Abstract
Rosacea is a disorder the affects millions of people and remains unexplained in terms of its pathophysiology. Many hypothesis have been put forward bun none has led to the breakthrough that so many researchers want. I believe that this is due in part because of the nature of basic research that limits forward movement to small steps, each adding another piece to the puzzle, but not enough to allow for completion of the big picture. I have been fortunate enough to have treated a patient who developed Rosacea as a consequence of another medical problem, thus allowing me to start with the big picture and work back through the pathophysiology and determine how this could have happened. The disorder in question is renovascular hypertension which occurred as a result of an acute renal artery dissection. The renin angiotensin system is activated in this situation and the cascade of events that follows can both initiate and sustain a state of vasodilation in the vasculature of the face that results in the clinical expression of Rosacea. Hypertension and Rosacea are recognized as comorbid conditions that are linked in s severity dependent manner and the hypothesis presented in this paper explains why this is so. It also presents the Angiotensin AT2 receptor as a possible target for therapeutic intervention.
Highlights
Effective therapy for Rosacea has been described as one of the great unmet needs in dermatology [1]
In a recent review in 2018, the authors concluded that what we need to know most is what the key mediators and receptors involved in Rosacea are [2]
I will offer a proposal of what I believe to be the pathophysiology of Rosacea and the clinical case which serves as a model for it
Summary
Effective therapy for Rosacea has been described as one of the great unmet needs in dermatology [1]. This is a disease which has eluded talented researchers for many years and continues to present questions which remain unanswered. Rosacea is an external manifestation of an internal disorder characterized by elevated levels, either local or systemic or both, of Angiotensin II. This causes stimulation of the AT2 receptor, production of bradykinin, nitric oxide, and a cascade of inflammatory mediators in the vasculature of the face which result in a state of chronic vasodilation and inflammation. Journal of Clinical and Cosmetic Dermatology Open Access Journal arm- that cause vasodilation and inflammation by acting through one common pathway (Figure 1)
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