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Q1: Definition and clinical presentation (2 min)
A 16-year-old boy has a unilateral brown patch with coarse dark hair on his left shoulder, first noticed at age 13. What is the diagnosis and what are the key clinical features?
Model answer: Becker's naevus (Becker melanosis) — a benign, androgen-dependent cutaneous hamartoma presenting at puberty as a large, unilateral, light- to dark-brown, irregularly bordered (geographic) patch with hypertrichosis confined to the patch on the shoulder, upper chest or upper back, predominantly in adolescent males. The three-phase evolution is characteristic: faint pigment at peripuberty, then enlargement and darkening, then terminal hair growth after puberty.
[2] [3]Q2: Pathophysiology (3 min)
Why does Becker's naevus appear at puberty, and what is the underlying biology?
Model answer: It is a hamartoma of three native skin structures — epidermis (acanthosis, papillomatosis, increased basal melanin without more melanocytes), hair follicle (terminal hair) and arrector pili smooth muscle (hyperplasia). It is androgen-dependent: immunohistochemistry shows up-regulated androgen receptors in basal keratinocytes and follicular outer root sheath, so the lesion declares at the pubertal androgen surge — explaining the onset, male predominance, hypertrichosis and intralesional acne. The unilateral, mosaic pattern reflects a postzygotic somatic (paradominant) mutation; familial cases show paradominant inheritance (silent germline allele plus a second somatic hit).
[2]Q3: Differential diagnosis and investigations (3 min)
How do you distinguish it from other pigmented lesions, and do you need to investigate?
Model answer: It is a clinical diagnosis. Biopsy is reserved for atypical sites (face, lower limb), absent hair, or changing lesions. Distinguish from: congenital melanocytic naevus (present at birth, darker, nodular, contains naevus cells); cafe-au-lait macule (flat, smooth-bordered, hairless, multiple in NF1); congenital smooth-muscle hamartoma (near-birth, firmer, less epidermal change); post-inflammatory hyperpigmentation (preceding rash, fades); linear epidermal naevus (verrucous surface, present at birth); naevus of Ota/Ito (blue-grey dermal melanocytosis, no hair). Histology: basal hyperpigmentation, acanthosis, arrector pili smooth-muscle hyperplasia, no naevus cells.[2][3]
Q4: Management (3 min)
Outline your stepwise approach to management.
Model answer: Step 1: reassurance — benign, no malignant potential, stabilises after puberty. Step 2: camouflage make-up. Step 3: Q-switched laser (Nd:YAG 1064 nm, ruby 694 nm, alexandrite 755 nm) for pigmentation — variable, partial, may recur. Step 4: long-pulsed laser (alexandrite, diode, Nd:YAG) for hair — better response. Step 5: combination protocols for best cosmetic result. Excision rarely appropriate. No role for topical bleaching agents or retinoids. Counsel on realistic, partial improvement and post-inflammatory hyperpigmentation risk.
[1]Q5: Associations, complications and prognosis (2 min)
What must you screen for, and what is the prognosis?
Model answer: Screen for Becker's naevus syndrome — examine the ipsilateral breast (hypoplasia), spine (scoliosis, vertebral anomalies) and limbs (asymmetry, hypoplasia); image if any anomaly is found.[3] Complications are mainly cosmetic and psychological; underlying smooth-muscle hamartoma may cause pruritus. Prognosis is excellent: benign, stabilises after puberty, persists lifelong, no malignant transformation, no impact on lifespan.
References3ShowHide
- [1]Zhong Y, et al. Lasers for Becker's nevus Lasers Med Sci, 2019.PMID 30762191
- [2]Grande Sarpa H, et al. Androgen receptor expression patterns in Becker's nevi: an immunohistochemical study J Am Acad Dermatol, 2008.PMID 19119099
- [3]Patel P, et al. Sebaceus and Becker's Nevus: Overview of Their Presentation, Pathogenesis, Associations, and Treatment Am J Clin Dermatol, 2015.PMID 25782676