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    Bowen Disease PDF

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    Rifky Budi Triyatno

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    © All Rights Reserved
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    Bowen's Disease Myung-Moo Lee, MO Michael M. Wick, MD, PhO Introduction In 1912John T. Bowen described two cases of “precancerous dermatoses" that had clinical and histologic similarities to other precancerous conditions known atthe time (for example, Paget's disease, xeroderma pigmentosum, x-ray dermatitis, and “"ker- atosis senilis").' Based on these similar ties, Bowen concluded that the lesions ‘would have ‘‘imminent'™ malignant se- uelae. His description of the disease that ‘now bears his name is classic for squamous cell carcinoma in stu Epidemiology ‘Bowen's disease is predominantly adisease of the elderly, with a mean age at diagnosis. inthe sixth decade and an age range begin- Dr. Wik is Chie of be Laboratory of Motecu- larDermatlogse Oncology at Dana Faber Ca erntute and Arointe Profesor of Derma: tology a Harvard Media! School in Boson. Matachuets Dr. Le isa Fellow inthe Laboratory of Mole: Une Dermatologic Oncology at Dana-Farber ‘Cancer istute and a Clinieal Resident inthe Departmen of Dermatology of Harvard Media Stoo in Boston, Massochse ‘The autor. grafuly acknowledge the a- ‘tance of Ms Katherine Defuse prep draonof his manvecit ‘This work was supported by 2 grant from the Josephine M. Lil’ Memocal Melanoma Re- ‘each Fund VOL.40,NO.& JULYAUGUST 1990 ning in the late 20s. The male-to-female ratio shows a slight male preponderance (12:1) insome studies,” while the larg- est study to date, comprising 617 patients, the ratio is reversed (0.8:1, male 10 fe- tale) The lesion may appear anywhere fon the skin and may involve a mucosal Surface or nal bed"? Clinical Presentation Bowen's disease may appear as a macule, papule, or plaque (Fig. 1). Most often the lesion appears asa sealy, crusted, fissured, ‘erythematous plaque. The border is sharply demarcated from the surrounding tissue, ‘and the size of the plaques may vary consi ‘erably, ranging from a few millimeters to several centimeters. Cutaneous lesions are rarely pigmented. Upon removal of the seale or crus, a moist granular surface may be seen. Symptomatology consists of a combination of ulceration, and scaling or crusting. For the majority of lesions, the time of, onset to diagnosis is five to eight yeeiAbout half of the lesion occur on the head (4 to 54 percent), and the majority (72 percent) appear on the sun-exposed sur- faces (head, neck, hands). In a retro spective series of 19 black patients, how= ever, non-sun-exposed areas were found 10 be three times more common than exposed * Other areas such as the anogeni- talia, oral mucosa, nal beds, and conjunc tivae may be affected as well, Mucosal lesions appear as red velvety plagues oF ‘may be verrucous and polypoid. Alters: tively, they may be multiple hyperpig- mented papules on an underlying velvety ‘base. Lesions in the nail bed appear with periungual scaling with nail discoloration * While in the intertriginous areas they app as an erythematous dermatitis, a chronic nonspecific dermatitis, or dark patches." Bowen’s disease of the penis is often re. ferred to as erythroplasia of Queyrat. The presence of an isolated or few chronic, scaly plagues is suggestive of Bowen's disease. Lesions may closely re semble psoriasis or eczema (Fig. 2), and the differential diagnosis also includes mul- ticentric superficial basal cell carcinoma, ‘mammary and extramammary Paget's dis ease, lichen simplex chronicus, actinic ker atoses, intraepidermal epithelioma of Ja- dassohn, and verrucae. The pigmented variety of Bowen's disease may be difficult to distinguish from lentigo maligna mela- noma. The diagnosis is made by histologic Histopathology ‘The histopathology of Bowen’s disease is that of squamous cell carcinoma in situ and ishistolopicaly indistinguishable fromery- throplasia of Queyrat or bowenoid papu- losis. The results of treatment of a lesion with’ podophyllin prior to biopsy may mimic Bowen's disease, with a pattem of pseudoepitheliomatous hyperplasia and bi- 2arre keratinocyte forms, 12 The epidermis in Bowen's disease shows hyperkeratosis With parakeratosis, and marked acanthosis With elongation and thickening of the rete ridges. There is full thickness atypia with intense mitotic activity throughout. In con- trast to that for actinic keratosis, the basal layer is relatively intact without significant atypia, Many of the epidermal cells appear atypical, with pleomorphic and enlarged nuclei (Fig. 3). Occasionally, there is marked vacuolization of cells, especially in the upper epidermis, The clear and abun- dant cytoplasm appears homogeneous and strongly eosinophilic. Two types of mult nucleated cells are seen in the epidermis: fone has the appearance of a dyskeratotic 208 The lingerie @ common site for Bow 26. Note the ulcerated characteristic plaque witha sharply defined margin. cell engulfed in the cytoplasm of another keratinocyte, while the other as mult ple nuclei within a giant cell. The dermal epidermal junction remains sharp without invasion into the dermis, while inthe upper dermis, there is a moderate Iymphohistio- cyt ingiltrate,"® Etiology/Pathogenesis There have been a number of etiologic agents that predispose to or have been as- sociated with Bowen's disease. In some cases, as with basal and squamous cell car- ccinomas, the sun-exposed distribution of Bowen's disease implicates ultraviol light exposure. Similarly, a genetic predis- position as related to skin type and subtle defects in DNA repair might also contribute to the development ofthe disease ‘Among the chemical compounds are the inorganic arsenicals. These are found ina wide variety of formerly used medica- tions, in occupational chemicals, and in Well water, It is therefore essential to be as specific as possible when taking a patient's history. Inorganic arsenic is present in some herbal medications, in Fowler's so: lution (previously used for psoriasis), in epilepsy medications (those containing ‘bromine and arsenic), and in Gay's solution (used for asthma)."*"* Inorganic arsenic |was a common ingredient in vitamin and iton tablets in Denmark until the early ‘CAACCANCER JOURNAL FOR CLINICIANS Fig 2. Bowen's disease presenting asa soltary patch onthe lower eg. (a) The existence ofan icles conc scaly lesion or gezera may suggest Bowen's disease and should be bopsed (b}Oesasionaly the lesion can be pigmented 1960s. Patients treated before 1940 for a variety of conditions such as syphilis, eczema, psoriasis, lichen planus, and lupas may have been treated with arsenicals. ‘Health food calcium supplements like do- Jomite and bone meal may contain arse as may fungicides, pesticides, weed-killer, sheep-ip, and mildewcide used in German Vineyards * Similarly, mining and smelting of copper and other metals, silver electro plating, and recovery of silver from x-ray plates all may result in exposure."®"* An- other factor associated with Bowen's dis- tase is bipyridine pesticide (paraquat) ‘manufacturing."* ‘Of recent interest has been the etiologic role of human papilloma virus (HPV). Use of the technique of DNA-probe hyiridiza- tion has identified HPV-16-specific DNA in lesions of Bowen's disease, bowenoid papulosis, and “an. invasive cutaneous ‘The incidence of squamous cell earei- ‘nom arising from Bowen's disease lesions has been reported as three to five per- cent," and as high as 20 percent.> In addition to invasive squamous cell care- rom, there has been one reported case of Sebaccous carcinoma arising from Bowen's disease ofthe vulva.” The possible mech- anisms by which Bowen's disease pro- sresses to invasive carcinoma include im- paired DNA repair (demonstrated in the lymphocytes of patients with Bowen's dis- cease lesions after exposure to UY light *) VOL. 40,NO.4 JULYIAUGUST 1090 and the tumorigenic potential of HPV 16. ‘The question ofan association between Bowen's disease and primary intemal can- cers has been a controversial one. In 1959, Graham and Helwig originally proposed the existence of such an association." Since that time, a number of studies have affirmed this relationship." The rates of intemal cancers have varied among these studies, ranging from 151070 percent, with most between 15 and 30 percent?!" One group has proposed that Bowen's disease occurting on non-sun-exposed skin hhas& higher statistical correlation with in- temal malignancy.” Other studies. how- ever, have failed to confirm this reltion- ship.’ A recent Danish study of 581 patients found no statistically significant difference between observed and “ex pected” rates of intemal cancers in Bow. tn’s disease patients." Neither were these researchers able to discern any differences ininternal malignancy rates associated with sun-exposed versus non-sun-exposed Bow- en's disease lesions.” “Another recent study pointed out three ‘major methodologic deficiencies in seven previous cohort studies investigating the Correlation of Bowen's disease with inter- nal malignancy: (1) most of the prio stud- ies lacked an adequate comparison group: {@) six of the seven studies included pa- tients with preexistent or concurrent iner= nal cancers (recalculation of two of these studies” yielded no statistically significant 20 Fig. &.(@)_ The histopatro 9 of Bowen's dsoase shows hyperkeratos's, parakeraosis, and ‘Seanthosle. Despite Tull ieknoss epidermal stypia, the basal layet rermains intact winout corelation); and (3) six ofthe seven studies ‘and compare the cancer incidence rates lover time,*!In agreement with the concept that Bowen's disease is not a marker for internal malignaney is a matched case- control study in which SO patients were matched by age, sex, race, and date of ski biopsy.** The two control groups used in- cluded patients with basal cell carcinoma sand patients with other dermatoses. ‘These latest findings refute the earlier studies correlating Bowen’s disease with internal malignancy. However, it has been proposed that the relationship may exist Indirectly (i.e., via arsenic and HPV). Arsenic, for example, increases the risk of both Bowen's disease and pulmonary tumors." ‘Therapy Surgical excision isthe therapy of choice for Bowen's disease lesions. A five-mm surgical margin is advisable witha depth to Subeutaneous ft for removal of & posible underlying carcinoma.” Electroessica- curettage and cryotherapy are also ‘widely used modes of therapy. However, these methods have thei imtatons, since they may not be feasible for large or multi- ple lesions orf the patient refuses or cannot Undergo surgery “Topical agents such as $-fluorourail (6-FU) can bean alternative to surgery. In Siqicart apa. () Mary epedama ele appea” apical win lrorpne and elrged one reported case, a man with 60 Bowen's disease lesions was treated with topical dinitrochlorobenzene (DNCB) in conjunc- tion with 5-FU. Most ofthe lesions disap- peared within two to six weeks of twice- aily application of DNCB cream alone. (One large (12 Tem) lesion was refractory but regressed after addition of topical S-FU tothe regimen.” Radiotherapy is also an alternative to surgery, with good functional as well as cosmetic results. Indications include: (1) location of the lesions on cosmetically or functionally important areas, such a the nose, eyelids, fingers, or periungual orano- ‘genital areas: (2) large or multiple lesions: {G) patients who refuse or cannot undergo surgery; (4) patients on anticoagulant the apy: (3) patients who are predisposed to hypertrophic. scars oF keloid formation. ‘Suspicion of disease extension into the pi losebaceous apparati, however, isan ind cation for another treatment option, since this area may extend beyond the range of ‘conventional x-rays." (Ff relatively recent interest has been laser therapy. The Nd:YAG and CO, lasers ‘can be used for extensive and leukoplakia- like or verrucous lesions. The Nd:YAG laser has a deep coagulating effect that smakes it particularly suitable for various skin tumors, including exophytic, papillo- rmatous lesions. The duration of wound baling is the longest, however, requiring up to eight weeks, The CO, laser has CCAACANCERJOUANAL FOR CUNICIANS ‘vaporizing effect, requiring less time for ‘wound healing than does the Nd:YAG (four tosix weeks). The depth of dermal destruc- tion may be controlled visually and there- fore more precisely. Recurrences usually ‘occur on the border of the lesions during ‘wound healing and probably reflect incom- plete therapy. >® Conclusion ‘Since its original description early in this ‘century. much has been elucidated about References: 1. Bowen JT: Precancerous dermatoses: A Stady of two cases ofehrone atypical epithe proliferation. JCut Dis 30:241-255,1912, 2 Thestrup-Pedersen K, Ravnborg L, Rey- ‘mann F: Morbus Bowen: A description ofthe disease in 617 patients. Acta Derm Venereol (8:236-239, 1988. 3. Reymann F, Ravnborg L, Schou G, eta: Bowen's disease and internal malignant dis eases: A study of 581 patients. Arch Dermatol 128:677-679, 1988 4, Mora RG, Pemiciaro C, Lee B: Cancer of the skin inbacks. I: A review of nineteen black patients with Bowen's disease, J Am Acad Der mato 11557-5602, 1984 5. Eedy DJ, Gavin AT: Thineen-year ro spective study of Bowen's disease in Northern Teland. Br J Dermatol 117:715-720,1987 6. Callen JP, Headington J: Bowen's and non- Bowen's squamous intracpidermal neoplasia of the skin: Relationship to internal malignancy. ‘Arch Dermatol 116:422—£26,1980, 7. Peterka ES, Lynch FW, Goltz RW: An as Seciaton between Bowen's disease and internal Cancer. Arch Dermatol 84:623~629, 1961 8. Baran RL, Gorey DE: Polydactylous Bowen's dscate ofthe mail J Am Acad Der. ‘matol 17-201-204,1987, 9. Maize JC, Rasmussen JE: Precancerousle- sions, in Heim F (ed): Cancer Dermatology. Philadelphia, Lea & Febiger.1979 10. Graham JH, Helwig EB: Bowen's disease tnd its relationship to systemic cancer, Arch Dermatol 80:133-159,1989. 1 Schwartz RA, Stoll HL: Epithelial precan- VOL. 40,NO.4- JULVAUGUST 1990 Bowen's disease. The tobe squamous cell malignant predisposition foreseen by Bowen himself. Several etiologic agents have been identified, with some of them linked to the carcinogenic process. Recent evidence suggests no correlation with other primary intemal tumors, and the existence ofthe disease should not prompt an exten- sive search for internal cancers other than ‘what is age-appropriate. The therapy of the disease itself is straightforward, and pa- tientshave an excellent prognosis. &@

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