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INTRODUCTION

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  • Acne is a common, usually self-limiting disease involving inflammation of the sebaceous follicles of the face and upper trunk.

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PATHOPHYSIOLOGY

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  • Acne usually begins in the prepubertal period 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 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 Propionibacterium 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.

  • The closed comedone (whitehead) is the first visible lesion of acne. It is almost completely obstructed to drainage and has a tendency to rupture.

  • An open comedone (blackhead) is formed as the plug extends to the upper canal and dilates its opening. Acne characterized by open and closed comedones is termed noninflammatory acne.

  • 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. Inflammatory lesions that may form and lead to scarring include pustules, nodules, and cysts.

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CLINICAL PRESENTATION

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  • Lesions usually occur on the face, back, upper chest, and shoulders. Severity varies from a mild comedonal form to severe inflammatory acne. The disease is categorized as mild, moderate, or severe, depending on the type and severity of lesions.

  • Lesions may take months to heal completely, and fibrosis associated with healing may lead to permanent scarring.

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DIAGNOSIS

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  • 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.

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TREATMENT

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  • Goals of Treatment: The goals are to reduce the number and severity of lesions, improve appearance, slow progression, limit duration and recurrence, prevent disfigurement associated with scarring and hyperpigmentation, and avoid psychologic suffering.

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GENERAL APPROACH

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  • Acne is treated as a chronic disease that warrants early and aggressive treatment (FIG. 15–1). Maintenance therapy is often needed for optimal outcomes. Patient adherence to lengthy treatment regimens is crucial ...

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