(Stroke. 2002;33:1163.)
© 2002 American Heart Association, Inc.
Letters to the Editor |
Institute of Clinical Physiology, National Research Council - CNR, Pisa, Italy
Department of Experimental Pathology, University of Pisa Medical School, Pisa, Italy
To the Editor:
In a recent issue of Stroke, Jousilahti et al reported on the association of stroke with serum levels of gamma-glutamyltransferase (GGT) and alcohol consumption in a cohort of more than 14 000 subjects.1 In particular, the authors observed that the incidence of ischemic stroke had a good correlation with serum GGTwhich they interpreted as a surrogate marker of alcohol consumptionin both genders (relative risk in men 1.29, 95% CI 1.04 to 1.60; in women 1.42, 95% CI 1.10 to 1.84). On the other hand, no correlation of ischemic stroke was observed with the self-reported individual alcohol intakes, although "a significant linear increasing trend in the mean levels of self-reported alcohol drinking by quartiles of the serum GGT" was found. The obvious conclusion is that GGT is an independent risk factor for ischemic stroke, irrespective of alcohol drinking, whereas the authors concluded that answers given by patients to questionnaires concerning their lifestyles are unreliable and that serum GGT is a more faithful indicator of alcohol consumption, ie, the actual determinant of stroke occurrence.
We would like to suggest an alternative explanation to the findings of this study, based on previous evidence in the literature in favor of a direct GGT involvement in atherosclerotic plaque complication. GGT, present in serum and on the surface of most cell types, is the enzyme responsible for the extracellular catabolism of glutathione, the main antioxidant in mammalian cells, and its role in cardiovascular diseases may be more complex than currently thought.2 While it is certainly
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