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Acne vulgaris is a self-limited disorder of the pilosebaceous unit that is seen primarily in adolescents. Most cases of acne present with a pleomorphic array of lesions, consisting of comedones, papules, pustules, and nodules with varying extent and severity. While the course of acne may be self-limiting, the sequelae can be lifelong, with pitted or hypertrophic scar formation.
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Acne is sufficiently common that it often has been termed physiologic. Mild degrees of acne are frequently seen at birth, probably resulting from follicular stimulation by adrenal androgens, and may continue into the neonatal period. However, in the vast majority of cases it is not until puberty that acne becomes a more significant problem. Acne often heralds the onset of puberty. In girls, the occurrence of acne may precede menarche by more than a year. In these very young patients, the predominant lesions are comedones. Acne prevalence hits its peak during the middle-to-late teenage period, with more than 85% of adolescents affected, and then steadily decreases. However, acne may persist through the third decade or even later, particularly in women. One study demonstrated a prevalence of facial acne in women between ages 26 and 44 to be 14%.1 Acne severity seems to be familial. The prevalence of high school students with moderate-to-severe acne was 19.9% in those students with a family history of acne and 9.8% in those students without a family history of acne.2 In twin studies, 81% of the population variance in acne was found due to genetic factors (vs. 19% environmental factors).3 Nodulocystic acne has been reported to be more common in white males than in black males, and one group of investigators has found that acne is more severe in patients with the XYY genotype.4,5
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Etiology and Pathogenesis
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Understanding the underlying basis for acne, and the mechanisms of action of the multitude of therapeutic options in treating acne will assure better therapeutic results. The pathogenesis of acne is multifaceted, but four basic steps have been identified. These key elements (Fig. 80-1) are: (1) follicular epidermal hyperproliferation, (2) excess sebum production, (3) inflammation, and (4) the presence and activity of Propionibacterium acnes. Each of these processes are interrelated and under hormonal and immune influence.
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