A 12-year-old boy presents to the dermatology clinic with a 2-year history of a brown patch on his chest. The 8-cm patch had been asymptomatic, but over the past 6 months, it has become darker, with hair and acne vulgaris developing within the lesion. The patient is self-conscious about the lesion’s appearance and wishes to learn if it can be treated to lessen the hyperpigmentation.
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Becker nevus is an acquired patch or thin plaque of hyperpigmentation and excessive hair growth that was first described in 1949 by William Becker.1 These benign, hamartomatous lesions commonly occur in a unilateral distribution across the upper trunk, shoulders, and back. They are asymmetrical, with sharply demarcated borders. Classically, patients report the appearance of increasing brown pigmentation, followed by progressive hair growth over several years.1
Becker nevi typically develop or become more pronounced in peripubertal adolescents when androgen levels rise and lead to increased genital skin pigmentation, hair growth, and muscle hypertrophy.2 The lesions may first appear in early adulthood, but this is less common. These nevi are believed to be the result of increased androgen sensitivity and upregulation of androgen receptors within the lesions, which cause varying degrees of localized melanosis, smooth muscle hyperplasia, and hair thickening.3
Due to the androgen-dependent nature of their pathogenesis, Becker nevi are identified more frequently in men. The diagnosis may be missed in women whose lesions are lighter in color or have less hair growth because of comparatively lower androgen levels.4
These nevi may occur as isolated lesions or as part of a constellation of other developmental anomalies of the breast or skeleton, known as Becker nevus syndrome.5 The syndrome arises sporadically, following a somatic mutation during embryogenesis that results in subsequent mosaicism with loss of heterozygosity. Although the presentation of Becker nevus syndrome occurs on a spectrum, the most common clinical manifestations that accompany the nevi are hypoplasia of the breast or limb ipsilateral to the lesion6 or vertebral defects, such as scoliosis or spina bifida occulta.5
Becker nevi occasionally are diagnosed based on their clinical appearance and patient history.2 Patients describe sudden-onset or worsening dark pigmentation of the lesion, with subsequent development of androgen-dependent changes within the lesion, such as thick hair growth or acne vulgaris. A biopsy and microscopic examination are performed to make a definitive diagnosis and differentiate Becker nevi from other pigmented lesions.1,2
On histologic examination, Becker nevi display many features of nevoid lesions, including acanthosis with bridging of elongated rete ridges and increased basal melanin. However, unlike true nevi, Becker nevi lack nevomelanocytic structures.1,5, Histologic examination reveals smooth muscle proliferation rather than nests of melanocytes.
Identification of a Becker nevus should prompt further evaluation for other developmental malformations including a thorough physical examination and radiographic imaging of the spine to rule out Becker nevus syndrome.7
The differential diagnosis includes other pigmented lesions commonly seen in adolescence, such as café au lait macules, congenital smooth muscle hamartomas, and congenital melanocytic nevi. Ordinarily, these congenital lesions are present at birth, whereas Becker nevi develop after the first decade of life.8,9 When the diagnosis is unclear based on clinical history and appearance, a biopsy should be performed to make a definitive diagnosis and determine the correct management.9
Clinically, congenital smooth muscle hamartomas may present similarly to Becker nevi—as hyperpigmented lesions with increased hair growth. A distinctive finding of congenital smooth muscle hamartomas absent in Becker nevi is the pseudo-Darier sign, in which the lesion becomes increasingly elevated or indurated in response to tactile stimulation.8 Histologically, both lesions demonstrate dermal smooth muscle hyperplasia, but this finding is more pronounced in congenital smooth muscle hamartomas; Becker nevi exhibit greater pigmentation in the basal layer.9
The clinical course of these lesions also differs. The hyperpigmentation and hypertrichosis associated with congenital smooth muscle hamartomas decreases over time but increases in Becker nevi. Congenital smooth muscle hamartomas frequently are observed in the lumbosacral area as opposed to the upper trunk with Becker nevi.9
Congenital melanocytic nevi can be differentiated from Becker nevi on microscopic examination by the presence of melanocytes with nevoid features.9
Due to the absence of melanocytic variants in Becker nevi, malignant transformation is unlikely to occur. Therefore, isolated, asymptomatic lesions can be managed conservatively, and surgical excision is not indicated.4 However, patients often request treatment for cosmetic purposes.
Hyperpigmentation traditionally is addressed with either ablative or Q-switched laser treatment. Laser therapy is time consuming, often requiring several treatment sessions. Ablative lasers are used to completely remove the epidermis, eradicating the lesion with residual scarring. Q-switched lasers target intralesional pigment within the dermis and epidermis. However, because the epidermis is not removed, complete removal of the lesion rarely is accomplished. Fractional resurfacing has been shown to be clinically effective and less invasive.10
After evaluating the patient in this case for associated bony and soft tissue abnormalities, we discussed treatment options. He and his parents opted to defer treatment.
Rachel Graubard, BS, and Emily Burns, BA, are students at Baylor College of Medicine, and Christopher Rizk, MD, is a dermatology fellow at Elite Dermatology in Houston, Texas.
1. Becker SW. Concurrent melanosis and hypertrichosis in distribution of nevus unius lateris. Arch Derm Syphilol. 1949;60(2):155-160.
2. Tymen R, Forestier JF, Boutet B, Colomb D. [Late Becker’s nevus. One hundred cases (author’s transl)]. Ann Dermatol Venereol. 1981;108(1):41-46.
3. Person JR, Longcope C. Becker’s nevus: an androgen-mediated hyperplasia with increased androgen receptors. J Am Acad Dermatol. 1984;10(2 Pt 1):235-238.
4. Hsu S, Chen JY, Subrt P. Becker’s melanosis in a woman. J Am Acad Dermatol. 2001;45(6 suppl):S195-S196.
5. Happle R, Koopman RJ. Becker nevus syndrome. Am J Med Genet. 1997;68(3):357-361.
6. Glinick SE, Alper JC, Bogaars H, Brown JA. Becker’s melanosis: associated abnormalities. J Am Acad Dermatol. 1983;9(4):509-514.
7. Ghosh SK, Majumder B, Agarwal M. Becker’s nevus syndrome: a report of a rare disease with unusual associations. Int J Dermatol. 2017;56(4):458-460.
8. Schmidt CS, Bentz ML. Congenital smooth muscle hamartoma: the importance of differentiation from melanocytic nevi. J Craniofac Surg. 2005;16(5):926-929.
9. Bilgiç Ö, Tunçez Akyürek F, Altınyazar HC. Pseudo Darier sign: a distinctive finding for congenital smooth muscle hamartoma. J Pediatr. 2016;169:318.
10. Glaich AS, Goldberg LH, Dai T, Kunishige JH, Friedman PM. Fractional resurfacing: a new therapeutic modality for Becker’s nevus. Arch Dermatol. 2007;143(12):1488-1490.