CASE #2: Sebaceous hyperplasia
This patient had sebaceous hyperplasia, a benign proliferation of the sebaceous gland that occurs in a periorbital location on patients of middle age or older. The condition is characterized by small, painless, 1- to 3-mm, yellow-to-flesh-colored papules, often clustered together.
The main differential diagnosis for sebaceous hyperplasia is basal cell carcinoma (BCC). The similarly sized lesions are typically seen on sun-exposed areas of the face. Patients with either condition will have a history of prolonged sun exposure as well as actinic keratoses. While both BCC and sebaceous hyperplasia can present as yellow, flesh-colored, or translucent growths with a central depression, sebaceous hyperplasia papules are more yellow than translucent and rarely have scale or crust. Telangiectasias are rare.8 Unlike BCCs, sebaceous hyperplasia lesions do not bleed and are soft to palpation; changes in size or appearance are uncommon.
Additional conditions mistaken for sebaceous hyperplasia include trichoepithelioma, xanthoma, fibrous papules, epidermal inclusion cysts, molluscum contagiosum, and sebaceous carcinoma.
Biopsy is recommended only if the diagnosis is unclear.9 Sebaceous hyperplasia is a benign condition, and no treatment is necessary, although many patients seek removal of the lesions for cosmetic reasons. Cryotherapy, electrodesiccation at a low setting, shave excision, and application of trichloroacetic acid 35% are all reasonable treatments. However, scarring is a possible side effect. Removal by application of a carbon-dioxide laser has recently been found successful in removing sebaceous hyperplasia.10 With all of these treatments, lesions may recur unless the entire growth is destroyed. Daily isotretinoin has been used for severe cases because of its ability to temporarily shrink the sebaceous glands, but lesions return after discontinuing therapy. Our patient’s papule was removed with shave excision. He has had no recurrence of the lesion, and his prognosis is excellent.
Ms. Conley is a medical student at the University of California, San Diego. Dr. Buka is a pediatric dermatology fellow in the Division of Dermatology, Children’s Hospital San Diego.
1. Karagas MR, Greenberg ER, Spencer SK, et al. Increase in incidence rates of basal cell and squamous cell skin cancer in New Hampshire, USA. The New Hampshire Skin Cancer Study Group. Int J Cancer. 1999;81: 555-559.
2. Johnson RL, Rothman AL, Xie J, et al. Human homolog of patched, a candidate gene for the basal cell nevus syndrome. Science. 1996;272:1668-1671.
3. van Dam RM, Huang Z, Rimm EB, et al. Risk factors for basal cell carcinoma of the skin in men: results from the health professionals follow-up study. Am J Epidemiol. 1999;150:459-468.
4. Milan T, Verkasalo PK, Kaprio J, Koskenvuo M. Lifestyle differences in twin pairs discordant for basal cell carcinoma of the skin. Br J Dermatol. 2003; 149:115-123.
5. Karagas MR, Tosteson TD, Blum J, et al. Design of an epidemiologic study of drinking water arsenic exposure and skin and bladder cancer risk in a U.S. population. Environ Health Perspect. 1998;106 (Suppl 4):1047-1050.
6. Boonchai W, Green A, Ng J, et al. Basal cell carcinoma and chronic arsenicism occurring in Queensland, Australia, after ingestion of an asthma medication. J Am Acad Dermatol. 2000;43:664-669.
7. Lichter MD, Karagas MR, Mott LA, et al. Therapeutic ionizing radiation and the incidence of basal cell carcinoma and squamous cell carcinoma. The New Hampshire Skin Cancer Study Group. Arch Dermatol. 2000;136:1007-1011.
8. Benign neoplasms and hyperplasia, part 1 section VII. In: Fitzpatrick TB, Johnson RA, Wolff K, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology. 4th ed. New York, N.Y.: McGraw-Hill; 2000:200.
9. Epidermal growth. In: Heml KF, Marks JG, eds. Atlas of Differential Diagnosis in Dermatology. New York, N.Y.: Churchill Livingstone; 1998:218-219.
10. No D, McClaren M, Chotzen V, Kilmer SL. Sebaceous hyperplasia treated with a 1450-nm diode laser. Dermatol Surg. 2004;30:382-384.�