Acne

Acne

Daniel P. Krowchuk

ETIOLOGY

Acne is a disease of pilosebaceous units, composed of a follicle, sebaceous gland, and vellus hair. These structures are concentrated on the face, chest, and back, explaining the occurrence of acne in these areas. Although the pathophysiology of acne is not fully understood, several factors contribute:

Androgens and sebum production: At adrenarche, rising levels of dehydroepiandrosterone sulfate (DHEAS), likely after conversion to testosterone and dihydrotestosterone, cause sebaceous glands to enlarge and produce more sebum. Increased sebum production contributes to obstruction within follicles and correlates with acne severity.
Bacteria and the innate immune response: Propionibacterium acnes is an anaerobic gram-positive rod that colonizes pilosebaceous follicles following increases in sebum production. P. acnes elaborates lipases that can damage the follicle wall and releases a number of chemotactic factors and proinflammatory mediators.
Abnormal keratinization: Epithelial cells lining the follicle proliferate more rapidly and become more cohesive. The result is a collection of cells and sebum that leads to the development of the primary acne lesion, the microcomedo.¹ As obstruction increases, the follicle may rupture with spread of its contents into surrounding tissues, an event that contributes to inflammation.

CLINICAL MANIFESTATIONS

Acne Lesions

Obstructive lesions (comedones): Obstruction within follicles initially is microscopic (i.e., microcomedones) but ultimately becomes apparent as open and closed comedones. Open comedones (blackheads) have a dilated follicular orifice and a black color (thought to be due to oxidized melanin, altered transmission of light through epithelial cells, or the presence of certain lipids in sebum) (Fig. 21.1). Closed comedones (whiteheads) are small (1 mm in diameter) white to skin-colored papules (Fig. 21.2).

Inflammatory lesions: Rupture of obstructed follicles leads to the formation of erythematous papules (<5 mm in diameter), pustules, and nodules (>5 mm in diameter) (Fig. 21.1). As inflammatory lesions resolve, they often leave erythematous (Fig. 21.1), violaceous, or hyperpigmented (Fig. 21.3) macules that may persist for as long as a year. Patients often mistake these lesions for scars.

FIGURE 21.1 This patient has moderate mixed (inflammatory and comedonal) acne. He has inflammatory papules and pustules, erythematous macules (resolving inflammatory lesions), and open comedones. (From Jensen S. Nursing health assessment. Philadelphia, PA: Lippincott Williams & Wilkins, 2010.)

FIGURE 21.2 In this patient who has moderate mixed acne (inflammatory and comedonal), there are closed comedones (yellow arrows), papules (green arrow), and pustules (blue arrow).

FIGURE 21.3 In persons of color, resolving inflammatory lesions may produce hyperpigmented macules. (From Lugo-Somolinos A, McKinley-Grant L, Goldsmith LA, et al. Essential dermatology in pigmented skin. Philadelphia, PA: Lippincott Williams & Wilkins, 2011.)

FIGURE 21.4 On the face, acne scars appear as small pits seen here in the temporal fossa. Based on the presence of scars and numerous inflammatory lesions, this patient has severe acne. (From Burkhart C, Morrell D, Goldsmith LA, et al. Essential pediatric dermatology. Philadelphia, PA: Lippincott Williams & Wilkins, 2009.)

Scars: Scarring is most likely to occur in those who have large inflammatory lesions (i.e., nodules). On the face, scars appear as small pits (Fig. 21.4), while on the trunk they are hypopigmented macules. Occasionally, patients develop hypertrophic scars (i.e., keloids) or cysts (compressible nodules that lack overlying inflammation).

Acne Variants

Pomade acne: Caused by physical obstruction of follicles, most often from inadvertent application of hair styling products (e.g., pomades, greases) to facial skin. Comedones are concentrated on the forehead near the scalp and in the temporal fossae.
Acne conglobata: A severe form of acne in which cysts, abscesses, and draining sinuses develop on the face, chest, or back (e-Fig. 21.1). Extensive scarring and keloid formation are common.
Acne fulminans: This severe acne variant is characterized by the abrupt onset of painful nodules and cysts that become hemorrhagic and ultimately suppurate. Ulcers form and heal slowly, often leaving extensive scarring. Fever, chills, weight loss, myalgias, or arthritis may be present. Patients may have leukocytosis, anemia, elevated inflammatory markers and transaminases, and periosteal reaction suggestive of osteomyelitis.
Gram-negative folliculitis: Infection with gram-negative bacteria that complicates long-term oral antibiotic treatment of acne. The organisms most often responsible include Escherichia coli, Enterobacter spp, Serratia marcescens, and Klebsiella spp. Patients exhibit inflammatory papules and pustules concentrated around the nose.

EVALUATION

Elements of the history that may be helpful are presented in Table 21.1. At a minimum, the physical examination should include the face, chest, and back. To aid in assessing the effect of treatment, one can document the approximate number and types of acne lesions present on the face (forehead, each cheek, and chin), chest, and back. Including photographs in an electronic health record is especially helpful.

An assessment of acne severity serves to inform the development of a treatment plan. The method presented here focuses on the face, but involvement of the trunk should be considered.¹

Mild acne: A minority of the face is involved; a few papules and pustules are present, but there are no nodules or scars.
Moderate acne: Approximately one-half of the face is involved; papules and pustules are more numerous, but nodules are few (Fig. 21.1).
Severe acne: The majority of the face is involved; papules and pustules are numerous, and there are several nodules; scarring may be present (Fig. 21.4).

Although androgens play an important role in acne, most patients have normal hormone concentrations. As a result, measuring concentrations of DHEAS, free testosterone, and 17-hydroxyprogesterone should be reserved for young women who have acne and other evidence of androgen excess (e.g., oligo- or amenorrhea, hirsutism, female-pattern alopecia, clitoromegaly).

DIFFERENTIAL DIAGNOSIS

Some conditions that mimic acne and differentiating features are presented below. In each of these disorders, comedones are absent.

Keratosis pilaris (KP): Small skin-colored papules located on the cheeks. A keratin plug emanating from the follicular orifice may be seen or palpated (differentiating the lesions from those of acne) (e-Fig. 21.2). KP often also affects the upper outer arms, thighs, and buttocks, areas not involved by acne.
Periorificial dermatitis: Erythematous papules, pustules, and scaling concentrated around the mouth, nose, or eyes. Unlike in acne, lesions are not present on the forehead or cheeks (e-Fig. 21.3).
Rosacea: Erythematous papules, pustules, and scaling involve the central face. Unlike in acne, flushing and telangiectasias are present (e-Fig. 21.4).
Pityrosporum folliculitis: Folliculitis caused by Pityrosporum ovale results in pruritic erythematous papules and pustules on the back, chest, and shoulders. In contrast to acne, the face is spared (e-Fig. 21.5). A potassium hydroxide preparation performed on a pustule roof may reveal spores and short hyphae.
Facial angiofibromas (adenoma sebaceum): Erythematous papules or nodules involving the nasolabial folds, nose, and medial cheeks (e-Fig. 21.6). Lesions typically appear in childhood, earlier than would be anticipated for acne.

TABLE 21.1 Key Elements of the History

Questions For All Patients	Rationale
When did your acne begin?	Early- or late-onset acne may indicate the presence of androgen excess.
What medications have you tried, and how did they work for you?	If the patient has used a medication you’re planning to prescribe, was it effective? If not, is it possible that failure was the result of improper use or the occurrence of adverse effects?
Are you taking other medications?	—Are there potential drug interactions? —Could the medication be exacerbating acne (as might occur with depot medroxyprogesterone acetate, an oral corticosteroid, lithium, diphenylhydantoin, phenobarbital, or isoniazid)
Do you have “sensitive” skin or eczema?	Individuals who have sensitive skin or atopic dermatitis may be less likely to tolerate medications that are irritating or drying (e.g., topical retinoids)
What skin or hair care products do you use?	— Occlusive preparations placed on the skin may physically obstruct follicles and worsen acne. Advise the use of products that are labeled “nonacnegenic,” “noncomedogenic,” or “won’t block pores.” —Hair greases used for hair styling may obstruct follicles if inadvertently applied to facial skin.
Are there other factors that may worsen acne?	Pressure applied by athletic gear (especially pads or chin straps) or tight clothing may worsen acne.
Questions For Young Women	Rationale
Are you having menstrual periods and, if so, how often?	— Oligo- or amenorrhea may suggest androgen excess as might occur in polycystic ovary syndrome or late-onset congenital adrenal hyperplasia. —Premenstrual acne flares may occur.
Are you using birth control? If so, what form?	—Progestin-containing long-acting reversible contraceptives may worsen acne. — Combined oral contraceptives (COCs) (even those without a specific FDA indication for acne) likely result in improvement. — Young women using an oral contraceptive may need a secondary form of contraception (e.g., condom) if receiving an oral antibiotic for acne.

TABLE 21.2 Options for Managing Mild Acne

Face

Inflammatory or mixed
- Benzoyl peroxide (BPO) once daily
- Alternatives (once daily):
  - BPO/antibiotic fixed-dose combination product
  - BPO/topical retinoid fixed-dose combination product
  - Topical antibiotic/topical retinoid fixed-dose combination product
Comedonal
- Topical retinoid (as single agent) or topical retinoid-containing fixed-dose combination product once daily