Seborrheic Keratoses

Christopher G. Bunick

Amanda Zubek

Macrene Alexiades

BACKGROUND

Seborrheic keratoses (SKs) represent one of the most common presenting complaints in dermatology offices. They begin to develop around the fourth decade of life and increase in number over time. SKs can have a wide variety of clinical appearances as well as a wide variety of histologic characteristics. Treatment modalities for SKs are mostly destructive in nature, but recurrence is common.

PRESENTATION

Patients present with solitary, few, or numerous lesions, most commonly waxy or verrucous tan-brown papules or plaques.

DIAGNOSIS

Clinical Diagnosis

SKs are very common benign skin lesions that grow on tens of millions of people worldwide and are responsible for countless dermatology office visits. They commonly grow on the scalp, face, chest, back, and extremities. They can be flat (macular) or raised (papular or plaque); they may range in color from tan to brown to dark brown or black. Sometimes they are even white (eg, stucco keratosis on the lower legs) or pink to red. Furthermore, the surface texture can vary from smooth to waxy to wartlike. They are often described as “stuck-on,” implying that some can be peeled off easily.

Histopathology

As with the clinical presentation, there is a wide variety of histologic subtypes of SK. The acanthotic type demonstrates epidermal acanthosis with overlying smooth surface and pseudohorn cysts within the lesion. These acanthotic SKs may be pigmented and, when abundant pigment is found, are termed melanoacanthomas. The hyperkeratotic type of SK has papillomatosis, acanthosis with thicker hyperkeratosis, and pseudohorn cysts. The adenoid or reticulated SK shows thin strands (double layer) of epidermis extending into the superficial dermis in a lacelike pattern with variable pigmentation. When inflammatory infiltrate is present, the lesion is termed
an irritated or inflamed SK. Occasionally, inflamed SKs demonstrate a more dermal proliferation near a hair follicle and are then termed inverted follicular keratosis.¹

Subtypes

Macular SK
Acanthotic SK
Hyperkeratotic SK
Irritated SK
Melanoacanthoma
Stucco keratosis
Dermatosis papulosa nigra (see chapter 11.4)

PATHOGENESIS

The molecular pathways involved in SK formation are slowly being elucidated. In 2016, Mandinova and colleagues established that SKs have overactive Akt signaling and inhibition of the Akt signaling leads to activation of apoptotic cell death in the SKs.² Akt inhibitors for use in SK therapy in the dermatology clinic are not currently developed. Despite the benign nature of SKs, and their lack of progression to malignancy, studies have identified that 80% of SKs have 1 mutation and 45% have 2 mutations in FGFR3, KRAS, PI3KCA, or EGFR oncogenes.²,³

TREATMENT

There are multiple elective treatment options for the symptomatic or cosmetically undesired SK, although no longer marketed (Algorithm 11.3.1). The most common therapy by far is the use of cryotherapy (liquid nitrogen).⁴ However, if owing to the size or thickness of the SK cryotherapy is not used, shave excision can readily be performed. Electrosurgery techniques as well as direct curettage of the SK can be used. An investigational topical therapy using 40% hydrogen peroxide was approved by the US Food and Drug Administration (FDA).⁵ A focal chemical peel using trichloroacetic acid (TCA) can be effective,⁶ including in patients with darker skin tone.

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