Acne Vulgaris in Skin of Color: Understanding Nuances and Optimizing Treatment Outcomes

June 2014 | Volume 13 | Issue 6 | Supplement Individual Articles | 61 | Copyright © June 2014

Andrew F. Alexis MD MPH

Skin of Color Center, Mount Sinai St. Luke’s Roosevelt Hospital, New York, NY
Icahn School of Medicine at Mount Sinai, New York, NY

However, more recent evidence supports the notion that subclinical inflammation is not unique to skin of color, but rather a pathogenic feature of acne in general. In an immunohistochemical study examining biopsies of clinically normal perifollicular skin, clinically inflamed acne lesions, and control samples from subjects without acne, Jeremy et al15 found that levels of interlekin- 1 (a proinflammtory cytokine) were upregulated in perifollicular skin. In addition, numbers of CD3+, CD4+ T-lymphocytes were increased in perifollicular skin compared with controls.15 Taken together, inflammatory responses may be a primary event in the pathogenesis of acne and can precede the development of clinically detectable acne lesions.
Subclinical inflammation in acne is of particular importance to skin of color given the risk of postinflammatory pigment alteration. Inflammatory mediators including prostaglandins and leukotrienes have been shown to stimulate melanocyte pigment production.16 Therefore, it is plausible that effective control of inflammation (both clinical and subclinical) may reduce the severity and number of hyperpigmented macules associated with acne in skin of color.
An important driver of inflammatory responses associated with acne is the bacterium, Propionibacterium acnes. There is evidence that P. acnes activates innate immunity via tolllike receptor 2 (TLR-2) leading to release of interleulin (IL)-1α from keratinocytes, which in turn stimulates follicular hyperkeratinization and the formation of the microcomedo.17 It has recently been shown that P. acnes activates inflammasomes leading to the production of IL-1β by monocytes, which could contribute to increased inflammation.17,18 Targeting P. acnes is therefore a core strategy in the management of acne and its associated inflammatory responses.

Implications for Treatment

The greater tendency toward dyspigmentation and keloid scarring in patients with skin of color has important therapeutic implications.
  1. Early and aggressive control of acne-associated inflammation is imperative. This can be accomplished with the use of a well-rounded treatment regimen that targets multiple factors in the pathogenesis of the disease and includes agents with anti-inflammatory properties. Acne treatments with anti-inflammatory effects include topical retinoids, the oral tetracycline antibiotics, topical dapsone, and azelaic acid. Among the retinoids, the anti-inflammatory activity of adapalene has been the most studied. Adapalene has been shown in vitro and in vivo to decrease expression of toll-like receptor (TLR)-2 (a receptor of the innate immune system) and IL-10 (an anti-inflammatory cytokine). (Zuliani T et al. Exp Dermatol. 2011;20:850-853.) In addition, adapalene increases expression of CD1d – a cell surface glycoprotein that plays a role in antigen presentation and induction of cutaneous inflammatory responses. Other anti-inflammatory effects of adapalene include inhibition of arachadonic acid metabolism, neutrophil chemotaxis, and free radical production.19 Benzoyl peroxide (BPO), through its microbicidal effects, indirectly reduces inflammation by killing P. acnes – a trigger of acne-associated inflammation.

    A well rounded regimen includes a multi-pronged approach to address the multiple pathogenic factors associated with acne, including follicular hyperkeratinization, P. acnes inflammation, and increased sebum production. Therefore, combination topical regimens that include a topical retinoid, a BPO, and/or an immunomodulating agent (eg, dapsone, azelaic acid) tend to be the most effective.

    Under-treatment of acne in patients with skin of color should be avoided, given the greater risk of dyspigmentation and keloidal scarring (in more severe cases). As such, the threshold for using oral antibiotics (for their anti-inflammatory and anti-P. acnes effects) in the appropriate patient is low. Regimens that initially include oral doxycycline or minocycline in combination with a topical retinoid followed by maintenance with a topical retinoid is a well-established long-term treatment strategy in the general acne population,20,21 and is particularly well suited to patients with skin of color.

    Oral isotretinoin should also be considered for the appropriate patient with severe inflammatory acne who is at risk for scarring, as well as for patients who fail oral antibiotics. It has been reported based on U.S. National Ambulatory Medical Care Survey data that isotretinoin is less frequently prescribed to blacks than to whites; cost may contribute to this disparity, but patient and provider biases as well as racial differences in severity cannot be ruled out.22 When warranted, oral isotretinoin should be considered early in the course of nodulocystic or other severe forms of acne in patients with skin of color.

    In cases of severely inflamed papules or nodulocystic lesions, the use of intralesional corticosteroid injections (typically triamcinolone acetonide 2.5 mg/mL to 3.3. mg/ mL) to rapidly reduce local inflammation is an effective