Seborrheic Keratosis

Woman With a Slowly Growing Mass on Her Back

University of Calgary

Dr A. K. C. Leung is a clinical professor of pediatrics at the University of Calgary and pediatric consultant at the Alberta Children’s Hospital in Calgary, Alberta, Canada. Dr A. A. C. Leung is a clinical scholar in internal medicine at the University of Calgary in Alberta and a research fellow at the Brigham and Women’s Hospital and Harvard Medical School in Boston, Massachusetts.


A 61-year-old woman presents with a 2-year history of a slowly growing mass on her back. The lesion is asymptomatic. She works as a casino hostess and does not actively participate in any outdoor activities. Her medical history is unremarkable, and she reports no recent weight loss. No similar lesion has been noted in other family members.


On examination, a sharply defined light brown mass with a finely verrucous surface measuring 1 cm 3 2 cm is noted. The rest of the examination is unremarkable.


An excisional biopsy is performed at the request of the patient. Histopathologic examination of the specimen shows a papillomatous growth of basaloid cells and squamous epithelial cells with marked hyperkeratosis.



(Answer on next page)

Answer: Seborrheic Keratosis

Seborrheic keratosis is a common benign cutaneous tumor composed of epidermal keratinocytes that is seen mainly in middle-aged and older persons.1,2 Synonyms include senile wart, verruca senilis, verruca seborrheica, seborrheic wart, basal cell acanthoma, melanoacanthoma, and basal cell papilloma.3


Seborrheic keratosis usually does not appear before middle age but becomes increasingly common with advancing age.2,3 Most studies estimate the prevalence approaches 100% in patients older than 60 years in susceptible racial groups.1,3,4 Seborrheic keratosis is more prevalent among whites; it is rare among African Americans and Native Americans.3

Although the exact pathogenesis remains unknown, seborrheic keratosis is thought to be caused by a local maturational arrest of keratinocytes.1 Epidermal growth factors and somatic fibroblast growth factor 3 mutations likely contribute to the pathogenesis.1,5

Advanced age is an established risk factor.3,6 Exposure to ultraviolet light may also play a role.3,6 Patients with an unusually large number of lesions, particularly at a younger age, often have a family history of seborrheic keratosis.3 Accordingly, an autosomal mode of inheritance has been described.1


Characteristically, the lesion presents as a sharply demarcated, round or oval plaque with a “stuck on” warty appearance.2,3 It is typically brown but may be yellow or black.6 The lesion is usually asymptomatic but may occasionally be itchy.2 Often, lesions may appear oily and shiny, giving rise to the misnomer “seborrheic” (greasy) keratosis.3

Seborrheic keratosis can appear almost anywhere on the body, but it spares the palms and soles.3 The most common sites include the face, chest, back, and extremities.4,7 Mucosal surfaces are usually unaffected.3


The common histologic features of seborrheic keratosis include proliferation of basaloid cells and squamous epithelial cells, hyperkeratosis, papillomatosis, and acanthosis with elongation of the rete ridges.3,8 Horn cysts and horn pseudocysts are often present.7 Several histologic types have been described, namely, acanthotic, hyperkeratotic, adenoidal, clonal, macular, irritated (inverted follicular), and pedunculated seborrheic keratosis.8 Of these, the acanthotic subtype is by far the most common.8


The diagnosis is mainly clinical. Dermoscopy can be helpful to confirm the diagnosis. Typical dermoscopic features include comedo-like openings, milia-like cysts, fissures and ridges, fingerprint-like structures, hairpin blood vessels, moth-eaten border, network-like structures, and sharp demarcation.2,9 When the contact dermoscope is moved horizontally over the lesion, the seborrheic keratosis lesion itself, but not the other features, will follow the dermoscope (a response known as the “wobble” sign).9 If the diagnosis is still in doubt, histologic confirmation is warranted.


The differential diagnosis includes basal cell carcinoma, squamous cell carcinoma, Bowen disease, actinic keratosis, papilloma, keratoacanthoma, verruca vulgaris, verrucous epidermal hyperplasia, melanocytic nevus, melanosis, and malignant melanoma.5 The distinctive features of each condition usually allow for a straightforward differentiation from seborrheic keratosis.


Occasionally, the lesion may bleed or become painful as a result of friction with clothing. Rarely, seborrheic keratosis occurs in association with other cutaneous neoplasms, notably basal cell carcinoma.5 The occurrence of seborrheic keratosis in association with squamous cell carcinoma, Bowen disease, keratoacanthoma, and malignant melanoma has also been described.5,10 It is unclear whether these tumors develop directly from seborrheic keratosis or whether they appear coincidentally as a result of advanced age.3

Many researchers suggest that the sudden eruptive appearance of numerous seborrheic keratoses, especially on the trunk, may herald the presence of an internal malignancy, in particular, adenocarcinoma of the gastrointestinal tract (Leser-Trélat sign).11 Some researchers, disagree, however.12 On the other hand, this association appears to be even stronger in the presence of concomitant pruritus and acanthosis nigricans.3


Given the benign nature of the disorder, removal of the lesion is usually not necessary except for cosmetic purposes. Treatment options include shave excision, cryotherapy, electrodesiccation, and laser therapy (erbium-yttrium-aluminum-garnet or CO2 laser).3,6 


1. Kwon OS, Hwang EJ, Bae JH, et al. Seborrheic keratosis in the Korean males: causative role of sunlight. Photodermatol Photoimmunol Photomed. 2003;19(2):73-80.

2. Rajesh G, Thappa DM, Jaisankar TJ, et al. Spectrum of seborrheic keratosis in south Indians: a clinical and dermoscopic study. Indian J Dermatol Venereol Leprol.2011;77(4):483-488.

3. Hafner C, Vogt T. Seborrheic keratosis. J Dtsch Dermatol Ges. 2008;6(8):664-677.

4. Kennedy C, Bajdik CD, Willemze R, et al. The influence of painful sunburns and lifetime sun exposure on the risk of actinic keratoses, seborrheic warts, melanocytic nevi, atypical nevi, and skin cancer. J Invest Dermatol. 2003;120(6):1087-1093.

5. Noiles K, Vender R. Are all seborrheic keratosis benign? Review of the typical lesion and its varients. J Cutan Med Surg. 2008;12(5):203-210.

6. Brodsky J. Management of benign skin lesions commonly affecting the face: actinic keratosis, seborrheic keratosis, and rosacea. Curr Opin Otolaryngol Head Neck Surg. 2009;17(4):315-320.

7. Zhang RZ, Zhu WY. Seborrheic keratosis in five elderly patients: an appearance of raindrops and streams. Indian J Dermatol. 2011;56(4):432-434.

8. Bon-Mardion M, Poulalhon N, Balme B, et al. Ungal seborrheic keratosis. J Eur Acad Dermatol Venereol. 2010;24(9):1102-1104.

9. Takenoughi T. Key points in dermoscopic diagnosis of basal cell carcinoma and seborrheic keratosis in Japanese. J Dermatol. 2011;38(1):59-65.

10. Sharma P, Sarma DP, Adickes ED. Seborrheic keratosis with in-situ squamous carcinoma changes. Dermatol Online J. 2006;12(7):19.

11. Ceylan C, Alper S, Kilinc I. Leser-Trelat sign. Int J Dermatol. 2002;41(10):687-688.

12. Fink AM, Filz D, Krajnik G, et al. Seborrheic keratosis in patients with internal malignancies: a case-control study with prospective accrual of patients. J Eur Acad Dermatol Venereol. 2009;23(11):1316-1319.