Acne vulgaris is the most common skin disorder in adolescents. It is a multifactorial disease characterized by chronic inflammation of the pilosebaceous units of certain areas (most commonly the face and trunk) that manifests as comedones, papules, nodules, cysts, or papulopustules. Resolving lesions are often but not always followed by scars.
INSIGHT 
Neonatal acne (presenting between the age of 2 weeks and 3 months of life) is common and self-limited; it has been associated with inflammation in response to Malassezia overgrowth. Infantile acne (presenting between 3 and 6 months of age) may foreshadow more severe acne later in life.
AGE Typically begins at puberty.
GENDER M > F, and males tend to be more severely affected.
PREVALENCE Approximately 85% of 12- to 24-year-old patients have some form of acne. Forty to fifty million people in the United States have acne annually.
DRUGS Systemic corticosteroids, iodides, bromides, anticonvulsants (phenytoin and trimethadione), antidepressants (lithium), and epidermal growth factor receptor (EGFR) inhibitors can exacerbate acne in susceptible patients.
GENETIC ASPECTS Family history may be a predictor of acne severity. Additionally, individuals with an XXY karyotype are at increased risk for severe acne. Acne may rarely be a component of syndromes such as SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) and PAPA (pyogenic arthritis, pyoderma gangrenosum, acne).
OTHER FACTORS Emotional stress, lack of sleep, and menses can cause exacerbations. Pressure or rubbing of skin can cause local outbreaks (acne mechanica). Androgen excess can also lead to severe refractory cases.
The lesions of acne (comedones) are the result of genetics (increased number and size of sebaceous glands), mechanical factors (accumulation of sloughed corneocytes leading to pilosebaceous unit blockage), hormones (androgens), bacteria (Propionibacterium acnes), and the inflammatory response in the pilosebaceous unit. Androgens stimulate sebaceous glands to produce larger amounts of sebum; bacteria contain lipase that converts lipids into fatty acids. Both excess sebum and fatty acids cause the corneocytes to block the pilosebaceous unit and comedones are formed. If the comedo is open to the skin surface, the oxidized keratin and lipid debris, along with corneocyte melanin, protrudes and darkens in color (blackheads). Closed comedones may break under the skin and the contents (sebum, lipid, fatty acids, keratin) enter the dermis, provoking inflammation (papules, pustules, nodules). Rupture plus intense inflammation may lead to scarring.
DURATION OF LESIONS Weeks to months.
SEASON Worse in fall and winter.
SYMPTOMS Itching or pain in lesions (especially nodulocystic type). Rarely, systemic symptoms such as fever may be associated with extreme presentations of acne fulminans.
TYPE
Comedones: open comedones are “blackheads,” closed comedones are “whiteheads” (Fig. 6-1A).
Papules with or without inflammation, pustules (Fig. 6-1B).
Nodules, noduloulcerative lesions, 2 to 5 cm in diameter.
Postinflammatory hyperpigmentation (more common in darker skin types).
Scars. Atrophic depressed (often pitted), box-car, ice-pick, rolling, or hypertrophic (keloid) scars (Fig. 6-1C).
SHAPE Round; nodules may coalesce to form linear plaques.
ARRANGEMENT Isolated single lesion (e.g., nodule) or scattered discrete lesions (papules, cysts, nodules).
SITES OF PREDILECTION Face, chest, back, shoulders.
Acne has many morphologies and thus has a large differential including milia, miliaria, candidal infections, pustulosis, sebaceous hyperplasia, appendageal tumors, folliculitis, keratosis pilaris, and rosacea. Persistent lesions may mimic facial growths associated with genetic syndromes such as adenoma sebaceum of tuberous sclerosis.
Acne may have a mild self-limited course or a protracted recurrent course that may persist into adulthood.
Persistent acne may be a result of XYY chromosomal genotype or endocrine disorders such as polycystic ovarian syndrome, hyperandrogenism, hypercortisolism, or precocious puberty. Patients suspected of hyperandrogenism should have screening tests including serum levels of total and free testosterone (to detect ovarian excess androgen), didehydroepiandrosterone sulfate (DHEAS, detects excess adrenal androgen), and 17-hydroxyprogesterone (detects adrenal excess androgen). Patients suspected of hypercortisolism should have an AM serum cortisol checked.
Patients and parents should be educated on factors that may aggravate acne:
Repeated pressure, leaning, touching, or scrubbing acne-prone areas.
Occlusive garments such as headbands, chinstraps, helmets, and hats.
Oil and grease in moisturizers, face creams, makeup, or hair products.
Greasy air–filled environments such as fast-food kitchens.
Squeezing or popping pimples can lead to scarring.
Certain medications taken for other problems [e.g., oral contraceptives (OCPs), lithium, hydantoin, topical, and systemic steroids].
Emotional stress.
Hormonal changes with menses.
Foods typically do not play a major role, but some people find specific foods trigger their acne and are helped by avoiding them.
Topical antibiotics such as clindamycin or erythromycin help decrease bacterial load and inflammation.
Topical benzoyl peroxide also suppresses P. acnes and microbial resistance has not been reported. Topical benzoyl peroxide and topical antibiotics have synergistic effects when used in combination and help reduce bacterial resistance when combined.
Topical salicylic acid or α-hydroxy acid preparations can help slough the outer layer of skin preventing follicular blockage.
Topical retinoids (tretinoin, adapalene, tazarotene) are effective, but require detailed instructions and gradual increases in concentration. Retinoids help the skin turn over more rapidly to decrease follicular blockage and rupture.
Topical sulfur is antimicrobial and keratolytic.
Use of noncomedogenic cleansers and cosmetics should be encouraged in individuals who are acne-prone once clear to minimize recurrences.
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