CASE #2: Sebaceous hyperplasia

Sebaceous hyperplasia (SH) is the physical manifestation of enlargement of the sebaceous gland to the point where discrete raised yellow aggregations of cells can be visualized. The discrete papules measure 2-3 mm in diameter and have the consistency of flesh, unlike milia or calcinosis cutis, which are hard to the touch.

SH most commonly occurs on the face, in particular the forehead and/or cheek. Sebaceous glands are sensitive to androgens, and any hyperplasia is rare in prepubescents. SH is most common in whites and in the middle-aged and elderly.

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Focused examination often demonstrates a central hair follicle surrounded by yellowish lobules. Dermoscopy often reveals prominent blood vessels. Although the hyperplastic glands are large, the glands of SH secrete very little sebum. In contrast to normal sebocytes that contain lipids, the hyperplastic sebaceous glands of SH contain small, undifferentiated sebocytes with large nuclei and scant cytoplasmic lipid.

SH has been noted in body areas other than the face, including the areola, chest, mouth, penis, scrotum and vulva. On the buccal mucosa, SH is referred to as Fordyce spots; SH on the glans penis or clitoris is called Tyson’s glands; SH on the areolae is also known as Montgomery glands, and SH on the eyelids is hyperplasia of the meibomian glands. Intraoral SH has also been noted.

Although the distribution of papules is usually random, SH has been noted in blaschkoid, linear (on the chest and penis), and zosteriform distributions. Bilateral areolar sebaceous hyperplasia in a woman has been noted,9 as has pubertal giant sebaceous hyperplasia over the nose.

Muir-Torre syndrome (MTS) is a genetic disorder characterized by a variety of pathology of the sebaceous gland, including SH as well as sebaceous adenoma, sebaceous epithelioma, or sebaceous carcinoma combined with internal malignancy (usually GI or genitourinary carcinomas). MTS has autosomal dominant pattern of inheritance in 60% of cases with a high degree of penetrance and variable expression.10

The differential for SH includes any process that results in yellowish papules. Specifically, the related condition of juxtaclavicular beaded lines (yellow papules in parallel or rippled distributions on the chest)11 basal cell carcinoma (in particular with sebaceous differentiation), xanthelasma, flat warts, epidermodysplasia verruciformis and epidermal nevus.

In particular, neoplasms of the sebaceous gland (e.g. sebaceous adenoma, seboacanthoma, sebaceous epithelioma, sebaceoma, mantleoma, sebomatricoma, and sebaceous carcinoma) can mimic SH. Preputial ectopic sebaceous glands mimicking molluscum contagiosum12 and giant solitary sebaceous gland hyperplasia clinically simulating epidermoid cyst13 have been reported. Sebaceous trichofolliculoma and trichofolliculoma rare adnexal tumors can resemble SH.

Rosacea is closely associated with SH of the discrete type. Rhinophyma, a key manifestation of rosacea, can be viewed as a variant of SH. Otophyma and blepharophyma, two rarer forms of sebaceous gland hyperplasia-type phymas, can also occur. Histology of the classic type of rhinophyma usually shows the histopathologic features of fully developed rosacea with the presence of prominent SH.

Sometimes phymas demonstrate marked dermal thickness, absence of folliculosebaceous structures, sclerotic collagen bundles with large amounts of mucin and spreading telangiectasia features akin to the elephantiasis caused by chronic lymphedema. Sebaceous gland hyperplasia and senile comedones (Favre-Racouchot syndrome) often manifest in the same patient. 

Oztas and colleagues reported on a series of 17 patients with 30 SH lesions, all of which were evaluated dermatoscopically.14 Cumulus sign, crown vessels, and milia-like cysts were detected in 100%, 86.6%, and 53.3% of the lesions, respectively. In 80% of the lesions, a feature with central umbilication surrounded by cumulus sign was observed (the Bonbon toffee sign). 

A variety of treatments have been reported for SH, including oral isotretinoin, antiandrogens (in women), electrodesiccation, CO2 laser surgery, cryosurgery, chemical peeling agents (in particular, bichloracetic acid and trichloracetic acid) and shave excision with curettage.

Limited cases are best treated with electrodesiccation with curettage. Photodynamic therapy with 5-aminolevulinic acid and a blue light source or intense pulsed-light source has been successful. Premature familial SH has been effectively treated with oral isotretinoin. 

This patient’s papules were effectively treated with low-voltage electrodesiccation with curettage. Three weeks later the area had healed, and the patient was happy with the cosmetic results. 

Noah 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.


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All electronic documents accessed December 13, 2011.