Acne Vulgaris

Descriptive text is not available for this image BASICS

DESCRIPTION

Acne vulgaris is a disorder of the pilosebaceous units, and a chronic inflammatory dermatosis notable for open/closed comedones, papules, pustules, and/or nodules.Geriatric Considerations
Favre-Racouchot syndrome: comedones on face/head due to sun exposurePregnancy Considerations

  • May result in a flare or remission of acne; typically, improves in 1st trimester, may worsen in 3rd trimester
  • Can use topical benzoyl peroxide, azelaic acid, erythromycin, or clindamycin; salicylic acid, oral erythromycin, azithromycin, cephalexin, or amoxicillin
  • Avoid topical tretinoin, trifarotene, and adapalene—may cause retinoid embryopathy; class C
  • Contraindicated: isotretinoin (Category X), tazarotene, tetracycline, doxycycline, minocycline, sarecycline, spironolactone

Pediatric Considerations

  • Neonatal acne (neonatal cephalic pustulosis)— newborn to 8 weeks; lesions limited to face; usually self-limited, Rx topical ketoconazole 2% cream
  • Infantile acne—6 weeks to 1 year; lesions on face, neck, back, chest; topical/systemic Rx
  • Early to middle childhood acne—1 to 7 years; rare; consider hyperandrogenism.
  • Preadolescent acne—7 to 12 years; common, 47% of children, usually due to adrenal awakening, comedonal lesions
  • Do not use tetracyclines in those <8 years old; other therapies similar to adolescent

EPIDEMIOLOGY

  • Predominant age: early to late puberty, may persist in 20–40% into 4th decade
  • Male > female (teen), female > male (adult)

Prevalence

  • 80–95% of adolescents affected; 8% of adults aged 25 to 34 years; 3% at 35 to 44 years
  • African Americans 37%, Hispanic 32%, Caucasians 24%
  • 9.4% globally, 8th most common disease worldwide

ETIOLOGY AND PATHOPHYSIOLOGY

  • Androgens (testosterone and dehydroepiandrosterone sulfate [DHEA-S]) stimulate sebum production/qualitative sebum changes and proliferation of keratinocytes in follicles. Keratin plug obstructs follicle os, causing sebum accumulation and follicular distention.
  • Cutibacterium acnes phylotype IA1, an anaerobe, colonizes and proliferates within a biofilm in the plugged follicle. C. acnes promote proinflammatory mediators/cytokines (IL-1), causing inflammation of follicle/dermis.

Genetics

Familial association in 50%

RISK FACTORS

  • Increased endogenous androgenic effect
  • Oily cosmetics, cocoa butter, polyvinyl chloride, chlorinated hydrocarbons, cutting oil
  • Occluding skin surface (e.g., sports equipment such as helmets and shoulder pads), cell phones, hands against the skin, or pandemic masks (“maskne”—subset of acne mechanica)
  • Numerous drugs, including androgenic steroids (e.g., steroid abuse, some birth control pills), lithium, phenytoin
  • Endocrine disorders: PCOS, Cushing syndrome, congenital adrenal hyperplasia, androgen-secreting tumors, acromegaly
  • Psychological stress
  • High-glycemic load, possibly high-dairy diets (skim milk), and whey protein supplements may exacerbate acne.
  • Severe acne may worsen with smoking.

GENERAL PREVENTION

Avoidance of risk factors

COMMONLY ASSOCIATED CONDITIONS

Acne conglobata, hidradenitis suppurativa, pomade acne—hair oils, SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis), pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) and seborrhea, acne, hirsutism, and alopecia (SAHA), dark-skinned patients: 50% keloidal scarring and 50% acne hyperpigmented macules

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