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Actinic keratosis (AK) is a very frequently diagnosed disorder in dermatological practice that mostly arises on the parts of the body that are exposed to the sun. This cutaneous lesion has been historically considered pre-cancerosis, but currently it is recommended to classify it as squamous cell carcinoma (SCC) in situ. The course of the disease is usually heterogeneous. Individual lesions may -- regress spontaneously, -- recur, -- persist without changes for a long time, or -- can progress to invasive cancer. It is known that AK and SCC of the skin represent a continuous evolutionary process that begins with ultraviolet radiation-induced damage of keratinocyte DNA, continues with clonal expansion of genetically altered cells, and ends with invasive carcinoma. The process of the malignant transformation of AK and cutaneous SCC development is similar to a mechanism of uterine cervix SCC development called cervical intraepithelial neoplasia. Therefore, an analogous classification scheme for the neoplastic changes of epidermis has been proposed named keratinocyte intraepidermal neoplasia. This 3-tiered grading system better reflects the process of gradual malignant transformation of the epidermis, but controversy still persists about its practical application. Although the malignant potential of AK is relatively low, we do not know any reliable clinico-pathological factors to predict disease outcome. That is why there is still a need for new studies focusing on the pathogenesis and biological behaviour of AK. In clinical practice, this is illustrated by the dilemma of whether all lesions unconditionally require treatment, and which is the most appropriate therapy for individual lesions. [ABSTRACT FROM AUTHOR]

Introduction: Jellyfish burning is not commonly part of the professional finding in the central Europe health care laboratory. Holiday seaside tourism includes different and unusual presentations of diseases for our worklplaces. Sea water-sports and leisure is commonly connected with jellyfish burning and changes in the skin, that are not precisely described., Aim: Authors focused their research on detection of morphological and quantitative changes of some inflammatory cells in the skin biopsy of a 59-years-old woman ten days after a jellyfish stinging. Because of a comparison of findings the biopsy was performed in the skin with lesional and nonlesional skin., Methods: Both excisions of the skin were tested by imunohistochemical methods to detect CD68, CD163, CD30, CD4, CD3, CD8, CD20 a CD1a, to detect histiocytes, as well as several clones of lymphocytes and Langerhans cells (antigen presenting cells of skin), CD 117, toluidin blue and chloracetase esterase to detect mastocytes and neutrophils. Material was tested by immunofluorescent methods to detect IgA, IgM, IgG, C3, C4, albumin and fibrinogen. Representative view-fields were documented by microscope photocamera Leica DFC 420 C. Registered photos from both samples of the skin were processed by morphometrical analysis by the Vision Assistant software. A student t-test was used for statistical analysis of reached results., Results: Mean values of individual found cells in the sample with lesion and without lesion were as follows: CD117 -2.64/0.37, CD68-6.86/1.63, CD163-3.13/2.23, CD30-1.36/0.02, CD4-3.51/0.32, CD8-8.22/0.50, CD3-10.69/0.66, CD20-0.56/0.66, CD1a-7.97/0.47 respectively. Generally mild elevation of eosinofils in lesional skin was detected. Increased values of tested cells seen in excision from lesional skin when compared with nonlesional ones were statistically significant in eight case at the level p = 0.033 to 0.001. A not statistically significant difference was found only in the group of CD163+ histiocytes., Conclusion: Authors detected numbers of inflammatory cells in lesional skin after the stinging by a jellyfish and compared them with the numbers of cells in the nonlesional skin of the same patient. Statistically significant differences were seen in the level of selected inflammation cells and numerically documented changes of cellularity in the inflammatory focus were caused by a hypersensitivity reaction after jellyfish injury in the period of 10 days after attack.

Epidermolysis bullosa and Bart´s syndrome are fairly accurately documented diseases by histopathology. In the article the authors describe interesting and hitherto undescribed phenomenon in the lungs male infant with epidermolysis bullosa junctionalis and Barts syndrome, who died 17 days after birth and 13 days after surgery for pyloric atresia, on multiorgan failure within basic congenital diseases.Histologically in lung alveoli was found to the massive presence of foamy macrophages and numerous globoid formations resembling morphological and immunohistochemical "Hassall´s" bodies in a thymus of the newborn. It was a acidophillic spherical bodies concentric tracks in the connective tissue with focal presence of fibrin, as a unique proof CKAE1/AE3 and CKHMW positive epithelial cells and CD68-positive histiocytic elements. An interesting finding was the follicular skin structure in the center "hassalloid´s-like" body, which suggests an aspiration components of the skin during intrauterine life.Normal Apgar score at birth of the child (10/10/10 s.) and severe histological features on the death of the child testify for the first pathogenetic formation "hassalloid´s-like" bodies in the lungs during the 17-day life of a disabled child.

Barts syndrome, in literature also known under the name CLAS (Congenital Localised Absence of Skin), first described by Bart in 1966 as congenital localized absence of skin, epidermolysis bullosa congenita and nail abnormalities. The authors present a macroscopic and histological findings of a newborn with Barts syndrome, with epidermolysis bullosa junctionalis and atresia pylori, who died 17 days after birth and 13 days after surgery for pyloric stenosis.