bradykinin and neurogenic inflamation - a possible aetiology ?

Seth Kendall has been a member of rosacea-support for a few years. He posted a message in March 2003 with the subject “A new explanation for rosacea”. This looked like a draft paper that was titled A NOVEL METHOD FOR INDUCING REMISSION IN ROSACEA AND A NEW HYPOTHESIS TO ACCOUNT FOR ITS AETIOLOGY. Since then Seth has succeeded in getting his ideas from this paper published in a journal. Well done Seth ! Seth’s ideas about the aetiology of rosacea centre around intestinal health and bradykinin (a vasoactive nonapeptide) acting on sensory neurons which then release vasodilatory substances.

Feel free to contact him for a full copy of the article. I hope we get to hear some more from Seth in the future.

Remission of rosacea induced by reduction of gut transit time, Clinical & Experimental Dermatology Volume 29 Issue 3 Page 297 - May 2004, Experimental dermatology, S. N. Kendall

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.

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