Dermatology · Acne Vulgaris
The facts most likely to be tested
The primary pathogenesis of acne involves follicular hyperkeratinization, sebum production, Cutibacterium acnes proliferation, and inflammation.
First-line therapy for mild comedonal acne is topical retinoids (e.g., tretinoin, adapalene).
First-line therapy for mild papulopustular acne is a combination of topical retinoids and topical benzoyl peroxide.
Moderate to severe inflammatory acne requires the addition of oral antibiotics (e.g., doxycycline or minocycline) to topical therapy.
Isotretinoin is the gold-standard treatment for nodulocystic acne or cases refractory to conventional therapy.
Isotretinoin is a potent teratogen requiring strict adherence to the iPLEDGE program and two forms of contraception.
Common side effects of isotretinoin include xerosis (dry skin), cheilitis (chapped lips), photosensitivity, and elevated triglycerides.
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A 17-year-old male presents to the clinic with a 6-month history of worsening facial breakouts. Physical examination reveals numerous open and closed comedones, several erythematous papules, and two tender nodules on the cheeks and forehead. He has previously failed a 3-month trial of topical benzoyl peroxide and adapalene. He has no history of systemic symptoms or scarring.
What is the most appropriate next step in management?
Oral doxycycline
The patient has moderate inflammatory acne that has failed topical therapy, necessitating the addition of an oral antibiotic to address the inflammatory component.
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Etiology / Epidemiology
Affects adolescents due to androgen-mediated sebum production and Cutibacterium acnes colonization.
Clinical Manifestations
Presents with comedones, inflammatory papules, and pustules; nodulocystic acne is the most severe form.
Diagnosis
Diagnosis is clinical; no laboratory testing is required for routine cases.
Treatment
Topical retinoids and benzoyl peroxide are first-line; teratogenic oral isotretinoin for severe cases.
Prognosis
High risk of permanent scarring and post-inflammatory hyperpigmentation if left untreated.
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Epidemiology & Etiology
Acne is a chronic inflammatory disorder of the pilosebaceous unit peaking during puberty. Increased androgen levels stimulate sebaceous gland hypertrophy and sebum production. Genetic predisposition and Cutibacterium acnes proliferation are primary drivers.
Pertinent Anatomy
The pilosebaceous unit consists of the hair follicle, sebaceous gland, and arrector pili muscle. Obstruction of the follicular infundibulum leads to the formation of microcomedones.
Pathophysiology
Pathogenesis involves four factors: follicular hyperkeratinization, increased sebum production, C. acnes colonization, and inflammation. Excess keratinocytes plug the follicle, creating a comedone. Subsequent bacterial lipase activity triggers an inflammatory cascade.
Clinical Manifestations
Lesions range from non-inflammatory open comedones (blackheads) and closed comedones (whiteheads) to inflammatory papules and pustules. Nodulocystic acne presents with deep, painful lesions and carries a high risk of permanent scarring. Red flags include sudden onset in adults or signs of hyperandrogenism like hirsutism or irregular menses.
Diagnosis
Diagnosis is clinical based on the presence of characteristic lesions in a seborrheic distribution. No gold standard lab test exists. Evaluate for endocrine disorders if the patient presents with sudden, severe, or treatment-resistant acne.
Treatment
Mild acne is managed with topical retinoids and benzoyl peroxide. Moderate cases require the addition of topical antibiotics or oral tetracyclines. Severe or recalcitrant acne is treated with oral isotretinoin, which is strictly teratogenic and requires the iPLEDGE program registration.
Prognosis
Early intervention is critical to prevent atrophic or hypertrophic scarring. Patients on isotretinoin require monthly monitoring of liver function tests and lipid panels due to potential hepatotoxicity and hypertriglyceridemia.
Differential Diagnosis
Rosacea: absence of comedones
Folliculitis: monomorphic papules/pustules
Perioral dermatitis: spares the vermilion border
Drug-induced acne: monomorphic lesions following medication initiation
Pseudofolliculitis barbae: associated with shaving