Diagnosis and treatment of acne

American Family Physician, May 1, 2004 by Steven Feldman, Rachel E. Careccia, Kelly L. Barham, John Hancox
Acne is a disease of pilosebaceous units in the skin. It is thought to be caused by the interplay of four factors. Excessive sebum production secondary to sebaceous gland hyperplasia is the first abnormality to occur. (1) Subsequent hyperkeratinization of the hair follicle prevents normal shedding of the follicular keratinocytes, which then obstruct the follicle and form an inapparent microcomedo. (2) Lipids and cellular debris soon accumulate within the blocked follicle. This microenvironment encourages colonization of Propionibacterium acnes, which provokes an immune response through the production of numerous inflammatory mediators. Inflammation is further enhanced by follicular rupture and subsequent leakage of lipids, bacteria, and fatty acids into the dermis.

Diagnosis

The diagnosis of acne is based on the history and physical examination. Lesions most commonly develop in areas with the greatest concentration of sebaceous glands, which include the face, neck, chest, upper arms, and back.

Acne vulgaris may be defined as any disorder of the skin whose initial pathology is the microscopic microcomedo. (3) The microcomedo may evolve into visible open comedones ("blackheads") or closed comedones ("whiteheads"). Subsequently, inflammatory papules, pustules, and nodules may develop. Nodulocystic acne consists of pustular lesions larger than 0.5 cm. The presence of excoriations, postinflammatory hyperpigmentation, and scars should be noted.

Acne may be triggered or worsened by external factors such as mechanical obstruction (i.e., helmets, shirt collars), occupational exposures, or medications. Common medications that may cause or affect acne are listed in Table 1. (4) Cosmetics and emollients may occlude follicles and cause an acneiform eruption. Topical corticosteroids may produce perioral dermatitis, a localized erythematous papular or pustular eruption. (5)

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Endocrine causes of acne include Cushing's disease or syndrome, polycystic ovary syndrome, and congenital adrenal hyperplasia. (6) Clinical clues to possible hyperandrogenism in women include dysmenorrhea, virilization (i.e., hirsutism, clitoromegaly, temporal balding), and severe acne.

Classification

In 1990, the American Academy of Dermatology developed a classification scheme for primary acne vulgaris. (7) This grading scale delineates three levels of acne: mild, moderate, and severe. Mild acne is characterized by the presence of few to several papules and pustules, but no nodules (Figure 1). Patients with moderate acne have several to many papules and pustules, along with a few to several nodules (Figure 2). With severe acne, patients have numerous or extensive papules and pustules, as well as many nodules (Figure 3).

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Acne also is classified by type of lesion--comedonal, papulopustular, and nodulocystic. Pustules and cysts are considered inflammatory acne.

Therapy

TOPICAL AGENTS

Selection of topical therapy should be based on the severity and type of acne. Topical retinoids, benzoyl peroxide, and azelaic acid are effective treatments for mild acne. Topical antibiotics and medications with bacteriostatic and anti-inflammatory properties are effective for treating mild to moderate inflammatory acne. The dosage, approximate cost, and side effects of selected topical medications are summarized in Table 2.

Proper selection of topical formulations may decrease side effects and increase patient compliance. Fortunately, most acne medications are available in several forms. Creams and lotions typically are reserved for dry or sensitive skin, whereas gels are prescribed for oil-prone complexions. During treatment with prescribed medications, patients should use bland facial washes and moisturizers.

Retinoids and Retinoid Analogs. Topical tretinoin (Retin-A) is a comedolytic agent that normalizes desquamation of the epithelial lining, thereby preventing obstruction of the pilosebaceous outlet. (8) This agent also appears to have direct anti-inflammatory effects. (9) A derivative of vitamin A, tretinoin is available in cream, gel, and liquid forms. In tretinoin microsphere (Retin-A Micro), tretinoin is encapsulated in a polymer that slowly releases the active medication, resulting in less irritation than with other tretinoin preparations. (10) With all retinoids, visible improvement occurs after eight to 12 weeks of treatment.

Tretinoin is inactivated by ultraviolet (UV) light and oxidized by benzoyl peroxide. It therefore should be applied only at night and never with benzoyl peroxide. Tretinoin may decrease the amount of native UV protection by thinning the stratum corneum; thus, daily use of sunscreen is recommended. Because the irritation caused by tretinoin is dose-dependent, treatment should be initiated in a low dose. Patients only need a pea-sized amount of product per application.

There is no strong evidence for the teratogenicity of tretinoin, which remains pregnancy category C. A study (11) published in 1998 focused on the transdermal absorption of topical tretinoin and found the absorbed concentration to be below endogenous retinoid levels. However, no definitive consensus has been reached on the use of topical tretinoin in pregnancy. It may be wise to avoid use of topical retinoids or retinoid analogs in women who may become pregnant during treatment.