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Typically, acne vulgaris presents in adolescence with chronic, waxing and waning lesions. A variety of lesions are present, including inflammatory papules, pustules, comedones, and nodulocysts over the face, chest, and back.


  1. Description of lesion: inflammatory papules, pustules, comedones, and nodulocysts over the face, chest, and back (see Figure 29-2).

  2. Acne is a highly prevalent condition, most common during mid-to-late adolescence.

  3. Acne may persist beyond adolescence, especially in women.

  4. Acne is caused by the obstruction of sebaceous follicles on the face and trunk. Three factors are involved in the development of the lesions:

    1. Increased sebum is produced (androgen dependent) and accumulates in follicles.

    2. Desquamation of epithelial cells and keratin into sebum-rich follicles causes obstruction.

    3. Inflammation develops as the anaerobe Propionibacterium acnes proliferates in this closed environment.

  5. Although the 3 factors discussed above are responsible for most cases of acne, it is important to keep in mind other factors that may contribute to the disease.

    1. Hyperandrogen states (most commonly polycystic ovary syndrome [PCOS] or androgenic progestins in contraceptives).

    2. Exposure to topical comedogens (cocoa butter, mineral oil, lanolin, fatty acids).

    3. Numerous factors that lead to follicular obstruction (eg, habits or clothing that cause skin trauma or obstruct pores, hot humid environments or heavy sweating leading to keratin over-hydration).

    4. Medications known to trigger or exacerbate acne (eg, corticosteroids, isoniazid, lithium, androgens).


  1. The diagnosis is typically clinical.

  2. Work-up for hyperandrogenism is appropriate when there are signs of polycystic ovary disease, virilization, or an atypical presentation (such as later in life).


  1. Identify and remedy the acne precipitants discussed above.

  2. Review general skin care techniques for acne-prone skin.

    1. Vigorous scrubbing can aggravate acne by promoting the development of inflammatory lesions.

    2. Abrasive cleaners and mechanical devices also aggravate acne by promoting inflammation.

    3. Use of one’s hands and a mild cleanser with lukewarm water is best.

    4. Use of moisturizers should be minimized and all cosmetics and lotions should be oil-free.

    5. Minimize contact of facial skin with hair gels and other styling products (pomade acne).

  3. Medical therapy is aimed at the 3 factors involved in acne development.

    1. Decreasing sebum production

      1. No topical therapies are effective

      2. Estrogen

        1. Most effective at doses of > 50 mcg of ethinyl estradiol

        2. Common oral contraceptive pills containing ≤ 35 mcg ethinyl estradiol are still helpful.

      3. Antiandrogens (spironolactone)

      4. Isotretinoin (see later discussion)

    2. Alteration of epithelial turnover and cohesiveness

      1. Topical retinoids: tretinoin, tazarotene

      2. Adapalene: a naphthoic acid with retinoid activity

    3. P acnes proliferation and accompanying inflammation

      1. Topical antibiotics

        1. Erythromycin

        2. Clindamycin

        3. Metronidazole

        4. Benzoyl peroxide

      2. Systemic antibiotics

        1. Tetracycline class

        2. Macrolide class

        3. Trimethoprim/sulfamethoxazole

  4. Guidelines for the use of these medications are as follows:

    1. Predominantly comedonal acne: retinoid or adapalene

    2. Mild inflammatory acne: topical antibiotic and benzoyl peroxide with or without retinoid or adapalene

    3. Moderate to severe but noncystic inflammatory acne: systemic antibiotic in combination with a topical retinoid

    4. Nodular cystic acne: ...

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