| Increases in cerebrospinal fluid caffeine concentration are associated with favorable outcome after severe traumatic brain injury in humans. | |
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MedLine Citation:
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PMID: 17684518 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Caffeine, the most widely consumed psychoactive drug and a weak adenosine receptor antagonist, can be neuroprotective or neurotoxic depending on the experimental model or neurologic disorder. However, its contribution to pathophysiology and outcome in traumatic brain injury (TBI) in humans is undefined. We assessed serial cerebrospinal fluid (CSF) concentrations of caffeine and its metabolites (theobromine, paraxanthine, and theophylline) by high-pressure liquid chromatography/ultraviolet in 97 ventricular CSF samples from an established bank, from 30 adults with severe TBI. We prospectively selected a threshold caffeine level of > or = 1 micromol/L (194 ng/mL) as clinically significant. Demographics, Glasgow Coma Scale (GCS) score, admission blood alcohol level, and 6-month dichotomized Glasgow Outcome Scale (GOS) score were assessed. Mean time from injury to initial CSF sampling was 10.77+/-3.13 h. On initial sampling, caffeine was detected in 24 of 30 patients, and the threshold was achieved in 9 patients. Favorable GOS was seen more often in patients with CSF caffeine concentration > or = versus < the threshold (55.6 versus 11.8%, P=0.028). Gender, age, admission CGS score, admission blood alcohol level, and admission systolic arterial blood pressure did not differ between patients with CSF caffeine concentration > or = versus < the threshold. Increases in CSF concentrations of the caffeine metabolites theobromine and paraxanthine were also associated with favorable outcome (P=0.018 and 0.056, respectively). Caffeine and its metabolites are commonly detected in CSF in patients with severe TBI and in an exploratory assessment are associated with favorable outcome. We speculate that caffeine may be neuroprotective by long-term upregulation of adenosine A1 receptors or acute inhibition of A2a receptors. |
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Authors:
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Kathleen T Sachse; Edwin K Jackson; Stephen R Wisniewski; Delbert G Gillespie; Ava M Puccio; Robert S B Clark; C Edward Dixon; Patrick M Kochanek |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2007-08-08 |
Journal Detail:
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Title: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism Volume: 28 ISSN: 0271-678X ISO Abbreviation: J. Cereb. Blood Flow Metab. Publication Date: 2008 Feb |
Date Detail:
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Created Date: 2008-01-25 Completed Date: 2008-04-17 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8112566 Medline TA: J Cereb Blood Flow Metab Country: United States |
Other Details:
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Languages: eng Pagination: 395-401 Citation Subset: IM |
Affiliation:
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Department of Critical Care Medicine, Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aging / physiology Brain Injuries / cerebrospinal fluid* Caffeine / cerebrospinal fluid* Central Nervous System Depressants / blood Central Nervous System Stimulants / cerebrospinal fluid* Ethanol / blood Female Glasgow Coma Scale Glasgow Outcome Scale Humans Male Prospective Studies Theobromine / cerebrospinal fluid Theophylline / cerebrospinal fluid Treatment Outcome |
| Grant Support | |
ID/Acronym/Agency:
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DK68575/DK/NIDDK NIH HHS; NS30318/NS/NINDS NIH HHS; NS38087/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Central Nervous System Depressants; 0/Central Nervous System Stimulants; 58-08-2/Caffeine; 58-55-9/Theophylline; 611-59-6/1,7-dimethylxanthine; 64-17-5/Ethanol; 83-67-0/Theobromine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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