eMedicine Specialties > Dermatology > Malignant Neoplasms

Bowen Disease: Treatment & Medication

Author: Mark P Eid, MD, Resident Physician, Department of Dermatology, Milton S Hershey Medical Center, Pennsylvania State University College of Medicine
Coauthor(s): Bryan E Anderson, MD, Associate Professor, Department of Dermatology, Pennsylvania State University College of Medicine
Contributor Information and Disclosures

Updated: Dec 16, 2009

Treatment

Medical Care

Each treatment modality has advantages and disadvantages. Choosing the best therapeutic option involves an analysis of various factors such as lesional size, number, site, degree of functional impairment, modality availability, and cost. Because most treatments have a recurrence risk, follow-up at 6-12 months is recommended to evaluate for recurrence. Factors that dictate a shorter follow-up period include history of past recurrence, presence of multiple lesions, lesions in high-risk locations, and immunosuppression.

  • Topical therapy 
    • 5-Fluorouracil is a topical antineoplastic agent that interferes with DNA synthesis via inhibition of thymidylate synthetase and subsequently cell proliferation. It is used clinically as a 5% cream once or twice daily for a variable period, ranging from 1 week to 3 months. 5-Fluorouracil has also been applied under occlusion, with dinitrochlorobenzene as a vehicle, via iontophoresis or pretreatment with an Er:YAG laser. The main advantage is easy self-application by patients. The main adverse effect is irritation with erosions and ulcerations that may last several weeks.17,18,19,20 A disadvantage is that it may not be able to penetrate deep enough to treat any deep follicular extension of the tumor cells.
    • Imiquimod 5% cream,21,22,23,24 a topical immune response modifier, applied 3-7 d/wk, appears to possibly be a successful treatment option for Bowen disease. It is often used for larger-diameter lesions, lower leg lesions, and erythroplasia of Queyrat. Two reports indicate sustained clearance with at least 19 months of disease-free follow-up after treatment of perianal Bowen disease with single-agent therapy using imiquimod 5% cream. Topical treatment for perianal Bowen disease may minimize the risk of scarring, poor wound healing, and functional impairment. The ideal dosing regimen is still under investigation, but the most studied regimen at this time is imiquimod 5% cream once daily for 16 weeks. Also note, however, that a cautionary report describes Bowen disease of the scalp treated with imiquimod that evolved into invasive SCC.25
  • Consider x-ray or grenz-ray radiation therapy for poor surgical candidates or patients with multiple lesions.26 It should be avoided for lower extremity lesions due to impaired healing.
  • Photodynamic therapy (PDT) has also been used, with variable success, for the treatment of Bowen disease.27,28 Photodynamic therapy involves the introduction of a photosensitizing agent into the body, which is retained preferentially by the tumor cells. Then, a light source is used to stimulate the photosensitizing agent, causing the release of toxins and leading to the destruction of the tumor. Topical 5-aminolevulinic acid (ALA) or methyl aminolevulinate (MAL) are the most commonly used photosensitizers. Various illumination sources, wavelengths of light, and dosing schedules have been used. PDT is well-suited for large lesions, multiple lesions, and poor-healing sites. The adverse effects include local phototoxic effects such as burning and stinging and, rarely, erosions, ulceration, and hyperpigmentation hypopigmentation. Treatment guidelines are available from the Norwegian University of Science and Technology.29

Surgical Care

  • Simple excision with conventional margins 
    • This surgery is the most common and preferred treatment for smaller lesions and those not in problematic areas, such as the face and digits. For perianal Bowen disease, excision with wide margin is recommended.30 Lower leg lesions are often limited by the lack of skin mobility.
    • Although lesions are typically well demarcated, the actual extent of the disease may be well beyond the clinical margins. For this reason, the excision should be made at least 4 mm outside the clinical margin.
  • Mohs micrographic surgery31  
    • This is an excellent method for larger lesions, poorly demarcated lesions, recurrent lesions on the head and neck, or areas where tissue sparing is vital, such as digital or genital lesions. Mohs micrographic surgery uses the systematic surgical removal of skin cancers with very small margins of normal tissue followed by frozen section examination of nearly 100% of the tissue margin.
    • It offers the highest cure rate of all treatment modalities, and, because relatively thin layers are taken only in areas of proven tumor, it is a tissue-sparing procedure.
  • Curettage and electrodesiccation, cryotherapy, and laser ablation32,33,34  
    • These are blind surgical methods (no pathologic confirmation of removal) that are established treatment modalities for Bowen disease.
    • As compared with excision and Mohs surgery, they are less likely to remove tumors that are present down adnexal structures.
    • Curettage and electrodesiccation is a common and safe modality. Treatment efficacy is largely determined by the skill of the clinician. It is also one of the most cost-effective treatment modalities.
    • Cryotherapy is another common therapeutic option, especially for single and small lesions. Suggested regimens in the literature include a single 30-second freeze-thaw cycle, 2 freeze-thaw cycles of 20 seconds with a thaw period, or up to 3 single treatments of 20 seconds at intervals of several weeks. The risk of poor wound healing (eg, hypopigmented scarring) increase with prolonged freezing times. Treatment of broad lesions is often limited because of patient discomfort.
    • Case reports and series have shown a benefit of using argon, carbon dioxide, and Nd:YAG lasers in the treatment of some Bowen disease lesions.

Medication

The goals of therapy for Bowen disease are to reduce morbidity and to prevent complications.

Antineoplastic agents

Topical agents that may be used in the management of Bowen disease.


5-Fluorouracil (Efudex, Carac, Adrucil, Fluoroplex)

5-Fluorouracil administered topically under occlusion, following the use of keratolytic or cryotherapy, or by iontophoresis (an electrogradient-driven chemical delivery system), can be used. Interferes with DNA synthesis by blocking methylation of deoxyuridylic acid and inhibits thymidylate synthetase, which subsequently reduces cell proliferation.

Adult

Only 5% strength recommended; apply bid, sparingly to cover lesions (minimum 3 wk); therapy may be required for 10-12 wk

Pediatric

Administer as in adults

Documented hypersensitivity; potentially serious infections

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Incidence of inflammatory reactions may occur with occlusive dressings; porous gauze dressing may be applied for cosmetic reasons without increase in reaction


Imiquimod (Aldara)

Precise mechanism of action for treatment of Bowen disease is unknown. May increase tumor infiltration of lymphocytes, dendritic cells, and macrophages. Indicated when surgical methods are not appropriate.

Adult

Apply cream to treatment area (including 1 cm of skin surrounding tumor) 3-7 d/wk for up to 16 wk; leave on for at least 8 h, then wash area

Pediatric

Not established

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Mandatory follow-up to ensure treatment response; may cause redness, swelling, and sore development at application site; may cause itching or burning

More on Bowen Disease

Overview: Bowen Disease
Differential Diagnoses & Workup: Bowen Disease
Treatment & Medication: Bowen Disease
Follow-up: Bowen Disease
Multimedia: Bowen Disease
References
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References

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Further Reading

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Keywords

Bowen disease, Bowen’s disease, squamous cell carcinoma in situ, SCC, human papilloma virus 16, HPV 16, human papillomavirus 16

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Contributor Information and Disclosures

Author

Mark P Eid, MD, Resident Physician, Department of Dermatology, Milton S Hershey Medical Center, Pennsylvania State University College of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Bryan E Anderson, MD, Associate Professor, Department of Dermatology, Pennsylvania State University College of Medicine
Bryan E Anderson, MD is a member of the following medical societies: American Academy of Dermatology, American Contact Dermatitis Society, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Kelly M Cordoro, MD, Assistant Professor, Pediatric and Adult Dermatology, Department of Dermatology, University of California at San Francisco
Kelly M Cordoro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Association of Professors of Dermatology, Dermatology Foundation, Medical Society of Virginia, National Psoriasis Foundation, Society for Pediatric Dermatology, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania
Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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