Chapter 053. Eczema and Dermatitis (Part 13) Acne Vulgaris Acne vulgaris is a self-limited disorder primarily of teenagers and young adults, although perhaps 10–20% of adults may continue to experience some form of the disorder. The permissive factor for the expression of the disease in adolescence is the increase in sebum production by sebaceous glands after puberty. Small cysts, called comedones , form in hair follicles due to blockage of the follicular orifice by retention of keratinous material and sebum. The activity of bacteria (Proprionobacterium acnes) within the comedones releases free fatty acids from sebum, causes inflammation within the cyst, and results in rupture of the cyst wall. An inflammatory foreign-body reaction develops as result of extrusion of oily and keratinous debris from the cyst. The clinical hallmark of acne vulgaris is the comedone, which may be closed (whitehead) or open (blackhead). Closed comedones appear as 1- to 2-mm pebbly white papules, which are accentuated when the skin is stretched. They are the precursors of inflammatory lesions of acne vulgaris. The contents of closed comedones are not easily expressed. Open comedones, which rarely result in inflammatory acne lesions, have a large dilated follicular orifice and are filled with easily expressible oxidized, darkened, oily debris. Comedones are usually accompanied by inflammatory lesions: papules, pustules, or nodules. The earliest lesions seen in adolescence are generally mildly inflamed or noninflammatory comedones on the forehead. Subsequently, more typical inflammatory lesions develop on the cheeks, nose, and chin (Fig. 53-7). The most common location for acne is the face, but involvement of the chest and back is common. Most disease remains mild and does not lead to scarring. A small number of patients develop large inflammatory cysts and nodules, which may drain and result in significant scarring. Regardless of the severity, acne may affect a patient's quality of life. If adequately treated, this may be a transient effect. In the case of severe, scarring acne, the effects can be permanent and profound. Early therapeutic intervention in severe acne is essential. Figure 53-7 Acne vulgaris. An example of acne vulgaris with inflammatory papules, pustules, and comedones. (Courtesy of Kalman Watsky, MD; with permission.) Exogenous and endogenous factors can alter the expression of acne vulgaris. Friction and trauma (from headbands or chin straps of athletic helmets), application of comedogenic topical agents (cosmetics or hair preparations), or chronic topical exposure to certain industrial compounds may elicit or aggravate acne. Glucocorticoids, topical or systemic, may also elicit acne. Other systemic medications such as oral contraceptive pills, lithium, isoniazid, androgenic steroids, halogens, phenytoin, and phenobarbital may produce acneiform eruptions or aggravate preexisting acne. Genetic factors and polycystic ovary disease may also play a role. Acne Vulgaris: Treatment Treatment of acne vulgaris is directed toward elimination of comedones by normalization of follicular keratinization, decreasing sebaceous gland activity, decreasing the population of P. acnes, and decreasing inflammation. Minimal to moderate, pauci-inflammatory disease may respond adequately to local therapy alone. Although areas affected with acne should be kept clean, overly vigorous scrubbing may aggravate acne due to mechanical rupture of comedones. Topical agents such as retinoic acid, benzoyl peroxide, or salicylic acid may alter the pattern of epidermal desquamation, preventing the formation of comedones and aiding in the resolution of preexisting cysts. Topical antibacterial agents such as azelaic acid, topical erythromycin (with or without zinc), or clindamycin are also useful adjuncts to therapy. Patients with moderate to severe acne with a prominent inflammatory component will benefit from the addition of systemic therapy, such as tetracycline in doses of 250–500 mg bid, or doxycycline, 100 mg bid. Minocycline may also be useful. Such antibiotics appear to have an anti-inflammatory effect independent of their antibacterial effect. Female patients who do not respond to oral antibiotics may benefit from hormonal therapy. Women placed on oral contraceptives containing ethinyl estradiol and norgestimate have demonstrated improvement in their acne when compared to a placebo control. Patients with severe nodulocystic acne unresponsive to the therapies discussed above may benefit from treatment with the synthetic retinoid, isotretinoin. Its dose is based on the patient's weight, and it is given once daily for 5 months. Results are excellent in appropriately selected patients. Its use is highly regulated due to its potential for severe adverse events, primarily teratogenicity. Additionally, patients receiving this medication develop extremely dry skin, cheilitis, and must be followed for development of hypertriglyceridemia. Recently there have also been concerns that it is associated with severe depression in some patients. The latter has not been proved. At present, prescribers must enroll in a program designed to prevent pregnancy and adverse events while patients are taking isotretinoin. These measures are imposed to ensure that all prescribers are familiar with the risks of isotretinoin; that all female patients have two negative pregnancy tests prior to initiating therapy and a negative pregnancy test prior to each refill; and that all patients have been warned about the risks associated with isotretinoin. . Chapter 053. Eczema and Dermatitis (Part 13) Acne Vulgaris Acne vulgaris is a self-limited disorder primarily of teenagers and young adults, although perhaps. develop on the cheeks, nose, and chin (Fig. 53-7). The most common location for acne is the face, but involvement of the chest and back is common. Most disease remains mild and does not lead to scarring Kalman Watsky, MD; with permission.) Exogenous and endogenous factors can alter the expression of acne vulgaris. Friction and trauma (from headbands or chin straps of athletic helmets), application