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Acne vulgaris is one of the most common cutaneous disorders and occurs in more than 85% of individuals between the ages of 12 to 24 years.1The degree of involvement is quite variable. Many individuals have mild to moderate disease of a transient nature; however, others develop severe disease that can lead to significant scarring and emotional distress. The onset of clinical disease usually occurs between the ages of 12 and 14 years, but mild disease may develop as early as 7 to 8 years of age and tends to occur somewhat earlier in girls than in boys. This prepubertal acne may be the first sign of pubertal maturation. Acne in this group is primarily comedonal and midfacial, favoring the forehead, nose, medial cheeks, and chin.2 Acne generally resolves in the late teens or early 20s, but persistence into the third decade or onset in middle age, particularly in women, is not unusual. Although most acne may be thought of as physiologic, disease with unusual features such as early onset or severe recalcitrance to therapy warrants evaluation for underlying abnormalities of the adrenal or ovarian systems.

Acne is most commonly localized to areas of highest sebaceous gland concentration and activity, such as the face, chest, and upper back. Acne is a multifactorial disease, involving excessive or increased sebum production, abnormal epithelial cell proliferation and desquamation, microbial proliferation, and inflammation.3 Acne lesions begin with the development of the microcomedone, a small cyst plugged by accumulated sebum, desquamated epithelial cells, vellus hairs, and bacteria. The formation of closed comedones (whiteheads) and open comedones (blackheads) is initiated by abnormal cornification of the follicular orifice (Fig. 365-1). The epidermal cells lining the orifice form adherent cornified sheets of cells instead of desquamating as single cells to be carried away with the sebum flow. These cornified sheets occlude the follicular opening and lead to cystic dilatation of the follicle. Open comedones have a widely patent surface orifice.

Figure 365-1.

Comendonal acne with many open and closed comedones and a mild inflammatory component.

Inflammatory lesions (ie, papules, pustules, or nodules) develop when the intradermal wall of the comedone ruptures, releasing comedonal contents into the dermis and provoking an intense, suppurative, and later a foreign-body, granulomatous-type inflammatory reaction. In cystic acne, the inflammatory reaction is extreme, resulting in deep nodules, sinus tracts, and cysts.

The surge of androgen production that occurs in adolescence leads to increased sebum production. 5-Alpha-reductase, which converts testosterone to the more potent dihydrotestosterone (DHT), appears to be more highly concentrated in infrainfundibular keratocinocytes.3 Interleukin-1 located in the hair follicle can also stimulate hypercornification.3

Sebum serves as a substrate for Propionibacterium acnes. This anaerobic diphtheroid is a normal resident of the pilosebaceous unit and overgrows within the blocked sebaceous follicle. Bacterial lipases liberate free fatty acids from ...

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