Clinical Review

Clinical reviewAcne vulgarisCommentary: A UK primary care perspective on treating acne

BMJ 2002; 325 doi: 10.1136/bmj.325.7362.475 (Published 31 August 2002)
Cite this as: BMJ 2002;325:475.1

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Acne vulgaris

  1. Guy F Webster, professor (Guy.Webster@mail.tju.edu)
  1. Department of Dermatology, Jefferson Medical College, Philadelphia, PA 19107, USA
  2. aQueens Park Medical Centre, Stockton-on-Tees TS18 2AW
  3. bClinical Trial Unit, Department of Dermatology, General Infirmary, Leeds LS1 3EX

    Acne may be common, but it causes considerable distress and doctors should treat it effectively, not trivialise it

    Acne vulgaris is common and affects nearly all adolescents and adults at some time in their lives. Although overall health is not impaired, acne is not a trivial disease; it can produce cutaneous and emotional scars that last a lifetime. 1 2 Numerous psychological problems stem from acne, even resulting in decreased employability in adulthood.3 Fortunately, acne is eminently treatable, and this review provides an outline of current treatments.

    Summary points

    • Acne is a multifactorial disease which, although not life threatening, has profound effects on patients

    • The microcomedo is the primary lesion in acne

    • Reduction of comedones and Propionibacterium acnes is the main aim of treatment

    • Most effective acne regimens treat inflammatory and comedonal acne lesions with a combination of antibacterial and retinoid drugs

    Sources and selection criteria

    A literature review augmented my extensive experience of the topic. I used Entrez PubMed for all literature searches.

    Pathogenesis

    Acne has a complex aetiology, involving abnormal keratinisation, hormonal function, bacterial growth, and immune hypersensitivity. 1 2 The disease is limited to pilosebaceous follicles of the head and upper trunk because the sebaceous glands in these regions are particularly active. The primary acne lesion is the “blackhead” (microcomedo), an impaction and distension of the follicle with improperly desquamated keratinocytes and sebum. The stimulus for comedogenesis is uncertain.

    At puberty, when androgens stimulate the production of sebum, pre-existing comedones become filled with lipid and may enlarge to become visible. Subsequently, some patients also begin to show signs of inflammation. Comedones that become inflamed are nearly always clinically invisible before the pimple develops.

    Inflammatory acne is the result of the host response to the follicular inhabitant Propionibacterium acnes, 1 4 which is a member of the normal flora and is a harmless …

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