Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit. Acne lesions favor the face, neck, upper back, chest, and upper arms. Multiple clinical variants exist and they include comedonal acne, papulopustular acne, nodulocystic acne, acne conglobata, and acne fulminans.
Incidence and age: predominantly a disorder of adolescence; affects 85% of individuals between 12 and 24 years of age; may affect all age groups
Race: lower incidence in African-Americans and Asians
Sex: more severe forms in males
Precipitating factors: genetic predisposition, endocrine disorders, stress, mechanical factors (friction, pressure, occlusion), contact with acnegenic materials (oils, chlorinated hydrocarbons, cosmetics), and drugs (steroids, lithium, androgens, hydantoin)
Many patients with nodulocystic acne have a first-degree relative with a history of severe acne. The primary pathophysiology involves altered follicular keratinization resulting in obstruction of sebaceous follicles, increased sebum production, hyperproliferation of Propionibacterium acnes, and increased production of chemotactic factors which result in inflammation.
Comedones (closed and open), erythematous papules, pustules, nodules, and cysts. May resolve with residual hyperpigmentation or scarring.
Acne rosacea, steroid acne, acne mechanica, Pityrosporum folliculitis, and bacterial folliculitis.
No routine studies are needed. If history and physical examination raise concerns then consider ordering—screen for free and total testosterone, dehydroepiandrosterone, and follicle stimulating hormone/lutenizing hormone (FSH/LH) ratios to exclude polycystic ovary syndrome or other hormonal abnormalities especially in women with moderate-to-severe acne, hirsutism, irregular menses, and weight gain. Diet may play a role in flares of acne. High glycemic diets may exacerbate acne. Further studies are needed.
Pathology of early lesion (comedone) reveals obstruction of the follicular infundibulum by cornified cells leading to dilatation. Later lesions reveal follicular rupture with lymphocytes, neutrophils, and macrophages. Scarring may be seen.
This disease demonstrates a chronic course and remits spontaneously in the early-to-mid-third decade in the majority of patients. However, acne may persist much longer in some patients.
Early treatment of acne is essential for the prevention of dyschromia or associated scarring (see scar treatment chapter 61). Many acne patients benefit from combination therapies. A thorough history and physical examination are paramount to administering a maximally effective plan. This should include current cosmetics and sunscreens, skin type, lifestyle, occupation, medications, past treatments and response, diet, menstrual and oral contraceptive history.
Topical treatment may be required for the duration of this condition. Topical formulations should be applied to the lesions as well as to the adjacent acne-prone clinically normal skin.