possible pharmacological manipulation of the complement system in stroke.
The complement system has an important role in innate
and specific immune responses with functions that include the
augmentation of the acute phase
response.1 It can be
activated via two reaction pathways: the classic pathway, which
is triggered primarily by cell-bound immune complexes, and the
alternative pathway, which is activated primarily by foreign
bodies, such as microorganisms. The complement component C3 is a key
protein in both
Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, Michigan
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