Chapter 15: Acne Vulgaris

INTRODUCTION

• Acne is a chronic skin disease characterized by open or closed comedones and inflammatory lesions, including papules, pustules, and nodules (cysts).

PATHOPHYSIOLOGY

• Acne usually begins during prepuberty and progresses as androgen production and sebaceous gland activity increase with gonad development.

• Acne progresses through four stages: (1) increased sebum production by sebaceous glands, (2) Propionibacterium acnes (renamed Cutibacterium acnes) follicular colonization (and bacterial lipolysis of sebum triglycerides to free fatty acids), (3) release of inflammatory mediators, and (4) increased follicular keratinization.

• Circulating androgens cause sebaceous glands to increase their size and activity. There is increased keratinization of epidermal cells and development of an obstructed sebaceous follicle, called a microcomedone. Cells adhere to each other, forming a dense keratinous plug. Sebum, produced in increasing amounts, becomes trapped behind the keratin plug and solidifies, contributing to open or closed comedone formation.

• Pooling of sebum in the follicle facilitates proliferation of the anaerobic bacterium P. acnes, which generates a T-cell response resulting in inflammation. P. acnes produces a lipase that hydrolyzes sebum triglycerides into free fatty acids that may increase keratinization and lead to microcomedone formation.

• Noninflammatory acne lesions include closed comedones (whiteheads) and open comedones (blackheads). Closed comedones are the first visible lesion in acne; they are almost completely obstructed to drainage and have a tendency to rupture. Open comedones are formed as the plug extends to the upper canal and dilates its opening.

• Inflammatory acne lesions include papules, pustules, and nodules. Pus formation occurs due to recruitment of neutrophils into the follicle during the inflammatory process and release of P. acnes–generated chemokines. P. acnes also produces enzymes that increase permeability of the follicular wall, causing it to rupture, thereby releasing keratin, lipids, and irritating free fatty acids into the dermis.

CLINICAL PRESENTATION

• Lesions usually occur on the face, back, neck, shoulders, and chest and may extend to the buttocks or extremities. One or more anatomic areas may be involved; once present, the pattern of involvement tends to remain constant. The skin, scalp, and hair are frequently oily.

• Lesions may take months to heal completely. Nodules and deep lesions may result in scarring. Resolution of inflammatory lesions may leave erythematous or pigmented macules (hyperpigmentation) that persist for months or longer, especially in dark-skinned individuals.

DIAGNOSIS

• Diagnosis is established by patient assessment, which includes observation of lesions and excluding other potential causes (eg, drug-induced acne). Several different systems are in use to grade acne severity.

TREATMENT

• Goals of Treatment: Reduce the number and severity of lesions, improve appearance, slow progression, limit duration and recurrence, prevent disfigurement from scarring and hyperpigmentation, and avoid psychologic suffering.

General Approach

• Acne is a chronic disease that warrants early and aggressive treatment (Fig. 15-1...