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Bowen’s disease

Template:DiseaseDisorder infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]


Overview

Bowen’s disease (BD) is a neoplastic skin disease, considered either as an early stage or intraepidermal form of squamous cell carcinoma. It was named after Dr John T. Bowen, the doctor who first described it in 1912.

Causes

Causes of BD include solar damage, arsenic, immunosuppression (including AIDS), viral infection (human papillomavirus or HPV) and chronic skin injury and dermatoses.

Bowen’s disease as seen under a microscope

Signs and symptoms

Bowen’s disease typically presents as a gradually enlarging, well demarcated erythematous plaque with an irregular border and surface crusting or scaling. BD may occur at any age in adults but is rare before the age of 30 years – most patients are aged over 60. Any site may be affected, although involvement of palms or soles is uncommon. BD occurs predominantly in women (70-85% of cases); about three-quarters of patients have lesions on the lower leg (60-85%), usually in previously or presently sun-exposed areas of skin. A persistent progressive non-elevated red scaly or crusted plaque which is due to an intradermal carcinoma and is potentially malignant. Atypical squamous (resembling fish scales) cells proliferate through the whole thickness of the epidermis. The lesions may occur anywhere on the skin surface or on mucosal surfaces. The cause most frequently found is trivalent arsenic compounds. Freezing, cauterization or diathermy coagulation is often effective treatment.

Differentiating Bowen’s disease from other diseases

Bowen’s disease should be differentiated from other diseases causing papulosquamous or erythmatosquamous rash. The differentials include:

Disease Rash Characteristics Signs and Symptoms Associated Conditions Images
Cutaneous T cell lymphoma/Mycosis fungoides[1]

courtesy of wikipedia.org

Pityriasis rosea[2]
  • Pink or salmon in color, which may be scaly; referred to as “herald patch”
  • Oval shape
  • Long axis oriented along the cleavage lines
  • Distributed on the trunk and proximal extremities
  • Squamous marginal collarette and a “fir-tree” or “Christmas tree” distribution on posterior trunk
  • Secondary to viral infections
  • Resolves spontaneously after 6-8 weeks

courtesy of https://commons.wikimedia.org

Pityriasis lichenoides chronica
  • Recurrent lesions are usually less evenly scattered than in cases of psoriasis
  • Brownish red or orange-brown in color
  • Lesions are capped by a single detachable, opaque, mica-like scale
  • Often leave hypopigmented macules

courtesy of http://www.regionalderm.com

Nummular dermatitis[5]
  • Lesions commonly relapse after occasional remission or may persist for long periods
  • Pruritus

courtesy of your-doctor.net dermatology atlas

Secondary syphilis[6]
  • Round, coppery, red colored lesions on palms and soles
  • Papules with collarette of scales

courtesy of wikipedia.org

Bowen’s disease[7]
  • Erythematous, small, scaly plaque, which enlarges erratically over time
  • Scale is usually yellow or white and it is easily detachable without any bleeding
  • Well-defined margins

courtesy of wikipedia.org

Exanthematous pustulosis[9]

commons.wikimedia.org

Hypertrophic lichen planus[11]

courtesy of wikipedia.org

Sneddon–Wilkinson disease[13]
  • Flaccid pustules that are often generalized and have a tendency to involve the flexural areas
  • Annular configuration

courtesy http://www.atlasdermatologico.com.br/disease.jsf?diseaseId=427

Small plaque parapsoriasis[17]
  • Erythematous plaques with fine scaly surface
  • May present with elongated, finger-like patches
  • Symmetrical distribution on the flanks
  • Known as digitate dermatosis
  • Lesions may be asymptomatic
  • May be mildly pruritic
  • May fade or disappear after sun exposure during the summer season, but typically recur during the winter

courtesy http://www.regionalderm.com

Intertrigo[19]

courtesy of cdc.gov

Langerhans cell histiocytosis[20]
  • Scaling and crusting of scalp

courtesy http://www.regionalderm.com

Tinea manuum/pedum/capitis[24]
  • Scaling, flaking, and sometimes blistering of the affected areas
  • Hair loss with a black dot on scalp in case of tinea capitis

courtesy regionalderm.com

Seborrheic dermatitis

courtesy of wikipedia.com


Histology

Bowen’s is equivalent to squamous cell carcinoma in situ. The entire tumor is confined to the epidermis and does not invade into the dermis. The cells in Bowen’s are extremely unusual or atypical under the microscope and in many cases look worse under the microscope than the cells of many outright and invading squamous-cell carcinomas. The degree of atypia (strangeness, unusualness) seen under the microscope best tells how cells may behave should they invade another portion of the body.

Treatment

Photodynamic therapy (PDT), Cryotherapy (freezing) or local chemotherapy (with 5-fluorouracil) are favored by some clinicians over excision. Because the cells of Bowen’s disease have not invaded the dermis, it has a much better prognosis than invasive squamous cell carcinoma.

de:Morbus Bowen


Template:WikiDoc Sources

  1. ↑ “Mycosis Fungoides and the SĂ©zary Syndrome Treatment (PDQÂź)—Patient Version – National Cancer Institute”.
  2. ↑ Mahajan K, Relhan V, Relhan AK, Garg VK (2016). “Pityriasis Rosea: An Update on Etiopathogenesis and Management of Difficult Aspects”. Indian J Dermatol. 61 (4): 375–84. doi:10.4103/0019-5154.185699. PMC 4966395. PMID 27512182.
  3. ↑ Prantsidis A, Rigopoulos D, Papatheodorou G, Menounos P, Gregoriou S, Alexiou-Mousatou I, Katsambas A (2009). “Detection of human herpesvirus 8 in the skin of patients with pityriasis rosea”. Acta Derm. Venereol. 89 (6): 604–6. doi:10.2340/00015555-0703. PMID 19997691.
  4. ↑ Smith KJ, Nelson A, Skelton H, Yeager J, Wagner KF (1997). “Pityriasis lichenoides et varioliformis acuta in HIV-1+ patients: a marker of early stage disease. The Military Medical Consortium for the Advancement of Retroviral Research (MMCARR)”. Int. J. Dermatol. 36 (2): 104–9. PMID 9109005.
  5. ↑ Jiamton S, Tangjaturonrusamee C, Kulthanan K (2013). “Clinical features and aggravating factors in nummular eczema in Thais”. Asian Pac. J. Allergy Immunol. 31 (1): 36–42. PMID 23517392.
  6. ↑ “STD Facts – Syphilis”.
  7. ↑ Neagu TP, ĆąigliƟ M, Botezatu D, Enache V, Cobilinschi CO, VĂąlcea-Precup MS, GrinĆąescu IM (2017). “Clinical, histological and therapeutic features of Bowen’s disease”. Rom J Morphol Embryol. 58 (1): 33–40. PMID 28523295.
  8. ↑ Murao K, Yoshioka R, Kubo Y (2014). “Human papillomavirus infection in Bowen disease: negative p53 expression, not p16(INK4a) overexpression, is correlated with human papillomavirus-associated Bowen disease”. J. Dermatol. 41 (10): 878–84. doi:10.1111/1346-8138.12613. PMID 25201325.
  9. ↑ Szatkowski J, Schwartz RA (2015). “Acute generalized exanthematous pustulosis (AGEP): A review and update”. J. Am. Acad. Dermatol. 73 (5): 843–8. doi:10.1016/j.jaad.2015.07.017. PMID 26354880.
  10. ↑ Schmid S, Kuechler PC, Britschgi M, Steiner UC, Yawalkar N, Limat A, Baltensperger K, Braathen L, Pichler WJ (2002). “Acute generalized exanthematous pustulosis: role of cytotoxic T cells in pustule formation”. Am. J. Pathol. 161 (6): 2079–86. doi:10.1016/S0002-9440(10)64486-0. PMC 1850901. PMID 12466124.
  11. ↑ Ankad BS, Beergouder SL (2016). “Hypertrophic lichen planus versus prurigo nodularis: a dermoscopic perspective”. Dermatol Pract Concept. 6 (2): 9–15. doi:10.5826/dpc.0602a03. PMC 4866621. PMID 27222766.
  12. ↑ Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z, Binyou W (2009). “Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis”. Arch Dermatol. 145 (9): 1040–7. doi:10.1001/archdermatol.2009.200. PMID 19770446.
  13. ↑ Lutz ME, Daoud MS, McEvoy MT, Gibson LE (1998). “Subcorneal pustular dermatosis: a clinical study of ten patients”. Cutis. 61 (4): 203–8. PMID 9564592.
  14. ↑ Kasha EE, Epinette WW (1988). “Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) in association with a monoclonal IgA gammopathy: a report and review of the literature”. J. Am. Acad. Dermatol. 19 (5 Pt 1): 854–8. PMID 3056995.
  15. ↑ Delaporte E, Colombel JF, Nguyen-Mailfer C, Piette F, Cortot A, Bergoend H (1992). “Subcorneal pustular dermatosis in a patient with Crohn’s disease”. Acta Derm. Venereol. 72 (4): 301–2. PMID 1357895.
  16. ↑ Sauder MB, Glassman SJ (2013). “Palmoplantar subcorneal pustular dermatosis following adalimumab therapy for rheumatoid arthritis”. Int. J. Dermatol. 52 (5): 624–8. doi:10.1111/j.1365-4632.2012.05707.x. PMID 23489057.
  17. ↑ Lambert WC, Everett MA (1981). “The nosology of parapsoriasis”. J. Am. Acad. Dermatol. 5 (4): 373–95. PMID 7026622.
  18. ↑ VĂ€kevĂ€ L, Sarna S, Vaalasti A, Pukkala E, Kariniemi AL, Ranki A (2005). “A retrospective study of the probability of the evolution of parapsoriasis en plaques into mycosis fungoides”. Acta Derm. Venereol. 85 (4): 318–23. doi:10.1080/00015550510030087. PMID 16191852.
  19. ↑ Janniger CK, Schwartz RA, Szepietowski JC, Reich A (2005). “Intertrigo and common secondary skin infections”. Am Fam Physician. 72 (5): 833–8. PMID 16156342.
  20. ↑ Satter EK, High WA (2008). “Langerhans cell histiocytosis: a review of the current recommendations of the Histiocyte Society”. Pediatr Dermatol. 25 (3): 291–5. doi:10.1111/j.1525-1470.2008.00669.x. PMID 18577030.
  21. ↑ Stull MA, Kransdorf MJ, Devaney KO (1992). “Langerhans cell histiocytosis of bone”. Radiographics. 12 (4): 801–23. doi:10.1148/radiographics.12.4.1636041. PMID 1636041.
  22. ↑ Sholl LM, Hornick JL, Pinkus JL, Pinkus GS, Padera RF (2007). “Immunohistochemical analysis of langerin in langerhans cell histiocytosis and pulmonary inflammatory and infectious diseases”. Am. J. Surg. Pathol. 31 (6): 947–52. doi:10.1097/01.pas.0000249443.82971.bb. PMID 17527085.
  23. ↑ Grois N, Pötschger U, Prosch H, Minkov M, Arico M, Braier J, Henter JI, Janka-Schaub G, Ladisch S, Ritter J, Steiner M, Unger E, Gadner H (2006). “Risk factors for diabetes insipidus in langerhans cell histiocytosis”. Pediatr Blood Cancer. 46 (2): 228–33. doi:10.1002/pbc.20425. PMID 16047354.
  24. ↑ Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G (2004). “Dermatology for the practicing allergist: Tinea pedis and its complications”. Clin Mol Allergy. 2 (1): 5. doi:10.1186/1476-7961-2-5. PMC 419368. PMID 15050029.
  25. ↑ Schwartz RA, Janusz CA, Janniger CK (2006). “Seborrheic dermatitis: an overview”. Am Fam Physician. 74 (1): 125–30. PMID 16848386.
  26. ↑ Misery L, Touboul S, Vinçot C, Dutray S, Rolland-Jacob G, Consoli SG, Farcet Y, Feton-Danou N, Cardinaud F, Callot V, De La Chapelle C, Pomey-Rey D, Consoli SM (2007). “[Stress and seborrheic dermatitis]”. Ann Dermatol Venereol (in French). 134 (11): 833–7. PMID 18033062.

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