Seborrheic Keratoses

39
Seborrheic Keratoses
Silvia Soohyun Kim and Shang I. Brian Jiang
I.BACKGROUND Seborrheic keratoses (SKs) are common benign epi-
dermal tumors found in middle-aged and elderly populations. The term
“seborrheic” refers to the lesion’s greasy appearance and location in areas that
have many sebaceous glands. However, there is no known relationship to sebaceous gland function, seborrhea, or seborrheic dermatitis. The cause of SKs is
unknown. Genetics (polygenic), sun exposure, and infection are all implicated
as possible predispositions to developing SKs. In mature SKs, deoxyribonucleic
acid (DNA) synthesis is decreased, while ribonucleic acid and protein synthesis
is increased with irregularities in the expression patterns of apoptosis markers.
Many patients with SKs have positive family history for the condition, but
validated studies are lacking. Sun exposure has been shown to increase the
prevalence of SKs, but there are some studies disagreeing with the role of genetics in SK development. Viral infection has also been explored as a possible cause
of SKs. SKs from the genital region may contain human papillomavirus (HPV)
DNA, but the role of HPV in developing SKs has been controversial. A recent
study reported that HPV-positive genital SKs arise in younger, sexually active
age groups.
While concern about these lesions is primarily cosmetic, some lesions
with multiple dark colors raise the question of melanoma. Rarely, malignant
lesions (i.e., basal cell carcinoma [BCC] and squamous cell carcinoma [SCC])
can arise within SKs, especially the reticulated type on sun-damaged skin. In a
retrospective study of 813 histologically diagnosed SKs, 5.3% were associated
with nonmelanoma skin cancer. No melanomas were observed. The most
common malignancy was Bowen disease, followed by BCC, then ­invasive
SCC.
II.CLINICAL PRESENTATION SKs are generally asymptomatic.
Irritated lesions or those in intertriginous areas may cause intense pruritus.
SKs start as small flesh-colored, yellow, or tan-colored waxy papules that
may grow to become dark brown or black greasy verrucous lesions with
a distinct border (Fig. 39-1). The rough scale may sometimes flake or be
rubbed off but will regrow. The keratoses appear to be “stuck on” the skin
(Fig. 39-2), and close inspection with a hand lens will expose the presence of
horn cysts or dark keratin plugs. Stucco keratosis, a variant of SKs, is 1- to
5-mm lightly colored keratotic papules on the dorsa of the hands and feet
and lower legs. A variant of SKs known as dermatosis papulosa nigra is seen
primarily on the cheeks in blacks or other dark-skinned individuals with a
familial predisposition. These lesions are small, pigmented papules that may
be pedunculated.
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300 MANUAL OF DERMATOLOGIC THERAPEUTICS
Figure 39-1. Seborrheic keratosis with “stuck-on” appearance. (From
Goodheart HP. Goodheart’s Photoguide of Common Skin Disorders. 2nd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)
Figure 39-2. Multiple seborrheic keratoses on the back. (From Goodheart
HP. Goodheart’s Photoguide of Common Skin Disorders. 2nd ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2003.)
III. WORKUP Any rapidly growing, symptomatic, atypical lesions should be
pathologically examined, and the base of all cutaneous horns submitted to rule
out any malignancies such as nonmelanoma skin cancer or melanoma. Shave
biopsies or curettage specimens are often not sufficient for definitive histologic
diagnosis. Please see Table 39-1 for differential diagnoses.
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Chapter 39 • Seborrheic Keratoses TABLE 39-1
301
Differential Diagnosis
1. Actinic keratosis
2. Basal cell carcinoma
3. Bowen disease
4. Bowenoid papulosis
5. Cutaneous horn
6. Epidermodysplasia verruciformis
7. Lentigo
8. Melanoma
9. Nevus sebaceous
10. Psoriasis (guttate or plaque)
11. Squamous cell carcinoma
12. Stucco keratosis
13. Warts
The development of multiple SKs has been attributed to estrogen therapy,
preexisting inflammatory dermatoses, chemotherapy (especially cytarabine),
and various internal malignancies. The latter association (Leser-Trélat sign),
although somewhat controversial, should at least arouse one’s suspicion when
multiple eruptive SKs arise rapidly in association with skin tags and acanthosis
nigricans. Adenocarcinoma of the stomach or lung is the most commonly associated malignancy with the sign of Leser-Trélat sign.
IV.TREATMENT SKs are benign lesions but may be symptomatic with pruritus or bleeding. Any destructive modality may be used to treat these lesions.
However, the patient must be warned that destructive treatments may lead to
scarring, hypopigmentation, or recurrence (Table 39-2).
A. Cryosurgical Application of liquid nitrogen for 15 to 20 seconds is generally the simplest method of destruction. Multiple areas can be treated easily
without anesthesia.
B. Simple Curettage, with or without anesthesia, leaves an excellent cosmetic
result. Lesions lightly frozen with a refrigerant, CO2, or liquid nitrogen may
sometimes be scraped off more easily. Monsel solution (ferric subsulfate),
ferric chloride, aluminum chloride, Gelfoam, weak acids (30% trichloroacetic), or pressure may be used for hemostasis. Light electrodesiccation
will accomplish the same end but may induce a small scar. Lesions should
remain uncovered or have only a light ointment applied such as Aquaphor
Healing Ointment.
C. Very Thick or Pedunculated SKs may be best removed with a shave excision or with sharp scissors. For lesions with a possibility of malignancy,
removal should be done to yield a pathology sample.
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302 MANUAL OF DERMATOLOGIC THERAPEUTICS
TABLE 39-2
Primary Treatment Options
1. Cryotherapy
2. Cryotherapy with curettage
3. Shave excision after anesthesia
4. Electrodesiccation
5. Laser ablation
D.Lesions of Dermatosis Papulosa Nigra are best treated by simple curettage but may also be treated by Gradle scissor excision, very light electrosurgery, laser surgery, or cryosurgery. It is particularly important not to treat
too aggressively so as to avoid posttreatment hypopigmentation, especially
in darker skin patients.
E.Ammonium Lactate 12% Lotion (Lac-Hydrin) applied b.i.d. for 1 to
2 months may reduce the height of SKs but will not change the width or
color of the lesions.
F.SKs have also been managed with laser treatments such as 532-nm diode
lasers with color enhancement using a red marker or ferric subsulfate. In
a study of 326 patients with SKs, 93% of the lesions were resolved completely without any hyperpigmentation or hypertrophic scar formation
following laser treatment.
ACKNOWLEDGMENT
The authors wish to gratefully acknowledge the contributions made by Dr. Jeffrey
T.S. Hsu, the author of the previous edition chapter. Some of his material is incorporated into this chapter.
Suggested Readings
Culbertson GR. 532-nm diode laser treatment of seborrheic keratoses with color enhancement. Dermatol Surg. 2008;34(4):525-528.
Kennedy C, Bajdik CD, Willemze R, et al. The influence of painful sunburns and lifetime sun
exposure on the risk of actinic keratosis, seborrheic warts, melanocytic nevi, atypical
nevi, and skin cancer. J Invest Dermatol. 2003;120:1087-1093.
Kwon OS, Bajdik CD, Willemze R, et al. Seborrheic keratosis in the Korean males: causative
role of sunlight. Photodermatol Photoimmunol Photomed. 2003;19:73-80.
Tardio JC, et al. Genital seborrheic keratoses are human papillomavirus-related lesions. A linear array genotyping test study. APMIS. 2012;120(6):477-483.
Vun Y, et al. Seborrheic keratosis and malignancy: collision tumour or malignant transformation? Australas J Dermatol. 2006;47:106.
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