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ICD-9: 706.1 • ICD-10: L70.0   Image not available. Image not available. Image not available. Image not available.

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  • An inflammation of pilosebaceous units, very common
  • Appears in certain body areas (face, trunk, rarely buttocks)
  • Most frequently in adolescents
  • Manifests as comedones, papulopustules, nodules, and cysts
  • Results in pitted, depressed, or hypertrophic scars

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Epidemiology

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Occurrence

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Very common, affecting approximately 85% of young people.

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Age of Onset

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Puberty—10 to 17 years in females, 14 to 19 in males; however, may appear first at 25 years or older.

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Sex

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More severe in males than in females.

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Race

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Lower incidence in Asians and Africans.

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Genetic Aspects

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Multifactorial genetic background. Familial predisposition: majority of individuals with cystic acne have parent(s) with a history of severe acne. Severe acne may be associated with XYY syndrome.

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Pathogenesis

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Key factors are follicular keratinization, androgens, and Propionibacterium acnes (5185637).

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Graphic Jump Location

A–D. Acne pathogenesis [From Zaenglein AL et al. Acne vulgaris and acneiform eruptions, in Wolff K et al (eds): Fitzpatrick's Dermatology in General Medicine, 7th ed. New York, McGraw-Hill, 2008.]

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Acne results from a change in the keratinization pattern in the pilosebaceous unit, with the keratinous material becoming more dense and blocking secretion of sebum. These keratin plugs are called comedones and represent the “time bombs” of acne. Linoleic acid, which regulates keratinocyte proliferation, is decreased in acne. Comedonal plugging and a complex interaction between androgens and bacteria (P. acnes) in the plugged pilosebaceous units lead to inflammation. Androgens (qualitatively and quantitatively normal in the serum) stimulate sebaceous glands to produce larger amounts of sebum. Bacteria contain lipase, which converts lipid into fatty acids, and produce proinflammatory mediators, [interleukin 1, tumor necrosis factor TNF α]. Fatty acids and proinflammatory mediators cause a sterile inflammatory response to the pilosebaceous unit. The distended follicle walls break, and the contents (sebum, lipids, fatty acids, keratin, bacteria) enter the dermis, provoking an inflammatory and foreign-body response (papule, pustule, nodule). Rupture plus intense inflammation lead to scars.

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Contributory Factors

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Acnegenic mineral oils, rarely dioxin and others.

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Drugs
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Lithium, hydantoin, isoniazid, glucocorticoids, oral contraceptives, iodides, bromides and androgens (e.g., testosterone), danazol.

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Others
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Emotional stress can definitely cause exacerbations. Occlusion and pressure on the skin, such as by leaning face on hands, very important and often unrecognized exacerbating factor (acne mechanica). Acne is not caused by chocolate or fatty foods or, in fact, by any kind of food.

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Clinical Manifestation

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Duration of Lesions

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Weeks to months.

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