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Clinical Presentation

The pathogenesis of acne involves four key processes 1–3

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Four key processes

Androgens lead to increased sebum production 2 3

  • Sebum is produced by the pilosebaceous glands, which are predominantly found on the face, back and chest
  • This may be due to an increased response to normal levels of androgens

Comedone formation 2 3

  • Abnormal proliferation and differentiation of keratinocytes leads to comedone formation

Colonisation with Propionibacterium acnes (P. acnes) 2 3

  • Sebum and comedone formation alters the micro environment in the pilosebaceous duct, which leads to colonisation of the duct

Inflammation 2 3

  • Acne lesions begin with an initial inflammatory event, triggered by an infiltration of inflammatory cells

Stages of acne 4

Stages of acne

Stages of acne. (A) Normal follicle; (B) open comedone (blackhead); (C) closed comedone (whitehead); (D) papule; (E) pustule.

  • Non-inflammatory lesions

    Comedones are non-inflammatory acne lesions that may be open or closed. 7

    Open comedones (blackheads):

    • Open comedones or blackheads are raised brown/black lesions up to 5 mm in diameter 1
    • They are small follicles with dilated openings to the skin allowing oxidation of the debris within the follicle leading to the black colour 7
    Open comedones

    Closed comedones (whiteheads):

    • Closed comedones or whiteheads are small plugged follicles, which are often inconspicuous (up to 3 mm diameter) with no visible follicular opening 1 7 8
    Closed comedones

  • Inflammatory lesions

    Papules:

    • When lesions become red and/or tender bumps they are termed papules (3-5 mm in diameter) 1 7

    Pustules:

    • When lesions fill with purulent material (pus) they become pustules (5 mm or less in diameter) 1 7

    Papulopustular acne

    Pustules

    Nodules:

    • As lesions progress to become larger and more tender, they are termed nodules 7
    • Nodules are defined as firm, inflamed lesions >10 mm diameter, painful by palpation 8

    Nodularcystic acne

    Nodules

Common causes of acne 2

  • Increased androgens/sebum production in puberty
  • Hormones
  • Resistance bacteria
  • Use of cosmetics
  • Drugs
  • Smoking
  • Stress (increased androgen production)
  • Genetics

References:

  1. Bhate K et al. Br J Dermatol 2013;168(3):474–485.
  2. Yentzer BA et al. Cutis 2010;86:94–99.
  3. Ayer J et al. Postgrad Med J 2006;82:500–506.
  4. Williams C et al. Am J Clin Dermatol 2006;7(5):281–290.
  5. Dunn LK et al. Derm Online J 2011;17(1):1.
  6. Krakowski AC et al. Pediatr Dermatol 2008;25(Suppl 1):1–14.
  7. Primary Care Dermatology Society. Acne Vulgaris. Available at: www.pcds.org.uk/clinical-guidance/acne-vulgaris. (Accessed March 2017).
  8. Dawson AL, Dellavalle RP et al. Br Med J 2013;346:f2634.
  9. Goodman G. Am J Clin Dermatol 2009;10(Suppl. 1):1–6.
  10. Layton AM. Am J Clin Dermatol 2001;2(3):135–141.

Adverse events should be reported directly to the HPRA; Freepost, Pharmacovigilance Section, Health Products Regulatory Authority, Earlsfort Terrace, Dublin 2, Tel: +353 1 676 4971 medsafety@hpra.ie. Adverse events should also be reported to GlaxoSmithKline on 1800 244 255.

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