This condition, also known as squamous cell carcinoma in situ, manifests in two thirds of patients as a solitary asymptomatic, slowly enlarging, erythematous, scaly 3-mm to 3-cm hyperkeratotic plaque that is crusted, fissured, or ulcerated.
This condition, also known as squamous cell carcinoma in situ, manifests in two thirds of patients as a solitary asymptomatic, slowly enlarging, erythematous, scaly 3-mm to 3-cm hyperkeratotic plaque that is crusted, fissured, or ulcerated. The most important difference between Bowen disease and its mimics is that Bowen disease lesions sometimes have crusted serum and most of its mimics do not. Mimics of Bowen disease include psoriasis, chronic eczema, actinic keratosis, and melanoma. The lesions of Bowen disease often display a sharply demarcated, irregular border. The scale is sometimes accentuated, and removal of the scale exposes a dull surface that may be moist or papillated.
Bowen disease typically appears on the head and neck; the limbs are the next most common site. Bowen disease of the penis is known as erythroplasia of Queyrat; it often manifests as a glistening erosion and primarily affects uncircumcised men. On the vulva, Bowen disease presents as leukoplakia. The lesions of Bowen disease are sometimes brown, particularly in the anogenital area, where they may resemble melanoma. Bowen disease is most common in elderly white men (particularly those of Celtic descent) with a history of sun exposure. Diagnosis is sometimes delayed because Bowen disease is usually asymptomatic, and a variety of inflammatory processes mimic it.
The most important risk factor for Bowen disease is sun exposure. Other risk factors include arsenic exposure; infection with human papilloma virus (HPV) (most commonly HPV-16); immunosuppression from drugs such as cyclosporine or azathioprine; and ionizing radiation. A Minnesota study whose participants were almost exclusively white found that the annual average rate of Bowen disease was 14 cases per 100,000.1 A study from Hawaii reported a rate of 142 cases per 100,000 whites.2
The definitive diagnosis of Bowen disease is established by shave biopsy. Full-thickness atypical keratinocytes, which often have a jumbled appearance, are common findings. Other features include vacuolization, mitoses, individually keratinizing cells, multinucleated cells, hyperkeratosis, parakeratosis, and acanthosis.
My preferred treatment for Bowen disease is electrodesiccation and curettage followed by the application of imiquimod 5% cream once daily. Either treatment alone is acceptable; however, I find that the combination prevents recurrences. Other treatment options include cryotherapy, photodynamic therapy, x-ray or grenz-ray radiation therapy, carbon dioxide laser ablation, simple excision with conventional margins, and Mohs micrographic surgery. If atypical keratinocytes extend down the follicle, local recurrence is possible. Mohs surgery has the highest cure rates but is the most expensive option and is best reserved for areas that require tissue-sparing therapy. Because the morbidity and mortality of Bowen disease are low, topical or destructive therapies may be tried initially, particularly in debilitated patients.
Chute CG, Chuang TY, Bergstralh EJ, Su WP.The subsequent risk of internal cancer withBowen’s disease. A population-based study. JAMA.1991;266:816-819.
Reizner GT, Chuang TY, Elpern DJ, et al. Bowen’sdisease (squamous carcinoma in situ) in Kauai,Hawaii. A population-based incidence report. J AmAcad Dermatol. 1994;31:596-600.