CASE #2: Sebaceous hyperplasia
Areolar glands (also called glands of Montgomery) are sebaceous glands in the nipple that secrete a lipoid fluid. The glands’ function is not fully known, but it has been suggested that the glands and their secretions contain a lubricating and protective substance that alters the skin’s pH and discourages bacterial growth. This secretion helps keep the skin healthy and the areola elastic. Areolar glands also secrete a small amount of milk.
Found on the surface of the skin, Montgomery tubercles can be barely noticeable, can be noticeable as protuberant projections on the areola, or can have increased turgor after exposure or stimulation. Montgomery tubercles and glands become more prominent during pregnancy and lactation. The number of Montgomery glands ranges from four to 28.
A study of samples from 12 modified radical mastectomy specimens looked at 1,536 serial sections of areolar tubercles.7 In 34 of 35 tubercles, a mammary lactiferous duct was associated with a sebaceous apparatus. This lactiferous duct ascended from deeper mammary parenchyma and entered the sebaceous gland. Histopathologic changes identified included features of fibrocystic disease, atypical intraductal hyperplasia, and carcinoma in situ. Because the areolar tubercle has two components — a sebaceous gland and a mammary duct arising from deeper breast parenchyma — diseases of the breast may also involve the areola independent of papilla-nipple involvement.
Areolar glands can be flesh-toned, yellow, pink, red, or white in color. They do not contain any distinct material; rather their color is an optical function of the thickness of the skin and the chromophores in the skin (water, hemoglobin, melanin, and secretory material). Some women squeeze the glands to extract the seemingly whitish-yellow contents, which can lead to scarring.
The areolar glands’ role in mother-infant interactions may pertain to protective, mechanical, and communicative functions. The secretion of areolar glands from lactating women elicits selective, unconditional responses in neonates. Areolar secretions from lactating women are especially crucial for optimal mother/neonate interaction in human newborns. Volatile compounds carried in these substrates appear to play a key role in establishing behavioral and physiologic processes pertaining to milk transfer and production, and hence, survival.
It is thought that the human breast areolae may function as scent organs, with morphologic data supporting the possible involvement of aereolar glands and tubercles in maternal-neonatal coadaptation and the early engagement of attachment and bonding.
A morphologic study of neonates between birth and day 3 compiled the number, secretory status, and spatial distribution of areolar glands. Researchers collected data on the infants’ weight variation, the mothers’ perception of the infant’s behavior at breast, and duration between delivery and onset of lactation. Areolar glands were seen in virtually all women, and great individual variations existed. The areolar distribution was nonrandom, and approximately 20% of the women had areolar glands giving off a secretion.
The quantity of areolar glands related positively with neonatal weight gain between birth and day 3 and the mother’s perception of the infant’s latching speed and sucking activity. The quantity of areolar glands also related positively with the onset of lactation in first-time mothers. The authors concluded that maternal endowment with areolar glands may contribute to an infant’s breastfeeding performance and early growth, and the mother’s lactation onset.8
Sebaceous hyperplasia is one reason for the yellow appearance of areolar glands and tubercles. A manifestation of rosacea that increases in frequency with age, sebaceous hyperplasia commonly occurs on the face and occasionally on the neck. Fordyce’s spot-like lesions have been seen on both areolae of women.9 The histology of the lesions showed sebaceous hyperplasia.
Areolar sebaceous hyperplasia in men — an uncommon entity first noted in 1985 — manifests clinically as yellowish thickening of the areolae and histopathologically by large numbers of mature hyperplastic sebaceous lobules connected to the surface of the skin through short, hairless, infundibular canals.10 A variety of morphologies of male areolar sebaceous hyperplasia occur, including unilateral areolar sebaceous hyperplasia and unilateral sebaceous hyperplasia as a plaque.11
In the female breast after age 25 years, apocrine metaplasia (aberrant growth of aprocrine glands) remains a most common clinical finding. The apocrine cell has a variety of atmans with complex nosology. Apocrine variants of both in situ and invasive cancer exist. Common iterations of apocrine metaplastic lesions include those with fibrocystic change and apocrine adenoma, apocrine change within sclerosing adenosis, atypical apocrine lesions and apocrine malignancies. Isolated areolar apocrine chromhidrosis — a rare phenomenon that usually occurs in the axilla — has been reported.12
A diagnosis of sebaceous hyperplasia was explained to the patient in this case. No treatment was necessary.
Noah S. Scheinfeld, MD, JD, is an assistant clinical professor of dermatology at Columbia University in New York City, where he has a private practice. The author has no relationships to disclose relating to the content of this article.
2. Scheinfeld NS. Molluscum contagiosum. Skinmed. 2008;7:89-92.
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6. van der Wouden JC, van der Sande R, van Suijlekom-Smit LW et al. Interventions for cutaneous molluscum contagiosum. Cochrane Database Syst Rev. 2009;4:CD004767.
7. Smith DM Jr, Peters TG, Donegan WL. Montgomery’s areolar tubercle. A light microscopic study. Arch Pathol Lab Med. 1982;106:60-63.
9. Tsuji T, Yamauchi R. Areolar sebaceous hyperplasia with a Fordyce’s spot-like lesion. J Dermatol. 1994;21:524-526.
10. Catalano PM, Ioannides G. Areolar sebaceous hyperplasia. J Am Acad Dermatol. 1985;13:867-868.
11. Fariña MC, Soriano ML, Escalonilla P, et al. Unilateral areolar sebaceous hyperplasia in a male. Am J Dermatopathol. 1996;18:417-419.
All electronic documents accessed November 7, 2011.