Pyogenic granuloma is a common benign vascular tumour occurring in all ages. Both skin and mucous membranes can be affected. Of pathogenetic importance are trauma, BRAF mutations and probably herpes virus type 1, Orf virus and/or human papilloma virus type 2. The tumour consists of capillary proliferations, venules and fibromyxoid stroma. The development of a lesion occurs in three stages and bleeding is a common symptom. The tumour can mimic various other vascular lesions, solid tumours, and soft tissue infections. In recent years, targeted tumour therapies have become the most common cause of drug-induced pyogenic granulomas. The backbone of treatment is surgical procedures including laser therapy. New developments in medical drug therapy include topical and systemic beta-adrenergic receptor antagonists timolol and propranolol. Drug therapy is an alternative for young children, ocular and periungual pyogenic granuloma.

For more than a century, radiotherapy has been an effective treatment for oncologic patients. The Authors report a brief history of the radiation therapy and its actual indication for the treatments of cutaneous malignant diseases.

The medical term onychomycosis should be understood as chronic infection of the nails caused by a fungus. The most common causative agents are the dermatophytes and Candida species. The less common are certain types of moulds (nondermatophyte moulds or NDMs). In approximately 60-80 % of the cases, onychomycosis is due to dermatophytes. Among dermatophytes, the most often isolated causative pathogen is Trichophyton (T.) rubrum. Other common species are T. interdigitale (formerly T. mentagrophytes), Epidermophyton floccosum, and T. tonsurans. The most significant yeasts causing onychomycosis are Candida albicans and Candida parapsilosis. Predisposing factors for onychomycosis include mainly diseases such as diabetes mellitus, peripheral vascular arterial disease, chronic venous insufficiency, polyneuropathies of diverse etiologies, and immunosuppression, e.g., myeloproliferative diseases (such as lymphoma and paraproteinemia), HIV/AIDS, etc. Other factors facilitating the fungal infection are frequent trauma in professional sportsmen, often accompanied by excessive perspiration. The diagnostic methods that are often applied in different dermatologic departments and ambulatory units are also different. This precludes the creation of a unified diagnostic algorithm that could be used everywhere as a possible standard. In most of the cases, the method of choice depends on the specialist's individual experience. The therapeutic approach depends mostly on the fungal organism identified by the dermatologist or mycologist. This review hereby includes the conventional as well as the newest and most reliable and modern methods used for the identification of the pathogens causing onychomycosis. Moreover, detailed information is suggested, about the choice of therapeutic scheme in case whether dermatophytes, moulds, or yeasts have been identified as causative agents. A thorough discussion of the schemes and duration of the antifungal therapy in certain groups of patients have been included.

The intention of this review on nevus comedonicus (NC) is to update on clinical features, pathogenesis, and therapy. NC is a rare epidermal nevus type. It is part of the nevus comedonicus syndrome, a neurocutaneous disorder with ocular, skeletal, and central nervous symptoms. Recently, acne-related signaling pathways and somatic mutations of tyrosine kinase receptors have been identified and may play a role in NC pathogenesis. On preexistent NC secondary skin tumors can develop, which are often benign. Treatment options of NC include topical therapy, laser, and surgery.

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.

Differentiating between sarcoidosis as an autonomous disease and sarcoid-like reactions requires considerable efforts. The epithelioid cell granuloma is not equivalent to sarcoidosis because it may be identified in a number of infectious and noninfectious disorders, including neoplastic diseases. At the current state of knowledge, accurate distinction between different causes of epithelioid cell granulomas is in many cases not possible. Despite being characteristic of sarcoidosis and sarcoid-like reactions, the epithelioid cell granuloma is not their synonym, as numerous other causes can give rise to such a type of granulomatous infiltrate. Its etiology should be sought through careful additional investigations, including the genetic signature of both conditions.Sarcoid-like reactions may be grouped generally into several subtypes. The differentiation between each one of them requires a certain combination of diagnostic tests. The major objective of these tests is to exclude or to prove the presence of an infectious, tumoral, or immunogenic antigen on the one hand, and to characterize the genetic profile of the affected patients (for example, sarcoidosis-specific genes) on the other. Only thus may one accurately differentiate between the two pathologic conditions described earlier in the abstract.The clear differentiation between sarcoidosis as a separate disease and sarcoid-like pathologies leads to the more precise clarification of the final diagnosis, which may in turn allow for a more appropriate therapy and improvement in the quality of life of the patients. Equating sarcoid granulomas with sarcoidosis can lead to serious consequences in a number of patients. Sadly enough, after scrutinizing the current available data in the world literature, one cannot find criteria to allow such distinction in a high percentage of the investigated cases.This critical review provides a completely new pathogenetic and diagnostic algorithm, helping in the differentiation between the disease sarcoidosis and the sarcoid-like pathologies with different etiology. An update on the inclusion criteria from the ATS/ERS/WASOG (American Thoracic Society/European Respiratory Society/World Association of Sarcoidosis and other Granulomatous Disorders) statement (which at the current state of knowledge seems to be ineffective) for the diagnosis of sarcoidosis is also suggested.In conclusion, molecular mimicry may be seen as the main pathogenic generator not only of sarcoidosis but also of sarcoid-like reactions. A completely new and exact definition of the notion of or the sarcoidosis disease itself will be possible only after 1. defining the genetic risk for the development of sarcoidosis as an autonomous disease and supplementing the sarcoidosis consensus of ATS/ERS/WASOG from 1999 with this important information, and 2. defining the notion of a sarcoid-like reaction and its subforms.

Prognosis of primary melanoma is presently based on morphological parameters, mainly tumor thickness. However, more reliable prognostic markers are needed that allow a better stratification of patients, especially with regard to therapeutic options. Here, a retrospective study was performed on patients with primary superficial-spreading melanoma (SSM, n=44) or nodular melanoma (n=16) of 1.5-4 mm thickness. Thirty patients had survived the follow-up of 10 years, whereas the other 30 patients developed metastases. Tumor sections were analyzed by immunohistochemistry for the expression of regulators of the cell cycle (p21; retinoblastoma protein (pRb)), of the intrinsic or extrinsic proapoptotic pathways (p53; murine double minute gene 2 protein; tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-R1/DR4; TRAIL-R2/DR5) and of Bcl-2-related proteins (Bcl-2, Mcl-1, Bax, Bak, Bok), which regulate the common mitochondrial apoptotic pathway. In SSM, decrease of Bax and Bak was significantly correlated with a poor prognosis: high Bax was associated with 10-year survival rates of 68%, whereas low Bax resulted in only 26% survival, and high Bak was associated with 10-year survival rates of 62%, whereas low Bak resulted in only 10% survival. Regulators of apoptosis may therefore candidate for independent prognostic markers for primary melanomas. The study underlines the particular role of the mitochondrial apoptosis pathway and of proapoptotic Bcl-2-related proteins for melanoma progression.

Malignant tumors of the female reproductive system are a serious health and social problem, as they are the second most common cause of death among women, after breast cancer. Their incidence has increased dramatically during recent years, probably due to the different sexual habits and changes in the prevalence of HIV/ AIDS and HPV virus carriers, among other factors. Vulvar tumors represent only 4% of all gynecological neoplasms, and they are fourth in frequency after tumors of the cervix, uterus, and ovary. Ninety eight percent of all vulvar tumors are benign and only 2% are malignant. The overall incidence of tumors with vulvar location is between two and seven cases per 100,000 women, and it increases with age, while the death rate is estimated at 0.7 per 100,000 women. Sarcomas of the vulva comprise approximately 1-3% of all vulvar cancers, with leiomyosarcomas, epithelioid sarcomas, and rhabdomyosarcomas being the most common among them. They are characterized by rapid growth, high metastatic potential, frequent recurrences, aggressive behavior, and high mortality rate. In this paper, we present the most common forms of sarcomas of the vulva (leiomyosarcoma, epithelioid sarcoma, malignant rhabdoid tumor, rhabdomyosarcoma) in order to emphasize the broad differential diagnosis, rare appearance, non-specific clinical picture, aggressive course, and high mortality.