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Wiley InterScience

Clinical and Experimental Dermatology

Clinical and Experimental Dermatology

Volume 29 Issue 3, Pages 297 - 299

Published Online: 29 Apr 2004

Journal compilation © 2010 British Association of Dermatologists



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Experimental dermatology • Concise report
Remission of rosacea induced by reduction of gut transit time
S. N. Kendall
Mathematics Institute, University of Warwick, Coventry, UK
Correspondence to S. N. Kendall, Mathematics Institute, University of Warwick, Gibbet Hill Road, Coventry CV4 7AL, UK.
E-mail: skendall@boltblue.net
Copyright 2004 Blackwell Publishing Ltd

Summary

AbstractReportAcknowledgementsReferences

Rosacea is a chronic disorder characterized by hypersensitivity of the facial vasculature, presenting with intense flushing eventually leading to chronic erythema and telangiectasia. Although the precise aetiology of rosacea is not known, numerous associations with inflammatory gastrointestinal tract disorders have been reported. Furthermore, substance P-immunoreactive neurones occur in considerably greater numbers in tissue surrounding affected blood vessels suggesting involvement of neurogenic inflammation and moreover plasma kallikrein–kinin activation is consistently found in patients. In this report, a patient without digestive tract disease is described, who experienced complete remission of rosacea symptoms following ingestion of a material intended to sweep through the digestive tract and reduce transit time below 30 h. It is possible that intestinal bacteria are capable of plasma kallikrein–kinin activation and that flushing symptoms and the development of other characteristic features of rosacea result from frequent episodes of neurogenic inflammation caused by bradykinin-induced hypersensitization of facial afferent neurones. The possible relevance of this hypothesis to other conditions featuring afferent hypersensitivity, such as fibromyalgia, is considered.


Accepted for publication 21 October 2003

DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1365-2230.2004.01461.x About DOI

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