This article represents a planned regular updating of the previous British Association of Dermatologists (BAD) guidelines for management of Bowen’s disease. They have been prepared for dermatologists on behalf of the BAD. They present evidence-based guidance for treatment, with identification of the strength of evidence available at the time of preparation of the guidelines.

Guidelines for management of Bowen's disease: 2006

These guidelines for management of Bowen's disease have been prepared for dermatologists on behalf of the British Association of Dermatologists. They present evidence-based guidance for treatment, with identification of the strength of evidence available at the time of preparation of the guidelines, and a brief overview of epidemiological aspects, diagnosis and investigation.

https://www.bad.org.uk/library-media/documents/Bowens%20disease%201999.pdf

Guidelines for management of Bowen's disease

Tumors of the epidermis

Presenilin (PS1) and (PS2) are the centers of gamma-secretase that release Abeta from APP in Alzheimer's disease (AD). They cleave signaling proteins like Notch and downregulate beta-catenin to modulate Wnt signaling. Inactivation of PS1 or PS1 and PS2 causes a prenatally lethal 'Notch phenotype,' which has hampered investigation of PS function in adulthood seriously. We have thus turned towards PS1+/-PS2-/- mice which carry the most severe reduction of PS alleles compatible with survival, to analyze the consequences of impaired PS function especially in adulthood. In these 'partial deficient' mice, PS1 protein concentration is considerably lowered, functionally reflected by reduced gamma-secretase activity and impaired beta-catenin downregulation. Their phenotype is normal up to approximately 6 months, when the majority of the mice develop an autoimmune disease characterized by dermatitis, glomerulonephritis, keratitis and vasculitis, as seen in human systemic lupus erythematosus. Besides B-cell dominated infiltrates, we observe a hypergammaglobulinemia with immune complex deposits in several tissues, high-titer nuclear autoantibodies and an increased CD4+/CD8+ ratio. The mice further develop a benign skin hyperplasia similar to human seborrheic keratosis as opposed to malignant keratocarcinomata observed in skin-specific PS1 'full' knockouts. A partial reduction of PS function in PS1+/-PS2-/- mice causes a novel phenotype in adulthood unrelated to the developmental defects of full knockouts. As PS1+/-PS2+/- mice remain healthy, this points towards a sharply defined minimum of PS function. Skin and immune system appear to be especially sensitive targets of impaired PS function and may need careful monitoring if gamma-secretase inhibitors are envisaged for treating AD.

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Partial loss of presenilins causes seborrheic keratosis and autoimmune disease in mice.

Objective To estimate the prevalence of melanoma clinically mimicking seborrheic keratosis. Design Retrospective review of cases submitted for histological examination with a clinical diagnosis of seborrheic keratosis or with a differential diagnosis that included seborrheic keratosis. Setting A tertiary medical care center–based dermatopathology laboratory serving academic dermatology clinics that have a busy pigmented lesion clinic. Materials and Methods A total of 9204 consecutive pathology reports containing a diagnosis of seborrheic keratosis in the clinical information field were identified between the years 1992 and 2001 through a computer database search. Reports with a final histological diagnosis of melanoma were selected for further review and clinicopathological analysis. Main Outcome Measure Histological diagnosis, which was correlated with the preoperative clinical diagnosis. Results Melanoma was identified in 61 cases (0.66%) submitted for histological examination with a clinical diagnosis that included seborrheic keratosis. Melanoma was in the clinical differential diagnosis of 31 cases (51%). The remaining lesions had a differential diagnosis of seborrheic keratosis vs melanocytic nevus (17 cases, 28%), basal cell carcinoma (7 cases, 12%), or a squamous proliferation (3 cases, 5%). In 3 cases (5%), seborrheic keratosis was the only clinical diagnosis. All histological types of melanoma were represented. Conclusions Our results confirm that melanoma can mimic seborrheic keratosis. These data strongly support the current policy of submitting for histological examination all specimens that have been removed from patients.

https://jamanetwork.com/journals/jamadermatology/articlepdf/479107/DST20084.pdf

Prevalence of melanoma clinically resembling seborrheic keratosis: analysis of 9204 cases.

The association of malignant neoplasms arising contiguous with or adjacent to seborrheic keratoses has been previously documented. In this study a retrospective analysis was performed to further characterize these combined neoplasms. A total of 54 examples of malignant neoplasms in conjunction with seborrheic keratoses were found, of which 43 were basal cell carcinomas, six were Bowen's disease, three were keratoacanthomas, and two were malignant melanomas. The average age of the patients was over 65 years. Men were affected more frequently then women. The posterior thorax was the most common site for malignant neoplasms associated with seborrheic keratoses. The superficial type of basal cell carcinoma was the most common type of basal cell carcinoma found in this association. All subtypes of seborrheic keratosis may be found together with malignant neoplasms. We believe the appellation collision tumor is not valid because it is unknown whether the association of seborrheic keratoses with malignant neoplasms is a random event or whether there is, in fact, a pathogenic relationship in the development of two distinctive neoplasms together. Therefore, the term compound tumor is proposed to designate the finding of two distinctive neoplasms either directly contiguous with each other or immediately adjacent to each other.

Malignant neoplasms associated with seborrheic keratoses. An analysis of 54 cases.

Inflammation of the subcutaneous tissue represents a dynamic process that shows different histopathologic findings at different stages of development; therefore, the stage of evolution of a lesion at the time of biopsy influences the microscopic appearance significantly. Furthermore, location and type of inflammation may vary among different examples of the same panniculitis independent of the stage of evolution. For these reasons, the histopathologic diagnosis of panniculitides is often difficult. Currently, the most common approach to diagnosis is differentiation between predominantly septal and predominantly lobular panniculitis, followed by the distinction between lesions with and without vasculitis. Although these criteria are important for diagnosis, they are often insufficiently specific. To determine an alternative method of diagnosis, 329 cases of panniculitis were histopathologically analyzed using the following parameters: location and type of inflammatory infiltrate within and around the subcutaneous tissue, presence or absence of fat necrosis, type of necrosis, presence or absence of vascular changes, and presence or absence of associated findings (e.g., hemorrhage, sclerosis). On the basis of the results of this study and of an extensive review of the literature, tables of histopathologic findings for the diagnosis of panniculitides are presented.

Panniculitis: definition of terms and diagnostic strategy.

REPORT OF A CASE Inpatient consultation was requested for a 13-year-old boy with a recurrent brain-stem glioma. He presented 9 months earlier complaining of balance problems, diplopia, and change in vision. At that time, a computed tomogram and magnetic resonance image demonstrated a mass in the brain stem. He underwent a proximal resection and was subsequently treated with radiotherapy and chemotherapy consisting of etoposide, mesna, ifosfamide, and carboplatin. No improvement was noted, and the tumor continued to enlarge despite multiple courses of chemotherapy. On first diagnosis, he had been prescribed dexamethasone to minimize edema of the tumor mass and compression of the brain stem. Over the subsequent 9 months, his dose of dexamethasone varied (1 g every morning to 4 g every 6 hours) depending on changes in his neurologic examination. As a result of long-term corticosteroid use, diabetes, fatty changes of the liver manifested by elevated liver

Carlos Diaz Cascajo

Papers

Malignant neoplasms associated with seborrheic keratoses. An analysis of 54 cases.

Panniculitis: definition of terms and diagnostic strategy.

Bilateral Jawline Nodules in a Child With a Brain-stem Glioma