Allergic contact dermatitis from hydrocolloid dressings.
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Colloids↗
Biomedical subjects
A Rauterberg
Publications and source records attributed to A Rauterberg.
[UV exposure, skin cancer and decrease in the ozone layer].
All over the world a remarkable increase in malignant tumors of the skin is reported. More than 90% of them are localized in areas of the skin exposed to sunlight. The incidence of malignant melanomas of the skin is tenfold higher today than 40 years ago. Experimental data and results of epidemiological studies indicate two different risk patterns of UV exposure for the development of skin cancer. The cumulative UV-light exposure during lifetime induces--especially in light-sensitive individuals older than 60 years--actinic elastosis, precanceroses and squamous cell carcinomas as well as lentigo maligna melanomas. Intense UV exposure in childhood and youth may lead to development of superficial spreading melanomas and nodular melanomas between the age of 20 and 40. The reduction of ozone in the stratosphere could still contribute to a higher incidence of tumors of the skin in the next decades. The evident role of UVB light in the induction of tumors of the skin offers the possibility for preventive strategies.
Atmosphere↗
Complement deposits in epidermal cells after ultraviolet B exposure.
Ultraviolet B (UVB) radiation is known to induce formation of sunburn cells (SBC) in the epidermis. Since it was unknown whether this process might be accompanied by complement (C) activation, we analyzed C-deposition in skin biopsies taken before and 24 h and 48 h after UVB exposure (fourfold minimal erythema dose or fourfold minimal phototoxic dose) from 14 patients (5 receiving potentially photosensitizing drugs and 9 without such medication) by immunohistology. Local C-activation was visualized by direct or indirect immunofluorescence staining with polyclonal antibodies against C3b, C3d, C5, C9 and monoclonal antibodies to C3b, C3d, C9 and neoantigens on the terminal complement complex (TCC). Neutrophils were identified immunohistologically by antibodies to polymorphonuclear elastase. All but one specimen taken before UVB irradiation were completely negative; biopsies obtained 24 h after UVB revealed complement C3b- and/or C3d-deposits within scattered cells of the epidermis, with wide individual variations in the number of C3-positive cells. C3b and TCC were found predominantly in the cytoplasma; C3d deposits were more often accentuated at the cell surface of C-positive cells. A significantly higher number of keratinocytes was C3d-positive 48 h after UVB exposure than in specimens taken 24 h after UVB. Such a reactivity pattern might indicate a rapid decay of intracellular C3b to C3d. Patients medicated with potentially photosensitizing drugs developed significantly higher numbers of strongly C3-positive cells than those without such medication. Infiltration with elastase-positive cells, presumably representing neutrophils, was observed in the upper third of the dermis and the epidermis in all but one biopsy (n = 9) after UVB.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗