Bowen's disease on the dorsum of hand

Abstract

A 59-year-old woman presented with a minimally itchy and tender plaque on the dorsum of the left hand since last 4 years. According to the patient it started as a small papule following blood collection at the site and gradually increased in size. She was a known diabetic; controlled on insulin for the past 15 years. She had used a topical antibiotic intermittently with no relief. On clinical examination, there was a well-defined erythematous plaque with hyperpigmented borders and overlying crust [Figure 1]. Rest of the dermatological and systemic examination of the patient was normal. Figure 1 Well-defined erythematous plaque with hyperpigmented borders and overlying crust present on the dorsum of the left hand A skin biopsy was performed. The histopathology showed epidermal acanthosis with focal ulceration. There were atypical pleomorphic hyperchromatic keratinocytes spanning the entire epidermis with loss of epidermal differentiation and polarity. Vacuolization and individual cell keratinization was appreciated [Figures 2 and 3]. Diagnosis of Bowen's disease (BD) was made. Figure 2 Hematoxylin and eosin, ×4-epidermal acanthosis with focal ulceration with inflammatory infiltrate in the upper dermis Figure 3 Hematoxylin and eosin, ×40 - pleomorphic, hyperchromatic, atypical keratinocytes spanning the entire epidermis with prominent vacuolization. Loss of differentiation and polarity seen DISCUSSION BD was first described by an American Dermatologist John T. Bowen in 1912. It is a squamous cell carcinoma in situ with potential for significant lateral spread. It can affect the skin and mucous membranes. The involvement of sun-exposed sites is more common in the whites, whereas that of the unexposed sites is more common in the pigmented skin.[1] It is more common on the head, neck, and extremities in men and lower limbs and cheeks in females. It ranges from very few millimeters to several centimeters in diameter. Lesions are usually solitary, but multiple lesions are seen in 10-20% of patients. Significant sun exposure, ionizing radiation, arsenic exposure,[2] immunosuppression,[3] and certain types of human papillomavirus[4] are predisposing factors for BD. Genetic factors, trauma, chemical carcinogens, and X-ray radiation are other factors implicated in the pathogenesis. Patients usually present with an asymptomatic slowly enlarging erythematous scaly patch or plaque. Histopathology shows full-thickness anaplasia of the epidermis with loss of normal maturation, although the basement membrane remains intact. Parakeratosis and hyperkeratosis, acanthosis with complete disorganization of the epidermal structure is present. Throughout the epidermis are numerous, atypical, pleomorphic hyperchromatic keratinocytes producing the windblown appearance. These cells are sometimes vacuolated and have a pale-staining cytoplasm. Loss of maturation and polarity of the cells, numerous mitotic figures, individually keratinized cells, multinucleated cells and atypical cells are seen throughout the pilosebaceous unit, within the acrotrichium, follicular infundibula, and sebaceous glands. The chances of development of squamous cell carcinoma (SCC) in a case of BD is 3%-5% and there are 33% chances of metastasis from a case of SCC that has evolved from BD. Therapy is guided by size and location of BD in addition to individual patient characteristics, such as age and healing capacity. Surgical excision is generally regarded as the treatment of choice for most BD lesions, if the lesions size and location permit such a procedure. Mohs micrographic surgery, electrodesiccation and curettage, cryosurgery, topical chemotherapy with 5-fluorouracil, topical immune response modifiers, such as imiquimod, laser therapy, radiotherapy, and photodynamic therapy are the known modalities of treatment.[5]