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KembaraXtra-Medicine: Acne Vulgaris
Acne vulgaris is a chronic disorder of the pilosebaceous unit caused by abnormal shedding of follicular epithelium that blocks the follicular canal and promotes inflammation. This process leads to the development of comedones, papules, pustules, nodules/cysts, and, in some patients, scarring and dyspigmentation. Lesions are broadly categorized as noninflammatory (open and closed comedones) and inflammatory (papules, pustules, nodules, and cysts). Inflammatory acne may be described as papulopustular, nodulocystic, or mixed. Although many grading scales exist, there is no universally accepted severity system; clinically, acne is often described as mild, moderate, or severe based on lesion type and burden.
In general, mild acne is dominated by comedones with few inflammatory lesions (often fewer than 10) and no nodules or cysts. Moderate acne involves more numerous inflammatory papules and pustules (often 10–40) along with comedones, and “moderately severe” acne includes higher inflammatory counts or a small number of deeper nodulocystic lesions. Severe acne includes extensive papules and pustules and/or many nodulocystic lesions, often with early scarring. A pattern of deeper lesions along the mandible and anterolateral neck, menstrual flares, and signs of androgen excess such as hirsutism or irregular menses suggests hormonally driven acne.
Acne is commonly referred to simply as acne and is coded under ICD-10-CM L70.0 (acne vulgaris), with additional codes for specific variants such as acne conglobata, infantile/neonatal acne, acne excoriée, and others. Acne is the most common skin disease in the United States and is most prevalent in teenagers, affecting up to 85% to some degree. Incidence peaks between ages 15 and 18 in all genders. While acne often improves before age 25, a substantial minority persists into adulthood, especially in women, with a portion continuing into the mid-40s. Increased “acne mechanica” related to prolonged mask use has also been observed.
Clinical findings include open comedones (blackheads) and closed comedones (whiteheads), inflammatory papules and pustules, deeper nodules or cysts, and occasionally ectatic pores. Many patients develop postinflammatory erythema or hyperpigmentation, and some develop scars such as ice-pick, rolling, boxcar/crateriform, or keloidal scars. Lesions often coexist at different stages of evolution. The typical distribution is the face, upper chest, and back, while hormonal patterns more often involve the jawline and neck.
The underlying pathogenesis centers on comedone formation driven by increased sebum production and abnormal keratinization, which blocks follicles. This environment allows overgrowth of Cutibacterium acnes (formerly Propionibacterium acnes), promoting inflammation. Acne can be worsened by environmental factors such as hot, humid climates; certain medications and exposures (including iodine-containing cough mixtures, pomades/hair greases, anabolic steroids, progestins, lithium, and halogenated hydrocarbons); mechanical friction from sports gear or excessive washing; and stress, which may exacerbate acne via hypothalamic–pituitary–adrenal axis effects and androgen activation.
Diagnosis is clinical, but the differential is broad and includes folliculitis (including gram-negative), perioral dermatitis, rosacea, steroid acne, hidradenitis suppurativa, pseudofolliculitis barbae, keratosis pilaris, seborrheic dermatitis, drug eruptions, and occupational oil/grease exposure. Workup relies on history and physical examination, including prior treatments, skincare products, cosmetic use, family history, medication review (including OTC agents), and in females, the presence of cyclic flares or hormonal features. Clinicians should consider hyperandrogenism in women with hirsutism, irregular menses, or androgenic alopecia, and in children with early-onset acne, seborrhea, or acanthosis nigricans.
Routine laboratory testing is not typically needed. Patients who may be treated with isotretinoin should have baseline liver enzymes and triglycerides checked, and pregnancy testing is required before starting and during therapy due to strong teratogenic risk. If hyperandrogenism is suspected, evaluation may include DHEAS, total/free testosterone, LH, and FSH, though women with regular menses often do not require serum androgen testing.
Treatment is best approached with combination therapy targeting multiple pathogenic pathways. Nonpharmacologic options include selected light-based therapies such as blue light for moderate inflammatory acne, though long-term benefit compared with standard therapy is uncertain. Dietary counseling is appropriate in obese patients, and some evidence suggests high glycemic diets and certain dairy patterns may worsen acne, though the strength of association is debated.
For mild acne, first-line therapy typically includes benzoyl peroxide, a topical retinoid, or combination topical regimens, including topical antibiotics when inflammation is present. Topical therapies require 6 to 8 weeks of consistent use to assess effectiveness. Comedonal acne responds best to topical retinoids (e.g., adapalene, tretinoin, tazarotene), which normalize follicular keratinization and are comedolytic; salicylic acid washes can be helpful as adjuncts. Benzoyl peroxide is often added to reduce bacterial burden and inflammation but may cause irritation and dryness.
For inflammatory acne, topical antibiotics (such as clindamycin or erythromycin) are commonly used with benzoyl peroxide to reduce resistance and improve efficacy, and fixed-dose combination products can simplify regimens. Moderate to severe inflammatory acne may require oral antibiotics (commonly doxycycline or minocycline), ideally limited to 3–6 months to reduce resistance and microbiome disruption. Patients with nodulocystic acne or moderate-to-severe acne unresponsive to standard therapy may need systemic options such as isotretinoin, hormonal therapy (combined oral contraceptives), and/or antiandrogen therapy such as spironolactone; intralesional corticosteroid injections can rapidly improve large nodules.
Referral to dermatology is appropriate for severe, scarring, refractory acne or when procedures are needed, including intralesional injections, comedone extraction, and treatments for scarring such as resurfacing lasers, dermabrasion, chemical peels, or other scar-directed interventions. Important clinical pearls include recognizing that acne may worsen during the first few weeks of retinoid therapy before improving, and that worsening inflammatory acne after prolonged antibiotic use should raise suspicion for gram-negative folliculitis. Patients should be counseled that acne is usually controllable but not quickly “cured,” and meaningful improvement generally requires at least 4–8 weeks of consistent therapy, with attention to adherence and gentle skin care to minimize irritation and scarring.
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