Management of Acne

Peter C. Schalock

Arthur J. Sober

Acne is a polygenic, multifactorial disease that in some form afflicts nearly all adolescents in the United States. It ranges in severity from a few scattered whiteheads and blackheads to disfiguring, painful, deep-seated, pus-filled, and bleeding nodulocystic lesions. About 15% of surveyed patients with acne seek medical care. The primary care physician is in a unique position to identify and treat many acne sufferers. Properly managing acne requires a thorough understanding of the development of acne in all its phases, so that therapy appropriate to the circumstances can be selected from the available modalities. Early effective treatment minimizes the physical scarring of the disease and prevents or reduces equally important psychological distress.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1, 2 and 3)

Pathophysiology

Acne is a disease of pilosebaceous units, which are predominantly on the face and central upper back and chest. The pathogenesis of acne results from the interplay of three factors: (a) hyperkeratinization and obstruction of the follicular infundibulum caused by abnormal desquamation of the follicular epithelium, (b) androgen-stimulated increases in sebum production, and (c) colonization of the follicle by Propionibacterium acnes, which generates inflammation.

The initial event of acne is conversion of the loose, easily shed, horny layer of the epithelium lining the follicular duct wall to a self-adhering mass that gradually obstructs the follicular duct. This has been called “retention hyperkeratosis.” A microcomedone is the initial lesion, a precursor to both open and closed comedones. It occurs following occlusion of the follicular ostia. An open comedone (blackhead) is this keratin plug that enlarges and does not become inflamed. The black color is due to oxidized lipids and melanin. Closed comedones (whiteheads) form from microcomedones after 1 to 2 months, once the accumulated mass of keratin, sebum, and bacteria reaches visible size. Whiteheads may expand the duct (“pore”) opening to communicate freely with the outside.

Chemotactic agents produced by bacteria within the duct attract leukocytes, leading to duct wall rupture and release of follicular contents into the surrounding dermis. This provokes a profound inflammatory response, leading to the development of papules, pustules, nodules, and suppurative nodules that are commonly but mistakenly termed cysts. These inflammatory lesions may lead to permanent scarring.

Propionibacterium acnes, a normal inhabitant of the follicular canal in humans, may participate in the initiation and aggravation of inflammatory lesions by elaborating enzymes, including lipases, that act on sebum to release potentially irritating free fatty acids. Its hyaluronidase may increase permeability of the follicular duct wall, and its protease can damage the duct wall, increasing leakage of materials into the surrounding dermis. In addition,

P. acnes produces chemotactic substances that contribute to the initiation and evolution of inflammatory lesions.

The debate about the role of diet and other environmental factors continues. It is hypothesized that adolescents in Westernized societies may be repeatedly acutely hyperinsulinemic due to their highly glycemic diets, which in turn may initiate an endocrine cascade (involving insulin growth factor [IGF], IGF-binding protein 3, testosterone, and retinoid signaling pathways) that affects sebaceous gland production and follicular keratinization. Whether adherence to a diet with a low glycemic load can reduce acne risk is unknown, but such diets are characteristic of non-Westernized populations that have low prevalences of acne. Milk consumption has been positively associated with the severity of acne; teenagers who consume greater amounts of cow’s milk, especially skim milk, had a greater number of acne lesions and severity of acne, perhaps related to high levels of bovine hormones, including estrogens, progesterones, and precursors to androstenedione.

Clinical Presentations

Acne can be categorized as obstructive or inflammatory; both types of lesions may be present. Obstructive disease results from impaction of horny material, bacteria, and sebum, which dilates follicular ducts and produces closed comedones (whiteheads) and open comedones (blackheads) (Figs. 185-1 and 185-2). Leakage of intrafollicular contents from comedones into the adjacent dermis produces an inflammatory response. Depending on the degree of leakage into the dermis and the amount of material released, inflammatory lesions vary from small, erythematous papules and superficial pustules to deeper pustules and larger, persistent, and occasionally suppurative nodules. Genetic immunologic factors may contribute to an exaggerated inflammatory response and more severe cystic forms of acne.

PRINCIPLES OF THERAPY (3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16 and 17)

Treatment is often initiated with topical agents, and with progression, systemic agents are added in more severely affected cases. An initial presentation of severe or scarring acne or with clear hormonal factors should hasten the use of systemic agents.

Removal of Acnegenic Factors

Eliminating precipitants is an important component of therapy. Some cosmetics, including makeup, hair sprays, oils, and
moisturizing creams, may be capable of producing comedones, and their use should be reduced or discontinued. The physician should advise against using acnegenic drugs such as androgens, systemic steroids, iodides, and bromides. Other medications such as lithium and epidermal growth factor receptor blockers (erlotinib/gefitinib) can cause acneiform reactions, but discontinuation of these medications is not typically recommended. The role of foods in the pathogenesis of acne is unclear, but recent epidemiologic and pathophysiologic evidence (see earlier discussion) suggests a potential benefit from the reduction of excessive carbohydrate and dairy intake (especially those forms that induce hyperinsulinism; see Chapter 102).

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