INTRODUCTION
Rosacea is a chronic inflammatory facial skin condition characterized by episodic or persistent erythema, edema, telangiectasias, and/or inflammatory papules and pustules.1 The global prevalence of rosacea is approximately 5.46%, with an estimated therapeutic market of 2.08 billion USD in 2024 that continues to grow.2,3 In some patients, phymatous or ocular changes may occur. Due to the visible nature of the disease and associated symptoms of pruritus, burning, and stinging, patients with rosacea experience significant psychosocial burden, including embarrassment, social anxiety, and depression.4,5
The four main subtypes of rosacea include erythematotelangiectatic (Type 1), papulopustular (Type 2), phymatous (Type 3), and ocular rosacea (Type 4).5 Acneiform or papulopustular rosacea (PPR) represents approximately 43% of cases and presents with papules and pus-filled blemishes, with or without facial flushing.6,7 While the pathogenesis is incompletely understood, rosacea arises from an interplay of environmental exposures, genetic susceptibility, and dysregulated innate and adaptive immune responses.8 Common triggers include ultraviolet exposure, temperature extremes, alcohol, spicy foods, and psychophysiologic stress.8 Increased signaling of the antimicrobial peptide LL-37 (cathelicidin), which interacts with toll-like receptor 2 (TLR2), further promotes activation of innate immune cells, neutrophilic infiltration, and the release of proinflammatory cytokines (eg, TNF-α, IL-6, IL-1β).9 Furthermore, Demodex mites are thought to play a central role in the pathophysiology of PPR, as high mite densities are observed in nearly all impacted patients.10 The mites may promote inflammation by burrowing into sebaceous glands and hair follicles, disrupting the skin barrier, and stimulating immune responses.10
Available therapies for PPR address distinct elements of disease pathophysiology. Ivermectin has antiparasitic activity against Demodex mites; azelaic acid, metronidazole, and tetracycline-class agents are used primarily for their anti-
The four main subtypes of rosacea include erythematotelangiectatic (Type 1), papulopustular (Type 2), phymatous (Type 3), and ocular rosacea (Type 4).5 Acneiform or papulopustular rosacea (PPR) represents approximately 43% of cases and presents with papules and pus-filled blemishes, with or without facial flushing.6,7 While the pathogenesis is incompletely understood, rosacea arises from an interplay of environmental exposures, genetic susceptibility, and dysregulated innate and adaptive immune responses.8 Common triggers include ultraviolet exposure, temperature extremes, alcohol, spicy foods, and psychophysiologic stress.8 Increased signaling of the antimicrobial peptide LL-37 (cathelicidin), which interacts with toll-like receptor 2 (TLR2), further promotes activation of innate immune cells, neutrophilic infiltration, and the release of proinflammatory cytokines (eg, TNF-α, IL-6, IL-1β).9 Furthermore, Demodex mites are thought to play a central role in the pathophysiology of PPR, as high mite densities are observed in nearly all impacted patients.10 The mites may promote inflammation by burrowing into sebaceous glands and hair follicles, disrupting the skin barrier, and stimulating immune responses.10
Available therapies for PPR address distinct elements of disease pathophysiology. Ivermectin has antiparasitic activity against Demodex mites; azelaic acid, metronidazole, and tetracycline-class agents are used primarily for their anti-
