Sarcoidosis of the skin may have an extremely heterogeneous clinical presentation, so that the definitions of 'great imitator' and 'clinical chameleon' have long been used. There is, in fact, a large group of skin diseases that can enter the differential diagnosis with cutaneous sarcoid manifestations, either clinically or/and pathologically. As the clinical consequences and the prognosis of these groups of diseases are often very different, it is important to correctly plan the diagnostic workup. The diagnostic process in this case often presents a challenge as no single test is sufficiently specific, so that a certain diagnosis can be only made in the presence of a compatible clinical and radiographic picture, along with histopathological evidence of non-necrotizing, epithelioid cell granulomas, and exclusion of other potential aetiologies. For practical reasons, four main groups of skin conditions capable of mimicking sarcoidosis can be identified: (i) transmissible, infectious diseases; (ii) allergic and immunological manifestations of various aetiologies; (iii) granulomatous diseases of various aetiologies; and (iv) lymphomas and pseudolymphomas. The aim of this article is to describe the main clinical and histopathological findings of such disease entities, and to discuss the role of those features (morphological, pathological and laboratory) that can help distinguish them from sarcoidosis of the skin.

The reason why the cutaneous form of sarcoidosis is well known in the literature is because of its spectrum of manifestations granting it the fame of a Great Imitator. The mystery shrouding the pathogenesis of this rare cutaneous disease is still there (in spite of the fundamental progress of the various diagnostic methods in current day medicine). The production of the morphological substrate-the epithelioid cell granuloma-which is considered to be characteristic of skin sarcoidosis, could, however, also be the end result of a reaction to i) various specific infectious agents such as Leishmaniasis cutis, coccidioidomycosis, etc., ii) certain residual bacterial or other mycobacterial antigens which, at the moment of setting the diagnosis are-by definition-non-infectious but still immunogenic, as well as iii) different tumor antigens in lesional tissue or other location. Often, differentiating between sarcodiosis and a sarcoid-like reaction, based on the updated criteria for cutaneous sarcoidosis, is problematic to downright impossible. A future characterization of the genetic signature of the two conditions, as well as the implementation of additional mandatory panels for i) the identification of certain infectious or ii) non-infectious but immunogenic and iii) tumor antigens in the epithelioid cell granuloma (or in another location in the organism), could be a considerable contribution to the process of differentiating between the two above-mentioned conditions. This will create conditions for greater accuracy when setting the subsequent therapeutic approaches.

Literature data analysis, providing an exact explanation of the lichen planus pathogenesis, as well as its transition into other rare forms such as Keratosis lichenoides chronica or Graham Lassueur Piccardi Little Syndrome are scant, or totally missing. The chronological course of the disease, known in the literature as lichen planus, varies. Some patients develop Lichen planus or lichen nitidus and there is no logical explanation why. It is also not clear why single patients initially develop ulcerative lesions in the area of the mucosa and only in a few of them these lesions affect the skin. Antigen Mimicry and Epitope Spreading could be the possible pathogenic inductor in cases of lichenoid dermatoses, as well as the cause for their transition into ulcerative, exanthematous or other rare forms. The Epitope Spreading is probably not the leading pathogenetic factor in lichen planus but a phenomenon which occurs later. This manuscript analyzes some basic pathogenic aspects and presents some possible medical hypotheses regarding the heterogenic clinical picture and pathogenesis of lichen planus and lichenoid like pathologies of the skin which, in the near future should be analyzed in details in order to clarify several dilemmas the clinical dermatologist has to face.

Summary Podoconiosis or mossy foot is a form of non‐filarial lymphedema. This geo‐chemical elephantiasis is a disabling condition caused by the passage of microparticles of silica and aluminum silicates through the skin of people walking barefoot in areas with a high content of soil of volcanic origin. Podoconiosis is widespread in tropical Africa, Central America and North India, yet it remains a neglected and under‐researched condition. The disabling effects of podoco‐niosis cause great hardship to patients. It adversely affects the economic (reduced productivity and absenteeism), social (marriage, education, etc.) and psychological (social stigma) well‐being of those affected. Podoconiosis can be prevented; the main primary preventive measure is protective footwear. Secondary measures include a strict hygiene regimen and compression therapy, which can reverse initial lesions. Tertiary approaches include surgical management, such as shaving operations to reduce hyperplastic and verru‐cous elephantiasis.

Piercing, i.e. perforation of skin or mucous membranes in order to attach mostly metallic jewelery as well as multicolored skin tattooing have become more popular than ever before and a considerable number of (young) people practise these methods of body art which are supposed to increase the individuality. But there is a lot of side effects, among them especially infections. The most important bacteria cultivated from such patients are Staphylococcus aureus, group A streptococci and Pseudomonas aeruginosa. Viruses which can be transmitted by piercing or tattooing are especially hepatitis B virus and hepatitis C virus. Besides local bacterial infections also systemic infections (sepsis, endocarditis) occur. The main aspects of diagnostics, therapy and prevention are discussed.

Mycobacterium marinum belongs to the non-tuberculous or "atypical" mycobacteria. The reservoirs for these ubiquitous and slowly growing bacteria are both fresh water and salt water. In particular, aquaria should be considered as important source of hobby-related infections especially of fingers, hands and forearms. Affected are both immunosuppressed patients and persons with an intact immune system. Distinctive are erythematous plaques and nodules with tendency for hyperkeratosis, crusting, and superficial ulcerations, sometimes as sporotrichoid lymphocutaneous infection. The histology shows non-caseation granulomas containing epithelioid cells and Langhans giant cells. Using the Ziehl Neelsen staining, typical acid-fast rods are not always detectable. The molecular biological detection of mycobacterial DNA using polymerase chain reaction represents the standard method of diagnosis. Cryotherapy is frequently used as first treatment. For the often long-term tuberculostatic therapy, rifampicin, ethambutol, and clarithromycin are the most used agents.

Fall 3091 Mediquiz Fall 3091 18-jähriger Patient mit Hyperpigmentierung am Zeh 18-year-old patient with hyperpigmentation on the toe Was sehen Sie? Abb. 1 Hautveränderung am zweiten Zeh des rechten Fußes des Patienten. Der 18-jährige Patient stellte sich mit einer seit vier Monaten bestehenden Hautveränderung am zweiten Zeh des rechten Fußes vor (q Abb. 1). Es wurden keine mechanischen Reizungen oder lokale Traumata infolge von Stoß oder Druck angegeben. Die Aufnahmen des Zehs zeigen einen pathologischen Befund.

Mycobacterium abscessus is the most pathogenic of the fast-growing mycobacteria, and it is resistant to most of the antimicrobial and tuberculostatic drugs available. This non-tuberculous mycobacterium is significant in medicine because it can contaminate post-traumatic wounds and be a causative agent in chronic skin and soft tissue infection after surgical procedures.A 60-year-old immunocompetent woman was suffering from chronic ulcers and abscesses on the heels and malleoli of both feet. Histological examination revealed a granulomatous inflammation with detection of acid-fast rods, albeit without fibrinoid necrosis. The repeated detection of atypical mycobacteria, which were ultimately identified as Mycobacterium abscessus, allowed the diagnosis of an atypical mycobacteriosis of the skin. This was successfully treated first with clarithromycin and rifabutin and later with a combination of ethambutol, minocycline, clofazimine and azithromycin.