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 ofthe cyst...
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Chapter 053. Eczema and Dermatitis (Part 13) Chapter 053. Eczema and Dermatitis (Part 13) Acne Vulgaris Acne vulgaris is a self-limited disorder primarily of teenagers and youngadults, although perhaps 10–20% of adults may continue to experience some formof the disorder. The permissive factor for the expression of the disease inadolescence is the increase in sebum production by sebaceous glands afterpuberty. Small cysts, called comedones , form in hair follicles due to blockage ofthe follicular orifice by retention of keratinous material and sebum. The activity ofbacteria (Proprionobacterium acnes) within the comedones releases free fattyacids from sebum, causes inflammation within the cyst, and results in rupture ofthe cyst wall. An inflammatory foreign-body reaction develops as result ofextrusion of oily and keratinous debris from the cyst. The clinical hallmark of acne vulgaris is the comedone, which may beclosed (whitehead) or open (blackhead). Closed comedones appear as 1- to 2-mmpebbly white papules, which are accentuated when the skin is stretched. They arethe precursors of inflammatory lesions of acne vulgaris. The contents of closedcomedones are not easily expressed. Open comedones, which rarely result ininflammatory acne lesions, have a large dilated follicular orifice and are filled witheasily expressible oxidized, darkened, oily debris. Comedones are usuallyaccompanied by inflammatory lesions: papules, pustules, or nodules. The earliest lesions seen in adolescence are generally mildly inflamed ornoninflammatory comedones on the forehead. Subsequently, more typicalinflammatory lesions develop on the cheeks, nose, and chin (Fig. 53-7). The mostcommon location for acne is the face, but involvement of the chest and back iscommon. Most disease remains mild and does not lead to scarring. A smallnumber of patients develop large inflammatory cysts and nodules, which maydrain and result in significant scarring. Regardless of the severity, acne may affecta patients quality of life. If adequately treated, this may be a transient effect. In thecase of severe, scarring acne, the effects can be permanent and profound. Earlytherapeutic 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 acnevulgaris. Friction and trauma (from headbands or chin straps of athletic helmets),application of comedogenic topical agents (cosmetics or hair preparations), orchronic topical exposure to certain industrial compounds may elicit or aggravateacne. Glucocorticoids, topical or systemic, may also elicit acne. Other systemicmedications such as oral contraceptive pills, lithium, isoniazid, androgenicsteroids, halogens, phenytoin, and phenobarbital may produce acneiform eruptionsor aggravate preexisting acne. Genetic factors and polycystic ovary disease mayalso play a role. Acne Vulgaris: Treatment Treatment of acne vulgaris is directed toward elimination of comedones bynormalization of follicular keratinization, decreasing sebaceous gland activity,decreasing the population of P. acnes, and decreasing inflammation. Minimal tomoderate, pauci-inflammatory disease may respond adequately to local therapyalone. Although areas affected with acne should be kept clean, overly vigorousscrubbing may aggravate acne due to mechanical rupture of comedones. Topicalagents such as retinoic acid, benzoyl peroxide, or salicylic acid may alter thepattern of epidermal desquamation, preventing the formation of comedones andaiding in the resolution of preexisting cysts. Topical antibacterial agents such asazelaic acid, topical erythromycin (with or without zinc), or clindamycin are alsouseful adjuncts to therapy. Patients with moderate to severe acne with a prominent inflammatorycomponent will benefit from the addition of systemic therapy, such as tetracyclinein doses of 250–500 mg bid, or doxycycline, 100 mg bid. Minocycline may alsobe useful. Such antibiotics appear to have an anti-inflammatory effect independentof their antibacterial effect. Female patients who do not respond to oral antibioticsmay benefit from hormonal therapy. Women placed on oral contraceptivescontaining ethinyl estradiol and norgestimate have demonstrated improvement intheir acne when compared to a placebo control. Patients with severe nodulocystic acne unresponsive to the therapiesdiscussed above may benefit from treatment with the synthetic retinoid,isotretinoin. Its dose is based on the patients weight, and it is given once daily for5 months. Results are ...