Evidence of Barrier Deficiency in Rosacea and the Importance of Integrating OTC Skincare Products into Treatment Regimens

April 2021 | Volume 20 | Issue 4 | Original Article | 384 | Copyright © April 2021


Published online March 16, 2021

Hilary Baldwin MDa, Andrew F. Alexis MD MPHb, Anneke Andriessen PhDc, Diane S. Berson MD FAADd, Patricia Farris MD FAADe, Julie Harper MDf, Edward Lain MD FAADg, Shari Marchbein MDh, Linda Stein Gold MDi, Jerry Tan FRCPCj

aAcne Treatment & Research Center, Brooklyn, NY
bIcahn School of Medicine at Mount Sinai, New York, NY
cRadboud UMC Nijmegen, Andriessen Consultants, Malden, The Netherlands
dCornell University Weill Medical College, Weill Cornell Medical Center, Dermatology, New York, NY
eTulane University School of Medicine, New Orleans, LA; Sanova Dermatology, Metairie, LA
fThe Dermatology and Skin Care Center of Birmingham, Birmingham, AL
gSanova Dermatology, Austin TX; Austin Institute for Clinical Research, Austin, TX
hNYU School of Medicine, New York, NY
iHenry Ford Health System, Detroit, MI
jRoyal College of Physicians and Surgeons of Canada; Schulich School of Medicine and Dentistry, Department of Medicine, Western University, Windsor, ON, Canada; Windsor Clinical Research Inc; The Healthy Image Centre, Windsor, ON, Canada



of a highly ordered 3-dimensional structure. Ceramides – of which there are many varieties - compose about 50% of the total lipids and are highly location-specific. Abnormalities in ceramide composition alter the stratum corneum's physiologic properties and contribute to barrier dysfunction and disease. Ceramide levels are reduced or structurally aberrant in psoriasis, ichthyosis, acne, AD, and skin damaged by surfactants.3,18-22 The use of ceramide-containing skincare products has been shown to restore ceramide composition and improve skin function and disease severity.23-26

Evidence for barrier dysfunction in rosacea
Although physicians may accept that rosacea is a barrier defect disorder, data have been primarily circumstantial until recently. Data that point to barrier deficiency in rosacea includes evidence of increased trans-epidermal water loss (TEWL), decreased skin hydration, increased stratum corneum (SC) pH, increased lactic acid stinger reaction, symptoms of itch, burn, and sting, and an increased incidence of irritant and allergic contact dermatitis.9,27-31 Still lacking is the identification of specific lipid abnormalities in rosacea-prone skin.

TEWL and skin hydration in both rosacea and AD were evaluated in a study exploring skin barrier function.9 The skin's irritation threshold to different sodium lauryl sulfate concentrations was assessed on the volar forearm and nasolabial fold in ninetyone patients with AD, rosacea, and healthy individuals. TEWL was higher (P=0.127) in AD patients compared to rosacea, which exceeded that of healthy patients. Skin hydration was decreased equally in atopic and rosacea patients compared to controls. Patients with AD showed enhanced susceptibility to sodium lauryl sulfate in comparison with rosacea and healthy subjects. In the rosacea patients, skin barrier impairment was limited to the area affected by rosacea, indicating that rosacea as an inflammatory disease is not generally related to an impaired barrier function, unlike AD. The authors, therefore, theorized skin physiology deterioration to be a consequence of inflammation.9

A study evaluating 135 patients with rosacea found that the erythematotelangiectatic form of rosacea occurs more frequently in dry skin than in seborrheic skin, while normal sebum levels were found in those with the predominantly papulopustular disease.7 However, the authors did note an imbalance in fatty acid concentration in patients with papulopustular disease that may influence skin barrier integrity. Notably, a significant reduction in skin hydration level persisted even after clinical improvement with oral minocycline.

Lonne-Rahm and co-workers evaluated a 5% lactic acid stinging reaction in 32 rosacea patients.29 This test is used to measure subjective skin irritation and constitutes a clinical measure of barrier function. Twenty-five patients were identified as having papulopustular disease, while seven had the erythematotelangiectatic type. They were compared to 32 healthy individuals. All patients with vascular disease were considered "stingers," compared to 68% of those with papules, pustules, and 19% of controls. SC permeability disruption was presumed to be the cause of the heightened response.