Prevalence of Nodulocystic Acne in White and Negro Males

Comparison of the epidemiology of acne vulgaris among Caucasian, Asian, Continental Indian and African American women

“…6 In the past, it was believed that inflammatory papulopustular acne was far more common among Caucasian patients than among African American patients. 19 A more recent investigation, however, found marked histological inflammation in comedonal acne lesions that appeared clinically to be non-inflammatory, which may explain why mild-to-moderate acne in African Americans results in scarring and hyperpigmentation. 20 In addition, it was observed that much of the melanin of postinflammatory hyperpigmented macules is epidermal and not dermal, suggesting that the relatively superficial location may facilitate topical approaches to the treatment of postinflammatory hyperpigmentation and that darker skin types may benefit from anti-inflammatory treatments.…”

Acne vulgaris in Nigerian adolescents – prevalence, severity, beliefs, perceptions, and practices

“…Three hundred and fifty-three of the 379 students (93.1%) had mild acne (GAGS score, 1-18), but only 26 of the 379 students (6.9%) had moderate disease (GAGS score, [19][20][21][22][23][24][25][26][27][28][29][30]. No student was adjudged to have severe or very severe disease (GAGS score, > 31).…”

Photodynamic therapy for acne vulgaris: A critical review from basics to clinical practice

“…7 Classically, acne vulgaris is classified according to lesion morphology and severity. Noninflammatory lesions (comedones) and inflammatory lesions (papules, pustules, nodules, and cysts) occur in mixed presentations.…”

“…Hypotheses on its pathophysiology include: (1) follicular hyperkeratosis with inflammation leading to obstruction of sebaceous follicles, mediated in large part by interleukin-1 (IL-1) 8 ; (2) subnormal levels of linoleic acid 9 ; (3) external causes of follicular occlusion; (4) local or systemic hormonal changes, notably androgens and especially dihydrotestosterone (DHT); (5) bacteria and other microorganisms that colonize sebaceous follicles, in particular Propionibacterium acnes, that may contribute to immune stimulation and that metabolize sebum to irritating substances, such as free fatty acids and triglycerides 10 ; and (6) hereditary (eg, XYY genotype), 7,11 (7) inflammatory, 12 and (8) immunologic 8,13 factors. P acnes is also implicated in triggering skin inflammatory/immune response, by activating Toll-like receptor 2 (TLR-2) on monocytes and macrophages surrounding the sebaceous follicle, 14 which release interleukins (eg, IL-1, IL-8, and IL-12) and tumor necrosis factor-alfa (TNF-a).…”