Porth's Essentials of Pathophysiology, 4e

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Integumentary Function

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overall the incidence and severity are greater in males. The disorder is very common, affecting more than 85% of teenagers, and a large percentage of young adults continue to show signs of the disorder. 20 Acne vulgaris is characterized by both noninflamma- tory and inflammatory lesions. The lesions are typically located on the face and neck and, to a lesser extent, on the back, chest, and shoulders. Noninflammatory lesions consist of comedones (whiteheads and blackheads). Blackheads are plugs of material that accumulate in sebaceous glands that open to the skin surface. The color of blackheads results from melanin that has moved into the sebaceous glands from adjoining epidermal cells. Whiteheads are pale, slightly elevated papules with no visible orifice. Inflammatory lesions consist of papules, pustules, nodules, and, in severe cases, cysts. Papules are raised areas less than 5 mm in diameter. Pustules have a central core of purulent material. Nodules are larger than 5 mm in diameter and may become suppurative or hemorrhagic. Suppurative nodules often are referred to as cysts because of their resemblance to inflamed epi- dermal cysts. The inflammatory lesions are believed to develop from the escape of sebum into the dermis and the irritating effects of the fatty acids contained in the sebum. The cause of acne vulgaris is largely unknown. There is a hereditary factor, multiple generations of family members being affected. Several factors are believed to contribute to acne, including (1) the influence of andro- gens on sebaceous gland activity; (2) increased prolif- eration of the keratinizing epidermal cells that form the sebaceous cells; (3) increased sebum production in rela- tion to the severity of the disease; and (4) the presence of Propionibacterium acnes, the microorganism respon- sible for the inflammatory stage of the disorder. These factors are probably interrelated. Increased androgen production results in increased sebaceous cell activity, with resultant plugging of the pilosebaceous ducts. The excessive sebum provides a medium for P. acnes growth, and the organism contains lipases that break down the free fatty acids that produce the acne inflammation. P. acnes is also thought to form a biofilm (an extracellular polysaccharide lining in which the bacteria are encased) that acts as a protective barrier to antibiotic treatment (see Chapter 14), explaining why prolonged antibiotic treatments are necessary. 21 The sebaceous glands also may serve as sites for immune reactions. 22 Acne may be triggered or worsened by external factors such as obstructions (e.g., head bands, collars), manipulation of the lesions, cosmetics, and occupational exposures. The diagnosis of acne is based on history and physi- cal examination. The severity of the acne is gener- ally assessed by the number, type, and distribution of lesions. 17 Mild acne is usually characterized by the pres- ence of a small number (generally <10) of open and closed comedones, with a few inflammatory papules; moderate acne by the presence of a moderate number (10 to 40) of erythematous papules and pustules (Fig. 46-11), usually limited to the face; and moderately severe acne by the presence of numerous papules and pustules (40 to 100) and occasionally larger, deeper, nodular inflamed lesions

involving the face, chest, and back. Treatment of acne focuses on clearing up existing lesions, preventing new lesions, and limiting scar formation. 17–20 Treatment measures include the use of topical antimi- crobials, oral antibiotics, topical retinoids, and isotreti- noin. Soaps are usually not effective in treating acne, and unless the skin is exceptionally oily, a mild soap should be used to avoid additional irritation that will limit the effectiveness of other topical treatments. Mild acne is usually treated with a topical preparation con- taining a combination of erythromycin or clindamycin and benzoyl peroxide. Topical antibiotics do not affect existing lesions but decrease the P. acnes on the skin, thereby reducing subsequent inflammation resulting from free fatty acid release and breakdown. Benzoyl peroxide, which is a bactericide, does not induce resis- tance, and when used with topical and oral antibiotics it protects against the development of lesions. Azelaic acid, products containing sodium sulfacetamide and sulfur, and salicylic acid preparations are also available. These agents are usually not considered as first-line ther- apies, but may be used in persons who cannot tolerate other topical agents. Moderate to severe cases of acne may be managed with systemic antibiotics (e.g., tetracycline), topi- cal vitamin A derivatives (retinoids), or oral retinoids (isotretinoin). Systemic antibiotics decrease P. acnes col- onization and have intrinsic anti-inflammatory effects. The action of topical vitamin A (e.g., tretinoin) has been attributed to decreased cohesiveness of epidermal cells and increased epidermal cell turnover. This is thought to result in increased extrusion of open comedones and transformation of closed comedones into open ones. Isotretinoin is approved for treatment of recalcitrant cases of acne and cystic acnes. Although the exact mode of action is unknown, isotretinoin decreases sebaceous gland activity, prevents new comedones from forming, reduces the P. acnes count through sebum reduction, and has an anti-inflammatory effect. Because of its many side effects, it is used only in persons with severe acne. The oral retinoids are known teratogens and must not FIGURE 46-11. Moderate acne. Erythematous papules and pustules are the predominant lesions, and lesions are limited to the face. (From JamesWD. Acne. N Engl J Med. 2005;352:1464. Copyright © 2005. Massachusetts Medical Society.)