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1
Question:

An 18-year-old man comes to the office due to acne.  The patient has had mild facial acne for the past 3 years that has responded well to topical agents.  Since he started college 2 months ago, the acne has worsened and has spread to his torso and neck.  Despite use of the topical agents, it has continued to worsen.  The patient plays on the university's baseball team, which requires him to practice outdoors for several hours 3 days a week.  He also swims in an indoor pool several hours a week.  Since starting college, the patient has adopted a dairy-free, low-glycemic-index diet.  Physical examination shows severe, nodulocystic acne on the face, neck, chest, and back.  Which of the following most likely caused this patient's worsening acne?

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Explanation:

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Acne vulgaris

Clinical features

  • Comedonal acne: closed or open comedones on forehead, nose & chin
  • Inflammatory acne: small, erythematous papules & pustules
  • Nodular acne: large, painful nodules; sinus tracts & scarring

Pathogenesis

  • Hyperkeratinization & obstruction of pilosebaceous follicle
  • Sebaceous gland enlargement & increased sebum production
  • Metabolism of sebaceous lipids by Cutibacterium acnes & release of inflammatory fatty acids
  • Follicular inflammation & rupture

Risk factors

  • Increased circulating androgens (eg, puberty, polycystic ovary syndrome)
  • Mechanical trauma/friction (eg, excessive scrubbing, tight clothing)
  • Comedogenic oil-based skin & hair products

This college athlete's rapidly worsening acne despite the previously effective use of topical agents raises concern for androgenic steroid supplementation.  Androgens (eg, dehydroepiandrosterone, testosterone) are produced predominantly by the adrenal glands and gonads; they may also be supplemented exogenously.  They bind to receptors in cytosol, translocate into the nucleus, and alter gene expression.  In the skin, this results in increased sebum production by sebaceous glands and follicular epidermal hyperproliferation, which promote acne formation.

The role that androgens play in acne pathogenesis is clearly demonstrated in the prepubertal and pubertal years, when a rise in adrenal and gonadal androgens coincides with acne formation.  Hirsute women with pathologic hyperandrogenic states (eg, polycystic ovary syndrome) also frequently have coexisting acne.  When acne suddenly becomes severe (eg, nodulocystic acne, acne fulminans), androgenic steroid supplementation should be considered as a possible cause, especially in athletes.

(Choices A and C)  Dairy consumption (particularly skim milk) and a high-glycemic-index diet are associated with acne.  Natural hormones in milk and increased levels of insulin-like growth factor may play a role.

(Choice B)  Chlorine has antibacterial effects against Cutibacterium acnes, the bacteria which promotes inflammation in acne.  Regular exposure to chlorinated water may improve acne.

(Choice E)  Ultraviolet radiation can cause sunburn or precipitate photodermatoses, such as the malar rash seen in systemic lupus erythematosus or drug-induced photosensitivity (eg, tetracyclines, sulfonamides).  However, ultraviolet radiation would not suddenly cause severe acne.

Educational objective:
Androgens stimulate follicular epidermal hyperproliferation and excessive sebum production, thereby promoting acne development.  Androgenic steroid supplementation is a known cause of acne, especially in competitive athletes.