This chapter discusses clinical and pathologic features of benign epithelial tumors, hamartomas, and hyperplasias of the skin. A review of relevant systemic and syndromic associations is provided when applicable.
Seborrheic keratosis is the most common benign epidermal tumor.
They usually begin as well-circumscribed tan brown patches or thin plaques with pseudo-horn cysts (keratotic invaginations).
Rapidly growing, symptomatic, or atypical lesions should be biopsied to rule out malignancy.
Clinical and histologic variants include common seborrheic keratosis (SK), reticulated SK, stucco keratosis, melanoacanthoma, dermatosis papulosa nigra, clonal SK, and irritated SK.
Hallmark histopathologic findings: acanthosis, papillomatosis, pseudo-horn cysts, and hyperkeratosis
Multiple eruptive seborrheic keratoses may be indicative of internal malignancy (Leser-Trélat sign). Gastrointestinal malignancy is most common followed by lymphoproliferative disease.
EPIDEMIOLOGY AND CLINICAL FEATURES
Seborrheic keratoses (SKs) are the most common acquired benign epithelial tumor of the skin. They can occur anywhere on the cutaneous surface, with the exception of the palms and soles. They are common in middle-aged and older adults and have a range of clinical appearances. Differences in clinical morphology often correspond with different microscopic variations.
SKs begin as circumscribed tan brown patches or thin plaques. Over time, they may become more papular or verrucous with a greasy scale and a stuck-on appearance (Figs. 108-1 and 108-2). Hallmark histologic findings include hyperkeratosis, acanthosis, papillomatosis, and pseudohorn cysts.
Seborrheic keratosis showing a rough surface and stuck-on appearance.
Multiple small seborrheic keratoses.
Multiple SKs may be patterned along the lines of skin cleavage or Blaschko lines.1,2 Eruptive lesions may be a sign of internal malignancy (Leser-Trélat sign).3 The most common associated malignancy is gastrointestinal, followed by lymphoproliferative disease. Eruptive SKs have been reported in other clinical settings, including erythroderma and HIV infection.4,5 Chemotherapeutic agents, such as cytarabine, may cause inflammation of preexisting SKs, which then become more clinically apparent (“pseudo-sign of Leser-Trélat”).6
On occasion, cutaneous malignancies arise from or adjacent to SKs, highlighting the importance of close examination and tissue biopsy of atypical, symptomatic, or changing lesions.7,8
ETIOLOGY AND PATHOGENESIS
Although the precise cause of SKs is unknown, most are sporadic. Interestingly, a family history of SKs is attainable in some instances, suggesting a genetic predisposition. Sun exposure may also contribute to their pathogenesis.9 The monoclonal nature of these neoplasms was established in 2001.10 By tracking polymorphisms in a human androgen receptor, researchers found that more than half of the 38 SKs sampled, regardless of subtype, were clonal in nature. Multiple oncogenic mutations have been reported ...