INTRODUCTION
Acne vulgaris is the most common inflammatory dermatosis worldwide. While it presents in 95% to 100% of men and 83% to 85% of women during puberty,1 acne commonly extends into adulthood,2 and can result in disfiguring sequelae such as scarring, post-inflammatory erythema (PIE), and post-inflammatory hyperpigmentation (PIH). This post-inflammatory dyschromia poses a significant psychological burden on acne patients, often accounting for greater concern than the original acne lesions, and reducing quality of life.3 For this reason, the management and treatment of post-inflammatory dyschromia represents a large proportion of the clinical, emotional, and economic burden associated with acne vulgaris.4 Importantly, this burden most commonly and disproportionately affects skin of color (SOC) patients,5 and can be the most distressing aspect of acne in skin of color patients with Fitzpatrick skin phototypes IV to VI.6,7
A disease of the pilosebaceous unit, acne vulgaris is a result of multiple different pathologic processes, ranging from increased sebum production, lipid oxidation, and free radical exacerbation in antioxidant-poor skin.8 The resultant inflammatory cascade has been hypothesized to stimulate angiogenesis and melanogenesis that underlie PIE and PIH.9,10 Recent observations have also implicated aberrant and long-term B-cell mediated inflammation in the development of post-inflammatory dyschromia and scarring following acne,11 suggesting a new potential mechanistic arm for treatment and the role of combination therapy.12 These dyschromias are amplified in phototypes rich in melanin, with some studies reporting PIH prevalence as high as 65% in Black patients and 48% in Hispanic patients, when compared with 25% PIH in White patients.13 This is likely related to the greater number and size of melanosomes in SOC, which may be overstimulated in the setting of chronic inflammation.14,15 Therefore, acne-related
A disease of the pilosebaceous unit, acne vulgaris is a result of multiple different pathologic processes, ranging from increased sebum production, lipid oxidation, and free radical exacerbation in antioxidant-poor skin.8 The resultant inflammatory cascade has been hypothesized to stimulate angiogenesis and melanogenesis that underlie PIE and PIH.9,10 Recent observations have also implicated aberrant and long-term B-cell mediated inflammation in the development of post-inflammatory dyschromia and scarring following acne,11 suggesting a new potential mechanistic arm for treatment and the role of combination therapy.12 These dyschromias are amplified in phototypes rich in melanin, with some studies reporting PIH prevalence as high as 65% in Black patients and 48% in Hispanic patients, when compared with 25% PIH in White patients.13 This is likely related to the greater number and size of melanosomes in SOC, which may be overstimulated in the setting of chronic inflammation.14,15 Therefore, acne-related
