Advancing the Understanding of Seborrheic Keratosis

May 2017 | Volume 16 | Issue 5 | Original Article | 419 | Copyright © 2017

Susan C. Taylor MD

Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA

Abstract

The seborrheic keratosis (SK), which is ubiquitous throughout all populations, is a benign tumor of the skin. SKs are among the top 20 dermatologic conditions treated by dermatologists. They have been reported to occur in individuals of all ages including children as young as age 15 years. Familial cases of SKs have been described with an autosomal dominant inheritance pattern. Mutations of the fibroblast growth factor receptor 3 gene (FGFR3) and the gene encoding for phosphoinositide 3-kinase (PIK3CA) have been demonstrated in SKs. In addition to a genetic predisposition, independent risk factors include advancing age and ultraviolet light exposure. It has been proposed that these two risk factors may also contribute to the development of SKs caused by the genetic mutation in FGFR3 gene, which is involved in regulating cell growth, differentiation, migration, and wound healing. The classic description of a SK is a papule or plaque with a soft, friable, hyperkeratotic surface, or a macule with a fine granular appearance. Variants include the stucco seborrheic keratosis and dermatosis papulosa nigra (DPN). Although diagnosed clinically, mimickers of SKs are well known with melanoma being the most concerning. Treatment of SKs is primarily procedural with new treatments in development.

J Drugs Dermatol. 2017;16(5):419-424.

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INTRODUCTION

The seborrheic keratosis (SK), which is ubiquitous throughout all populations, is a benign tumor of the skin. Nomenclature for the SK includes seborrheic wart, seborrheic verruca, basal cell papilloma, pigmented papilloma, verruca senilis, and senile keratosis.1 Wilmer analyzed data extracted from the National Center for Health Statistics’ National Ambulatory Medical Care Survey (NAMCS) from 2001 to 2010.2 The top 20 dermatologic conditions reported by dermatologists accounted for 85.4% of all diagnoses made by dermatologists and SKs were included in these conditions. Bickers estimated the prevalence of skin diseases in the United States (US) and determined that 83.3 million people in the US had SKs with direct health care cost due to SKs of $1092 million, indirect cost of $113 million (from lost productivity), and intangible cost of $6700 million (because of QOL impact).3 SKs occur in individuals of all ages including children as young as age 15.4 Familial cases of SKs have been described in the literature with a report of a German family with at least seven affected members in two generations and the onset of a large number of SKs at a young age.1 An autosomal dominant inheritance pattern has been identified in some families with familial SKs.5 The genetic basis of SKs is being elucidated and mutations of the fibroblast growth factor receptor 3 gene (FGFR3) and the gene encoding for phosphoinositide 3-kinase (PIK3CA) have been demonstrated in SKs.1 In addition to a genetic predisposition, independent risk factors for the development of SKs that have been proposed including advancing age and ultraviolet light exposure.6,7 These two risk factors may also contribute to the development of SKs caused by the genetic mutation in the FGFR3 gene, which is involved in regulating cell growth differentiation, migration, and wound healing.8 Although diagnosis is primarily clinical, mimickers of SKs are well known with melanoma being the most concerning. Treatment of the SK is primarily procedural with new treatments in development. Clinical PresentationThe diagnosis of the SK is primarily clinical. Clinical criteria for SKs include a “stuck on” appearance of papules or plaques with a soft, friable, hyperkeratotic surface, or macules with a fine granular appearance.6 The color can range from pink or white (nonpigmented) to grey, dark brown, or black. Lesions typically range from 0.5 -1.5 cm with the exception of the clinical variant, dermatosis papulosa nigra (DPN), which are smaller in size. SKs occur commonly on the head, trunk, and extremities. They have not been reported on the palms or soles. However, cases of subungual SKs have been reported and described as longitudinal leucoxanthonychia with filiform/globular haemorrhages and milia-like cysts.9 SKs are generally asymptomatic although they may become inflamed or pruritic due to rubbing by external forces, irritation, or infection. In a study by Del Rosso, 19% of subject had symptomatic lesions that were inflamed or irritated.10 Older patients, ages 60-69 years, were more likely to have a symptomatic SK than patients 40-59 years. Kyriakis studies 787 patients from Greece and found that body mass index did not differ between SK cases and non-SK cases. These authors also reported that skin type was more fair in SK patients.11Clinical variants of SKs include stucco keratosis and DPNs.12 DNPs seemingly occur more often in individuals with darker 

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