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At least 883 records · Page 49Linked to original sources
PubMed1998

Low humidity stimulates epidermal DNA synthesis and amplifies the hyperproliferative response to barrier disruption: implication for seasonal exacerbations of inflammatory dermatoses.

Although seasonal changes in humidity are thought to exacerbate various skin diseases, whether these flares can be attributed to prolonged exposure to extremes in environmental humidities has not been studied systematically. We recently showed that prolonged exposure to high versus low humidities induced profound changes in epidermal structure and permeability barrier homeostasis. Therefore, we asked here whether comparable extremes in humidity could initiate not only homeostatic, but also potentially pathophysiologic alterations. We showed first that exposure to low humidity increases epidermal DNA synthesis in normal murine epidermis. Moreover, exposure to a low humidity for 48 h further amplifies the DNA synthetic response to barrier disruption, resulting in marked epidermal hyperplasia. Additionally, exposure to a dry environment for 48 h prior to barrier disruption results in dermal mast cell hypertrophy, degranulation, as well as histologic evidence of inflammation. To demonstrate the role of changes in external moisture on these phenomena, we applied either an occlusive, water-impermeable plastic membrane, Petrolatum, or a nonocclusive humectant, both to nonperturbated and to perturbed skin. All three forms of treatment prevented the epidermal hyperplasia and dermal mast cell hypertrophy and degranulation induced by exposure to low humidity. These studies indicate that (i) exposure to changes in environmental humidity alone induces increased keratinocyte proliferation and markers of inflammation, and (ii) that these changes are attributable to changes in stratum corneum moisture content. Finally, these studies provide evidence that changes in environmental humidity contribute to the seasonal exacerbations/amelioration of cutaneous disorders, such as atopic dermatitis and psoriasis, diseases which are characterized by a defective barrier, epidermal hyperplasia, and inflammation.

Acetone↗
PubMed2003

Dermatoses from ticks.

Ticks are ectoparasites that cause dermatologic disease directly by their bite and indirectly as vectors of bacterial, rickettsial, protozoal, and viral diseases. In North America, where ticks are the leading cause of vector-borne infection, dermatologists should recognize several tick species. Basic tick biology and identification will be reviewed. Tick bites cause a variety of acute and chronic skin lesions. The tick-borne diseases include Lyme disease, tick-borne relapsing fever, tularemia, babesiosis, Rocky Mountain spotted fever, other spotted fevers, ehrlichiosis, Colorado tick fever, and others. The epidemiology, clinical features, diagnosis, and treatment of these diseases are reviewed with an emphasis on cutaneous manifestations. Finally, the prevention of diseases caused by ticks is reviewed.

Acute Disease↗