INTRODUCTION	Section 2 of 11
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Background: First described by John T. Bowen in 1912, Bowen disease is a squamous cell carcinoma (SCC) in situ with the potential for significant lateral spread. Larger lesions can reach several centimeters in diameter. Much controversy exists as to whether Bowen disease is associated with internal malignancies. Many early papers reported such an association in 15-70% of cases. Some later reports supported an association of internal malignancies with Bowen disease that was associated with arsenic ingestion but not with Bowen disease from other causes. Most of the recent studies, with a larger number of cases and better scientific methods, have refuted any association; currently, Bowen disease is not believed to be a paraneoplastic condition.

Pathophysiology: Both chronic solar damage and inorganic arsenic ingestion have been implicated as etiologic factors in the development of Bowen disease. The human papilloma virus (HPV) also has been documented as a cause of Bowen disease, especially HPV 16. Genetics, trauma, other chemical carcinogens, and radiation also may play a role. Quite often, no etiologic factor is determined.

Frequency:

• In the US: In 1991, a study from Minnesota reported the annual average rate of Bowen disease as 14 cases per 100,000 whites. In 1994, a study from Hawaii reported a rate 10 times that, 142 cases per 100,000 whites.

Mortality/Morbidity: Prognosis of Bowen disease is favorable, with less than 5% of cases advancing to invasive SCC, and metastases are even more rare.

Race: Bowen disease most commonly is reported in whites.

Sex: The ratio is approximately equal between males and females.

Age: Bowen disease has its highest incidence in the older age groups.

	CLINICAL	Section 3 of 11
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History: Patients often present with an asymptomatic, slowly enlarging, erythematous, scaly patch or plaque. It may occur anywhere on the mucocutaneous surface. A delay in diagnosis often is encountered because the lesion is asymptomatic; early skin changes may be subtle and overlap with clinical features seen in many benign conditions.

Physical: Bowen disease presents as a single lesion in two thirds of cases. Lesions may appear on sun-exposed or covered skin. The head and neck are the most commonly affected anatomic locations, followed by the limbs. Lesions vary in size from a few millimeters to several centimeters in diameter. A sharply demarcated, irregular border usually is present. Lesions are erythematous, scaly patches or plaques that may become hyperkeratotic, crusted, fissured, or ulcerated. Rarely, the lesions are pigmented, especially in the genital region and the nails. Lesions in these locations may simulate melanoma. Bowen disease also may occur on mucous membranes. When it arises on the glans penis, it is referred to as erythroplasia of Queyrat.

Causes:

• Chronic UV radiation: Sun-exposed distribution of Bowen disease (over one half of lesions occur on the head, neck, and hands) implicates chronic sun damage as one factor in its formation.

• Arsenic exposure: The main sources of arsenic exposure include Fowler solution, a medication formerly used to treat psoriasis; Gay solution, a medication formerly used to treat asthma; contaminated well water; and certain pesticides.

• Human papilloma virus: HPV 16 is by far the most common subtype isolated from lesions of Bowen disease, although other subtypes, such as HPV 2, also have been found.

• Other possible causes include genetic factors, trauma, other chemical carcinogens, and x-ray radiation.