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.
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.
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