Thursday, September 11, 2008

Acne Vulgaris

Acne ulgaris

Major points

  • Most prevalent skin disorder in pediatrics
1. Affects 40% of children aged 8–10 years
2. Affects 85% of adolescents aged 15–17 years
  • Lesion types:
1. Comedones: obstructive lesions
a. Microcomedone: microscopic plugging of the hair follicle that is the precursor lesion to
acne vulgaris
b. Open comedone (blackhead): plugging at the follicular opening; cellular plug of stratum
corneum with oxidized melanin within the follicle (Figure 1)

Figure 1 Comedonal acne - on forehead with open and closed comedones

c. Closed comedone (whitehead): plugging of the pilosebaceous unit just below the
follicular opening with cystic swelling of the duct; filled with cellular debris
2. Inflamatory lesions: papules, pustules, cysts, sinus tracts (Figures 2–4)
3. Scars: depressed, pitted, macular, papular, hypertrophic, keloidal
  • Acne is one of the earliest stages of adrenarche
  • Lesion type often correlates with pubertal stage
    1. Comedonal acne is predominant type in prepubertal children
    2. Inflammatory acne is more prevalent in adolescents
  • Develops in areas with high numbers of pilosebaceous units: face, chest, back
  • Increased severity often predicted by earlier onset and positive family history of scarring acne

Figure 2 Papulopustular acne - numerous erythematous papules and pustules on the face

Figure 3 Cystic acne on the chest with erythematous nodules, crusts and scarring

Figure 4 Inflammatory acne with comedones, erythematous papules and nodules on the back of a teenager


  • Acne development is a complex process that involves four main contributing factors :
    1. Abnormal keratinization and obstruction of the pilosebaceous unit
    a. Initial lesion is a microcomedone; caused by obstruction of the follicular opening with
    the accumulation of cellular debris
    b. Obstruction is due to abnormal keratinization of the cells lining the follicle with delayed
    shedding and increased cohesiveness
    2. Hormonal stimulation and increased sebum production
    a. Increased secretion and accumulation of sebum within the follicle which is stimulated
    by increased adrenal and gonadal androgens that occur with adrenache
    b. Poly cystic ovary syndrome, a heterogeneous disorder with altered gonadotropin
    secretion, hyperandrogenism (acne, hirsutism and virilization), chronic anovulation,
    obesity and insulin resistance
    3. Bacterial overgrowth
    a. Propionibacterium acnes overgrows within the dilated follicle
    b. Bacterial lipases convert accumulated sebum triglycerides into free fatty acids that
    cause inflammation
    c. P. acnes also releases other proteolytic enzymes and chemotactic factors that further
    stimulate inflammation and recruitment of polymorphonuclear cells (PMNs)
    4. Inflammatory reaction
    a. Inflammatory cells including PMNs are recruited to the area
    b. Ingestion of bacteria by PMNs causes release of hydrolytic enzymes that causes
    rupture of the follicular wall
    c. This leads to intense inflammation and a surrounding foreign body reaction
  • Clinical findings
Differential diagnosis
  • Drug-induced acne
  • Chemical-induced acne
  • Rosacea
  • Gram-negative folliculitis
  • Pityrosporum folliculitis
  • Topical retinoids: important for normalizing keratinization (e.g. tretinoin, adapalene)
  • Topical keratolytics: salicylic acid, azelaic acid
  • Topical benzoyl peroxide preparations
  • Topical antibiotics: clindamycin, erythromycin
  • Systemic antibiotics for inflammatory lesions
    1. Doxycycline, tetracycline and minocycline most commonly used in those >9 years of age
  • Systemic retinoids for severe cystic acne or early scarring
  • Oral contraceptives
  • Can have significant impact on social interactions and self-esteem and can lead to depression in severe cases
  • May produce significant scarring in inflammatory and cystic lesions
  • Can rarely be associated with an underlying endocrine disorder
Cunliffe WJ, Holand DB, Clark SM, Stable GI. Comedogenesis: some new aetiological, clinical and therapeutic strategies. Br J Dermatol 2000; 142: 1084–91
Harper JC, Thiboutot DM. Pathogenesis of acne: recent research advances. Adv Dermatol 2003; 19: 1–10
Lee DJ, VanDyke GS, Kim J. Update on pathogenesis and treatment of acne. Curr Opin Pediatr 2003; 15: 405–10
Leyden JJ. A review of the use of combination therapies for the treatment of acne vulgaris. J Am Acad Dermatol 2003; 49: S200–10
Lucky AW, Biro FM, Simbartl LA, et al. Predictors of severity of acne vulgaris in young adolescent girls: results of a five-year longitudinal study. J Pediatr 1997; 130: 30–9
Weiss JS. Current options for topical treatment of acne vulgaris. Pediatr Dermatol 1997; 14: 480–8


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