Acne vulgaris is one of the most common skin conditions in children and adolescents. It is a disorder of pilosebaceous units (PSUs). PSUs are found predominantly on the face, chest, back, and upper arms. Acne presents as comedonal or inflammatory lesions and can cause depressed scars and hyperpigmentation. Presentation, treatment, and associated systemic manifestations differ by age of presentation, pubertal status, and severity of disease.

  • Classification of acne by age:
    • Neonatal (birth to 6 weeks): affects up to 20% of neonates. Also known as neonatal cephalic pustulosis. Presents with a papulopustular eruption predominantly on face. Thought to be due to Malassezia colonization. No treatment necessary; for severe cases can use ketoconazole cream 2%
    • Infantile acne (6 weeks to 1 year): presents with comedonal and inflammatory lesions on face. Some evidence that it may predispose to severe adolescent acne. Often, no underlying endocrine abnormality; self-limited but in severe cases can use topical acne treatments
    • Midchildhood acne (1 to 6 years): uncommon. Presents with comedonal and inflammatory lesions on face. Suspect an underlying endocrinopathy.
    • Preadolescent (7 to 11 years): presents with predominantly comedonal lesions in “T-zone,” central face; can be first sign of onset of puberty
    • Adolescent (12 to 19 years): very common presentation, affects 85% of adolescents

Risk Factors


Familial patterns exist, but no inheritance pattern has been demonstrated.

General Prevention

  • Effective and early treatment limits scarring, postinflammatory pigment alteration, and minimizes psychosocial impact.
  • Use of oil-free and noncomedogenic moisturizers, sunscreens, and make-up


Pathogenesis of acne is multifactorial and involves four different components:

  • Increased sebum production: stimulated by an increase in androgen levels. The adrenal gland is active during the 1st year of life and then reawakens in preadolescent time period. Production peaks in teens and decreases in 20s.
  • Alteration in follicular growth and differentiation leading to the creation of a microcomedone, a precursor of inflammatory and comedonal acne lesions
  • Follicular colonization with Propionibacterium acnes, an anaerobic, gram-positive diphtheroid bacteria. P. acnes produces free fatty acids (FFAs) leading to inflammation.
  • Inflammation and immune response through the innate immune system


  • Androgen excess (physiologic vs. pathologic)
  • Medication-induced (corticosteroids, anticonvulsants, lithium, etc.)
  • Occlusion (from topical- or oil-based products)
  • Frictions from clothing or athletic gear such as helmets, shoulder pads, chin straps, or bra straps may worsen acne.

Commonly Associated Conditions

  • Polycystic ovarian syndrome (PCOS)
  • SAPHO syndrome: synovitis, acne, pustulosis, hyperostosis, and osteitis
  • Adrenal or gonadal/ovarian tumors
  • Late-onset congenital adrenal hyperplasia

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