Optimizing the Use of Topical Brimonidine in Rosacea Management: Panel Recommendations

January 2015 | Volume 14 | Issue 1 | Original Article | 33 | Copyright © January 2015

Emil A. Tanghetti MD,1 J. Mark Jackson MD,2 Kevin Tate Belasco DO MS,3 Amanda Friedrichs MD,4 Firas Hougier MD,5 Sandra Marchese Johnson MD,6 Francisco A. Kerdel MD,7 Dimitry Palceski DO FAOCD,8 H. Chih-ho Hong MD FRCPC,9 Anna Hinek MD MSc FRCPC,10 Maria Jose Rueda Cadena MD11

1Center for Dermatology & Laser Surgery, Sacramento, CA
2University of Louisville, Louisville, KY
3Blue Harbor Dermatology, Newport Beach, CA
4Dekalb Clinic, Sycamore, IL
5Family Dermatology, Atlanta, GA
6Johnson Dermatology Clinic, Fort Smith, AR
7Florida Academic Dermatology, Miami, FL
8Reflections Dermatology, Orlando, FL
9SkinFitMD, Surrey, British Colombia
10University of Toronto, Mississauga, Ontario
11Galderma Laboratories, Fort Worth, TX

Rosacea is a chronic inflammatory disease with a complex pathophysiology that manifests with central facial redness with or without papulopustular lesions. Often, patients with rosacea present with a constellation of signs and symptoms; for best results, the treatment plan should take into account all symptoms manifesting in the individual patient. The first available pharmacologic treatment to address the redness associated with rosacea is topical brimonidine. In the United States, brimonidine topical gel 0.33% is indicated for persistent facial erythema of rosacea; approval was based on clinically significant efficacy and good safety data from large-scale clinical trials. Use of brimonidine in routine clinical practice has yielded new insights that elaborate on the findings from clinical trials. For example, real-world use has shown that a percentage of patients (in our experience, approximately 10 to 20%) treated with brimonidine experience a worsening of erythema that has been called “rebound.” Our routine use of this agent for >1 year has yielded strategies to set patient expectations, optimize treatment initiation, and minimize potential problems; this article details those strategies. Because we believe that the term “rebound” has been used to describe several physiologically distinct events, we have also proposed more specific terminology for such events.

J Drugs Dermatol. 2015;14(1):33-40.


The clinical features of rosacea, including facial redness, papules/pustules, flushing and, oftentimes, skin sensitivity, have long been known.1-3 New information from molecular-level studies has shown that rosacea is an extremely complex disease with multiple aberrancies occurring in a variety of cutaneous neural, immune, and vascular pathways.4-8 An understanding of these pathways has given dermatologists a better knowledge of the most appropriate treatment options for this disease.2, 4, 5 It is not the purpose of this article to review the clinical presentations of rosacea, as these have been covered elsewhere.9, 10 It should be noted that while rosacea can be categorized into subtypes based on clinical presentation (erythematotelangiectatic rosacea, papulopustular rosacea, phymatous rosacea, and/or ocular rosacea), most experts today view rosacea as a chronic inflammatory disease with a spectrum of clinical features that can wax and wane over time.2, 11, 12 In 2013, the American Acne and Rosacea Society recommended that “rosacea management is best approached via assessment of the spectrum of clinical manifestations present in each individual patient.”12 New additions to the rosacea treatment armamentarium – like topical brimonidine gel 0.33%, the first treatment approved for topical treatment of persistent (nontransient) facial erythema (US indication) of rosacea – have prompted clinicians to re-assess the overall approach to this complex disease.
Facial redness is an extremely common finding in patients with rosacea, affecting up to 87% of rosacea sufferers; it can be present in all subtypes of rosacea.13 The erythema associated with rosacea poses a challenge for patients and clinicians alike.5 Both vascular and inflammatory events are involved in the clinical manifestations of redness.4, 6 The complete pathophysi-