Chapter 21 Acne and acneiform eruptions
1. How common is acne?
Acne vulgaris is the most common dermatologic disorder, affecting between 40 and 50 million individuals of all ages in the United States. Eighty-five percent of people between the ages of 12 and 24 years will have some acne. Direct costs related to acne, including factors such as loss of productivity and related depression, exceed $2.2 billion annually in the United States.
2. What is the pathophysiology of acne?
The pilosebaceous unit, made up of a follicle (pore), sebaceous gland, and a vellus hair, is the target organ affected in acne. The face, chest, and back are areas with the greatest concentration of pilosebaceous follicles, corresponding to the areas most commonly affected by acne lesions. The primary lesion of acne is the microcomedo. This is the result of obstruction of the sebaceous follicles by sebum and abnormally differentiated and desquamated keratinocytes that may produce large comedones (Fig. 21-1). The four main pathophysiologic factors in acne vulgaris are:
• Inflammation (recent evidence indicates that inflammatory events precede the hyperkeratinization of the follicle)
3. What are the acne subtypes.
Acne presents in many forms and variations. The most common form is acne vulgaris, which is classified according to the predominant lesion type as comodonal, papular, pustular, nodular, or cystic. It can be graded as mild, moderate, or severe (Fig. 21-2). Other clinical subtypes of acneiform skin lesions include:
4. How does the composition of sebum contribute to the formation of acne?
The major constituent of sebaceous lipid is triglyceride, which makes up over 50% of the lipid; wax esters account for 25%, squalene 15%, and there are small amounts of cholesterol esters and free cholesterol. Increased sebum production is characteristic of patients with acne, but the seborrhea itself is not sufficient to produce acne. Desaturation of the fatty acids in sebum may lead to the development of acne lesions. Lipoperoxidases characterize the sebum of acne patients, and this, along with other qualitative changes in the sebum lipids, induce alteration of keratinocyte differentiation and induce interleukin-1 (IL-1) secretion, leading to follicular hyperkeratinization.
5. Does stress exacerbate acne?
Yes, it seems to. Many patients report that emotional stress makes their acne worse. In one survey of 4576 consecutive patients with various dermatologic problems, 55% of those with acne reported that episodes of emotional stress were closely related to exacerbation of their acne. A prospective cohort study, published in 2003, of 22 university students with acne during exams showed increased acne severity that was significantly associated with increased stress levels. Another study in high school students also found that increased stress correlated with increased acne severity. There did not seem to be an increase in sebum production during times of stress in this study. New data regarding the physiology of sebaceous glands indicate that these skin organs have receptors for numerous neuropeptides (NPs), and these receptors modulate inflammation, proliferation, and sebum production and composition, as well as androgen metabolism in human sebocytes. Further elucidation of these neural skin connections may help our understanding of the connection between stress and acne.
Koo, JYM, Smith LL: Psychologic aspects of acne, Pediatr Dermatol 8:185–188, 1991.
6. Does diet affect acne?
Minimally. Association between diet and acne has long been postulated. Arguments for such an association include the observations that acne prevalence is low in rural, nonindustrialized societies and increases with the adoption of a Western diet. A study published in 1971 rechallenged patients with large amounts of foods that reportedly exacerbated their acne without showing any significant change in acne severity. In another study, 1925 patients kept food diaries and found milk to be most commonly associated with their acne flares. A study showing no association between chocolate bar consumption and acne has been criticized for several reasons most recently, because the chocolate bars given to subjects during the study did not contain milk, in contrast to the average chocolate bar of the time. To further examine the role of diet and acne, especially dairy consumption, a recent study examined data from the Nurses Health Study (NHS) II to see if there was a positive association between milk in the teenage diet and acne. Intake of milk during adolescence was associated with a history of teenage acne. The association was more marked for skim than whole milk. Interestingly, soda, French fries, chocolate candy, and pizza were not significantly associated with acne. The authors hypothesized that the hormonal content, not the fat in milk, may be responsible for the acne. Two other large studies have reported a similar positive association between milk intake and acne. Smith, Mann, Braue, et al. enrolled 43 men with moderate acne, ages 15 to 25, in a trial randomized to a low glycemic index diet or a high glycemic–index diet. The men on the low glycemic–index diet lost significantly more weight and had significantly improved acne over the other group. The relative contribution of the high glycemic–load diet on acne pathogenesis versus the improvement in insulin and hormone levels with weight loss is unknown.
7. When can teenagers with acne expect their acne to resolve?
Acne affects approximately 8% of adults aged 25 to 34, and 3% aged 35 to 44. Most teenage boys can anticipate clearing of their acne between 20 and 25 years of age. For women, the news is not so good. The majority of patients with adult acne, including adult-onset acne, are women. This can last up to and beyond age 40.
8. Discuss the topical therapy of acne vulgaris.
The single most important topical medications used to treat acne are retinoids. We now have numerous topical preparations to choose from that are less irritating and decrease the most common complaint associated with class of acne therapy. These include adapalene (Differin), tazarotene (Tazorac), and tretinoin (Avita, Retin-A, Retin-A Micro). Twelve weeks of use is required for maximum benefit. Retinoids are the only drugs that normalize keratinization within the follicular infundibulum and prevent comodone formation. Propironibacterium acnes, the anaerobic bacterium associated with acne pathogenesis, stimulates the innate immune response via Toll-like receptors (TLRs). This sets off an inflammatory cascade of cytokines. Retinoids are known to downregulate TLRs and inhibit downstream inflammatory transcription factors. Recent recommendations from a global alliance to improve outcomes in acne recommended that retinoid-based combination therapy (retinoid plus antimicrobial or benzoyl peroxide) be the first-line treatment for most forms of acne vulgaris. Retinoids have been shown to maintain improvement achieved with this initial combination therapy.
Other topical treatments include benzoyl peroxide (BPo), topical antibiotics (erythromycin, clindamycin, and sodium sulfacetamide), α-hydroxy acids, salicylic acid, and azelaic acid. Antibiotic resistance of P. acnes has become more common. More than half of patients undergoing therapy with a topical antibiotic will develop resistance. No bacterial resistance has been reported with topical benzoyl peroxide. The following are recommendations for preventing bacterial resistance in the treatment of acne: combining antimicrobials with a retinoid and BPo, limiting the duration of antimicrobial therapy, not using antimicrobials as monotherapy, and avoiding concurrent use of oral and topical antibiotics, especially if chemically different.
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