Bowen disease
Summary
Bowen disease is squamous cell carcinoma in situ (full-thickness epidermal dysplasia without breach of the basement membrane). It presents as a slowly enlarging, erythematous, scaly, well-demarcated plaque on sun-exposed skin, and it can progress to invasive SCC in about 3-5% of cases. Risk factors include chronic sun exposure, arsenic, and HPV (especially in anogenital disease).
Detail
**Definition:** Bowen disease is SCC in situ of the skin. Atypical keratinocytes involve the full thickness of the epidermis, and the basement membrane is intact. Related entities: erythroplasia of Queyrat (SCC in situ of the glans penis or prepuce, usually in uncircumcised men) and Bowenoid papulosis (HPV 16/18-associated, multiple pigmented papules on the genitals of younger adults, with a benign course and possible spontaneous regression).
**Pathophysiology/Risk factors:** - Chronic UV exposure (the most common cause, on sun-exposed skin of older adults) - Arsenic exposure (contaminated water, pesticides, some folk medicines). It can cause lesions on non-sun-exposed sites and is associated with visceral malignancies (lung, bladder, skin). - HPV, especially types 16 and 18 (anogenital and periungual lesions) - Immunosuppression (organ transplant recipients, HIV) - Ionizing radiation and chronic skin injury - Mutations in p53 (UV-induced) are implicated.
**Clinical presentation:** - A solitary, slowly growing, erythematous, scaly or crusted, well-demarcated plaque. It is often mistaken for psoriasis, eczema, or tinea, and it is persistent and unresponsive to topical steroids or antifungals. - Common sites are the head, neck, and lower legs (especially in women). - Periungual or subungual involvement may cause longitudinal erythronychia or melanonychia. - Mucosal and genital forms are possible.
**Histology:** Full-thickness epidermal atypia with a "windblown" appearance, loss of normal maturation, hyperkeratosis and parakeratosis, and atypical mitoses. Dyskeratotic cells and multinucleated cells may be seen. The basement membrane and dermis are intact. Invasion into the dermis means invasive SCC.
**Diagnosis:** Biopsy (shave or punch).
**Treatment:** - Surgical excision or Mohs surgery (for high-risk sites) - Curettage and electrodesiccation - Cryotherapy - Topical 5-fluorouracil or imiquimod - Photodynamic therapy - Radiation (for patients who cannot undergo surgery)
**Prognosis:** About 3-5% progress to invasive SCC, which has a higher metastatic potential than SCC arising from actinic keratosis.
**Board pearls:** - Bowen disease = SCC in situ. - Arsenic exposure leads to Bowen disease and to an association with internal malignancy (older teaching). - A scaly plaque that does not respond to topical steroids or antifungals should prompt a biopsy. - Erythroplasia of Queyrat = Bowen disease of the penis. - Actinic keratosis is the precursor lesion for SCC, with partial-thickness dysplasia. Bowen disease has full-thickness dysplasia.
Sources
- First Aid for the USMLE Step 1 (Dermatology)
- Robbins & Cotran Pathologic Basis of Disease (Skin tumors)
- Bolognia: Dermatology
- Fitzpatrick's Dermatology in General Medicine
- UpToDate: Cutaneous squamous cell carcinoma in situ (Bowen disease)
- AMBOSS: Squamous cell carcinoma of the skin
Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.