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Vitebsk, Belarus; Histopathology of lichenoid parapsoriasis. Kyiv, Ukraine, , March. Dermatopathology diagnosis in dermatology practice.

Conference Highlights

In: 1st Kyiv Dermatology days. Invited lecture. Kiyv, Ukraine; A case of Malassezia folliculitis in a 18 years old patient. Prague, Czech Republic; Efficacy of Itraconazole treatment in Patients with Inflammatory Diseases of the skin. International Congress, of October, Bangkok, Thailand; resident section. Research Activities. Auflage wurde um neue Krankheitsbeschreibungen erganzt Marginalzonenlymphom, Apokrines Hidrozystom, Mischtumor der Haut , der Abschnitt zum Basalzellkarzinom erweitert.

Geeignet als Nachschlagewerk und systematische Einfuhrung sowie fur die Schulung der Blickdiagnose. Fundamentals of dermatology by Theodor Nasemann Book 11 editions published in in English and held by WorldCat member libraries worldwide Why another dermatology text?

Burgdorf, Walter H. C.

In , when Drs. They promised their book would be concise and profusely illustrated to best teach the fundamentals of dermatology. The German text, now in its fourth edition, has been widely successful. In undertaking an American revised translation of their work, it was my hope to meet a need in the English-language literature similar to that met by the German text.

The practice of dermatology differs from country to country. This text is therefore not simply a translation, but an adaptation that incorporates much new material. In the pages that follow, I have built on the successful framework of the German text, incorporating its excellent photographs and other teaching aids. Discussion of therapy has been extensively revised to reflect current practice in the United States. Original chapters on male infertility and proctology two dermatologic domains in Germany are not included in this book.

They have been replaced by wholly new chapters on cutaneous surgery and tropical dermatology.

Burgdorf, Walter H. C. [WorldCat Identities]

We are grateful to Ronald G. Wheeland, M. In each chapter the differential diagnostic possibilities are shown in a table where the most important distinguishing features are summarized. Treatment is presented in considerable detail, reflecting the current literature as well as the clinical experience in two large German pediatric dermatology clinics.

The scientific names of all recommended medications are given so that the book can be used by readers around the globe, rather than just those with access to European medications. Recent advances in dermatologic therapy including tacrolimus, pimecrolimus, and imiquimod are included. The appendix contains detailed practical information on the choice of an appropriate vehicle, as well as on antibiotics, antihistamines, and topical corticosteroids.

Atlas of dermatology by Gernot Rassner Book 5 editions published in in English and held by WorldCat member libraries worldwide. EvG staining facilitates the visualization of invasive growth by the displacement of elastic fibers. These methods can also be used to more precisely classify tumors or to detect receptors in the context of specific therapies. Tissue formalin fixation alters the epitopes on target antigens.

This alteration may be reversed by mild proteolysis.


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Depending on the target structure, this method not only allows for the detection of cell membranes, cytoplasm, nuclei, and extracellular matrix but also specific mutations or translocations. Polymerase chain reaction PCR detects specific mutations or allows for the sequencing of a small number of genes.

If necessary, supplementary immunohistochemical or molecular pathology studies are performed. Apart from the clinical information previously provided, the dermatopathology report includes a description of the histological characteristics as well as a diagnosis that is as precise as possible and also indicates whether the tumor is benign or malignant. Below, the most important epithelial, melanocytic, and mesenchymal tumors, including Merkel cell carcinoma, are presented in a simplified manner.

The most important benign and malignant epidermal neoplasms are summarized in Table 2. Characterized by a heterogeneous histological appearance, seborrheic keratosis is one of the most common examples of a benign epidermal neoplasm. Common features of all variants include a regular, acanthotic and papillomatous epidermis with hyperkeratosis and intraepidermal proliferation of monomorphic basaloid cells as well as horn cysts and pseudohorn cysts Figure 3.

The term actinic keratosis refers to an incipient squamous cell carcinoma in situ. The basal epidermal layers show loss of regular maturation as well as dyskeratosis and isolated mitotic figures Figure 4 a. Histologically, various types of actinic keratosis hypertrophic, bowenoid, pigmented, lichenoid, and acantholytic can be distinguished. Bowen's disease is a squamous cell carcinoma in situ. Histologically, the regular architecture of all epidermal layers, including the epithelium of the follicular ostia, is lost.

Other features include numerous mitotic figures, dyskeratotic cells, and nuclear pleomorphism Figure 4 b. An important histological variant is clonal pagetoid Bowen's disease, which should be distinguished from extramammary Paget's disease positive for Cam5. Squamous cell carcinoma is a malignant epidermal tumor. Besides the loss of regular epidermal maturation, there is a variable degree of cellular and nuclear atypia.

Originating from the basal cell layers, there are focal proliferations of more or less dyskeratotic eosinophilic keratinocytes with large nuclei, prominent nucleoli, and mitotic figures. A mixed inflammatory infiltrate frequently surrounds the tumor cell aggregates Figure 4 c. The differential diagnosis encompasses other malignant tumors, such as Bowen's carcinoma, porocarcinoma, basal cell carcinoma, and cutaneous metastases of squamous cell carcinomas not just of epidermal origin.

Keratin pearls and dyskeratotic cells are suggestive of squamous cell carcinoma. A connection to the epidermis is considered an important indication of primary cutaneous squamous cell carcinoma. The hair follicle consists of a matrix, an inner and an outer hair root sheath made up of clear cells.

Both the ducts of sebaceous glands and those of apocrine glands open into the hair follicle. The hair follicle is characterized by a special mesenchyme that includes the follicular papilla and the perifollicular hair sheath. Table 3 provides an overview of the most important tumors with predominant follicular differentiation and their presumed histological origin; the exact classification of basal cell carcinoma epidermal vs. In everyday dermatopathology practice, the diagnostic differentiation between benign follicular tumors and basal cell carcinoma is of crucial importance.

Using trichoblastoma as an example, we would like to address this conundrum in more detail. Its nodular components consist of epithelial cell aggregates with follicular differentiation embedded in a typical follicular stroma Figure 5 a. Unlike basal cell carcinoma, there is no peritumoral clefting. The lesion is embedded in a fibrotic stroma with cleft formation solely between tumor cell nests a.

Basal cell carcinoma also exhibits characteristics of a tumor with follicular differentiation. Histologically, nodular basal cell carcinoma is characterized by nodular basaloid tumor cell proliferations with peripheral palisading and typical peritumoral clefting Figure 5 b. The cause of clefting in basal cell carcinoma is subject to controversial debate in the literature.

Detailed morphological descriptions of the individual subtypes are presented in a review by Liersch and Schaller Besides trichoblastoma, other benign follicular tumors such as trichofolliculoma, but also sebaceous gland tumors must be distinguished from basal cell carcinoma in the differential diagnosis.

Occasionally, it may be challenging to differentiate sclerosing basal cell carcinoma from microcystic adnexal carcinoma. With the exception of the palmoplantar region, sebaceous glands are ubiquitous in the skin.

They are particularly abundant in the face and on the upper back. While sebaceous glands usually open into the hair follicles, they may also occur in a nonfollicular variant as ectopic sebaceous glands in the buccal and areolar region as well as on the glans and the labia minora. The sebaceous gland consists of several lobules, which in turn consist of an outer layer with immature, basophilic, round to cuboidal sebocytes, and an inner layer with polygonal, fully differentiated sebocytes with vacuolated cytoplasm.

As a result of holocrine secretion, the excretory duct frequently contains an eosinophilic material.

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The detection of fully differentiated sebocytes or sebaceous ductal structures are a sine qua non for the diagnosis of tumors with sebaceous differentiation. A combination of patterns is also possible. The most important sebaceous tumors are summarized in Table 4. Sebaceous adenoma is an example of a benign sebaceous tumor that imitates the structure of normal sebaceous glands and has a connection to the overlying epidermis. The outer layer consists of small, monomorphic, basophilic germinative sebocytes and the inner layer of central mature sebocytes without cellular atypia Figure 7 a.

With respect to sebaceous carcinoma, a distinction is made between an ocular and an extraocular variant. Histology reveals aggregates of atypical, basaloid epithelial cells with variable sebaceous differentiation. In addition, there are structures resembling sebaceous ducts. Infiltrative tumor growth, cytological atypia, mitotic figures, and necrotic areas as well as the formation of spindle cells are suggestive of malignancy Figure 7 b. Sweat gland tumors are divided into lesions with apocrine and eccrine differentiation.

Eccrine sweat glands are abundant in the palmoplantar area, whereas apocrine sweat glands are predominantly found in the axillae and the anogenital region. Both apocrine and eccrine glands consist of a secretory and a ductal portion. The apocrine secretory portion has a large oval or round lumen that sometimes contains a pale eosinophilic material. The cells are marked by a round nucleus at the base and granular cytoplasm.

Apically, cytoplasmic structures are pinched off. The myoepithelial cells are surrounded by a basement membrane. Eccrine glands have a flat, secretory epithelium surrounded by a myoepithelial layer. Morphologically, secretion is not visible. It is impossible to distinguish apocrine and eccrine glands immunohistochemically.

Apocrine and eccrine ducts are morphologically indistinguishable. They consist of small cuboidal, eosinophilic cells with a round nucleus and cuticular cells that line the duct lumen. An overview of the most important sweat gland tumors is given in Table 5. Poroma is an example of a benign glandular tumor of eccrine lineage. While it typically occurs in acral areas, other sites, such as the trunk, are also possible. Based on location and morphology, the following types are distinguished: hidroacanthoma simplex intraepithelial poroma , nodular poroma, poroid hidradenoma, and dermal duct tumor Large areas of necrosis necrosis en masse are a typical feature of poroma.

Unlike poroma, porocarcinoma presents with epithelial atypia with numerous mitotic figures and an infiltrating growth pattern Figure 8 b. Intralymphatic metastasis is typical and frequently observed. Multiple benign or malignant adnexal tumors are indicator lesions for the syndromes presented in Table 6 While the exact histogenesis of Merkel cell carcinoma has not yet been elucidated, it has been proposed that it derives from epidermal or dermal neuroendocrine stem cells UV exposure, immunosuppression, and the detection of Merkel cell polyomavirus seem to play a key role in the tumor's pathogenesis The trabecular growth pattern corresponds to conventional Merkel cell carcinoma.

Immunohistochemical investigations should be performed to differentiate Merkel cell carcinoma from other tumors with small hyperchromatic, basophilic round cells By contrast, CD7 staining is not always positive Melanocytic neoplasms are characterized by the proliferation of melanocytes.

Table 7 provides an overview of benign and malignant melanocytic tumors. For the correct histological classification of melanocytic tumors, it is therefore crucial to provide the dermatopathologist with clinical details, possibly supplemented by a sketch or a clinical photo, and the location of the lesion.

Histologically, melanocytic nevi are divided into junctional and dermal lesions or a combination of the two compound nevus Figure In general, a distinction must be made between congenital and acquired nevi. Melanocytes originate from the neuroectoderm. Dermal nevus: exclusively dermal nests of monomorphic melanocytes without nuclear atypia; there is complete maturation. Junctional aggregates of monomorphic epithelioid melanocytes with large oval nuclei and broad cytoplasm, disposed as single cells or in nests; there is maturation with progressive descent.

Pigmented spindle cell nevus: similar epidermal pattern as in Spitz nevus. These are arranged as single cells or in large monomorphic nests along the dermoepidermal junction and in the upper dermis. Examples of various types of melanoma are given in Figure The most important histological criteria as regards malignancy are summarized in Table 8. Weighting these criteria is difficult and requires a lot of experience in the histological assessment of melanocytic lesions.

Melanoma in situ MIS : proliferation of atypical melanocytes in all epidermal layers with pagetoid infiltration of the entire epidermis. Lentigo maligna variant of MIS in actinically damaged skin : proliferation of atypical melanocytes and nests in actinically damaged skin, predominantly in the basal and suprabasal layers.

No maturation with progressive descent. Nodular melanoma: regular epidermis without proliferation of melanocytes. Immediately below, there is a nodular proliferation of atypical melanocytes with cellular and nuclear pleomorphism. Apart from the exact diagnosis, the melanoma dermatopathology report should include information on the vertical depth of invasion, the presence of ulceration, regression, neurotropism, or vascular infiltration as well as the T stage based on the most recent classification The classification no longer includes information on mitoses; based on tumor thickness, a distinction is now made between stage T1a and T1b.

Both benign and malignant melanocytic tumors are marked by an exceptionally wide clinical variety. Lesions designated as dysplastic nevi are a special variant whose biological significance is subject to controversial debate among dermatopathologists. In particular, it is still unclear whether this nevus represents an acquired nevus or a precursor lesion of melanoma.