Section 6. Disorders of the Sebaceous and Apocrine Glands

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 (face and trunk) that manifests as comedones, papules, nodules, cysts, or papulopustules, 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. Infantile acne (presenting between 3 and 6 months of age) may foreshadow more severe acne later in life.

Epidemiology

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), and antidepressants (lithium) can exacerbate acne in susceptible patients.

Genetic Aspects Family history may be a predictor of acne severity.

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.

Pathophysiology

The lesions of acne (comedones) are the result of genetics (increased number and size of sebaceous glands), 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 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.

History

Duration of Lesions Weeks to months.

Season Worse in fall and winter.

Symptoms Itching or pain in lesions (especially nodulocystic type).

Physical Examination

Skin Lesions

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.
• Scars. Atrophic depressed (often pitted) or hypertrophic (keloid) scars.

Shape Round; nodules may coalesce to form linear plaques.