- Email: [email protected]
S057 Environmental dry skin. From xerosis to eczema
Symposia
- Environmental
allergic contact dermatitis 1567 cases (= 35.9%) and contact urticaria 620 cases (= 14.2%). The most common causes of irritant dermatoses (n = 2181) were detergents (n = 729; 33%), wet work (10%) and oils, greases and cutting fluids (6%). The most common causes of occupational allergic contact dermatoses (excluding contact urticaria) (n = 1567 cases) were rubber chemicals (n = 328; 21%), metals (nickel, chromium, cobalt, mercury) (16%) and synthetic resins and plastics (9%). The most common causes during of occupational contact urticaria and protein contact dermatitis (n = 620) were: cow epithelium (n = 276; 44%), natural rubber latex (139 = 22%) and flour, grains and feed (7 1 = 11%).
Dermatoses
s17
tact with detergents or exposure to a hot and dry atmosphere. The delipidated and thinner cornea1 layer with scaling keratinocytes becomes permeable to irritants and allergens, even large proteins of fungi and Dermatophagoides, and granular keratinocytes produce cytokines, like IL-la and p, IL-8, GM - CSF and TNF-cr, which initiate cutaneous inflammation and T-cell migration. So, these patients get dry skin or xerosis, mainly in the dorsum of their hands or their anterior shins, and, as a next step, they develop chappy erythematous pruritic skin or an annular vesiculous eczema - erythema or eczema craquelee or aestheatotic eczema. On histology it may correspond to a spongiotic eczematous dermatitis and it needs treatment with topical corticosteroids, emollients and avoidance of environmental aggressive factors.
I SO56 Atopic dermatitis - An environmental
disease based on data from patch testing
K. Turjanmaa. Department University
Hospital,
of Dermatology,
Tampere,
I SO58 The ozone depletion and the skin J.-P. Ortonne. U385 INSERM, Faculte’ de Mkdecine,
Tampere
Finland
Since the observation of C. Bruynzeel-Koomen in 1986 that IgE molecules are present on epidermal Langerhans’ cells in atopic dermatitis, a lot of effort has been put on studying the mechanism and the consequences of this discovery. Under patch test cups, house dust mites and birch pollen have been found to produce eczematous skin reactions confirming that not only rhinitis and asthma are attributed to these aeroallergens. It has been shown that aeroallergens bind to allergen-specific IgE on Langerhans’ cells and are then presented to T lymphocytes. Allergen-specific T cells, mainly Th2 cells, are found in positive protein patch test (PPT) reactions. They are capable of secreting IL-4, leading to an inflammation similar to the delayed-type immune reaction. Aeroallergens have been shown to alter the epidermal barrier function which further facilitates the allergen penetration of the skin and keeps the eczema going on. These basic observations give us new insight into the pathomechanism of airborne contact dermatitis caused by protein allergens. In addition to mites and pollens, animal dander, flours in bakeries and milk products in dairies may cause even occupational problems. PPT has recently been used also for the diagnosis of delayed-type food allergy in children. Contact with food takes place via the gastrointestinal tract, but there is an increasing amount of information suggesting that atopic eczema caused by ingested food could be reliably diagnosed by patch testing with the allergenic food. For the time being, PPTs need to be standardized, including confirmation of clinical relevance by challenge tests. ElSO57 Environmental dry skin. From xerosis to
eczema
Margarida Goncalo. Clinica Vniversidade
P-3000,
de Dermatologia,
Hospital
da
Portugal
Cornea1 keratinocytes and epidermal lipids form a skin barrier which has its own reparative mechanisms, namely proliferating keratinocytes and enzymes like HMG-CoA reductase and serine palmitoyl transferase that regulate cholesterol and ceramide synthesis. When there are intrinsic defects on its constitution or reparative mechanisms, like in atopics or in old age, skin barrier may be easily disrupted by environmental factors, like con-
Dermatologie,
H6pital
de l’Archet,
Nice,
Service
de
France
Stratospheric ozone depletion (SOD) due to chlorofluorocarbons has long been predicted, Recent investigations demonstrate that the ozone layer shows definite thinning. Estimates suggest that ozone destruction will be enhanced for at least the next 70 years. SOD threatens to increase exposure to ultraviolet radiation in the range from 290-320 nm (UVB) reaching the surface of the earth, which is known to be a factor in a number of diseases including skin abnormalities: photoaging, photocarcinogenesis, alteration of the immune system of the skin. There is little doubt that cumulative exposure to UV-radiations is important in the aetiology of non-melanoma skin cancers. Evidence is also strong for a link with cutaneous malignant melanoma, also here it appears to be intermittent intense exposure that is most damaging. There is therefore great concern about the possible exacerbation of these impacts as a result of increased exposure of UV-radiation associated with SOD. Attemps are made to estimate these additional future risks for the development of skin cancer. The combination of predictions for changes in atmospheric ozone and effective UV with dynamic models for skin cancer induction allow full scenario studies. A recent report estimates for Northwest Europe the excess skin cancer cases due to SOD around the year 2100 at 550,000 (+315%) per year if the use of CFCs is not restricted (Slaper H et al, Nature 1996; 384: 256-258). As a consequence of international restrictions on the production of ozone-depleting substances recommended by the Copenhagen Amendments, the figure would be reduced at 4,000 (+2%) per year. Even if this latter scenario is fully implemented, the calculated number of excess cases caused by SOD would be 14,000 per year in Northwest Europe around the year 2050. These data demonstrate the importance of the restricitons protocols specified by recent international conventions. Dermatologists may play a key-role in this major public health problem by monitoring the incidence, mortality and morbidity of UV-exposure caused by current and future SOD and by evaluating prevention and early detection measures of photocarcinogenesis.
- Environmental
allergic contact dermatitis 1567 cases (= 35.9%) and contact urticaria 620 cases (= 14.2%). The most common causes of irritant dermatoses (n = 2181) were detergents (n = 729; 33%), wet work (10%) and oils, greases and cutting fluids (6%). The most common causes of occupational allergic contact dermatoses (excluding contact urticaria) (n = 1567 cases) were rubber chemicals (n = 328; 21%), metals (nickel, chromium, cobalt, mercury) (16%) and synthetic resins and plastics (9%). The most common causes during of occupational contact urticaria and protein contact dermatitis (n = 620) were: cow epithelium (n = 276; 44%), natural rubber latex (139 = 22%) and flour, grains and feed (7 1 = 11%).
Dermatoses
s17
tact with detergents or exposure to a hot and dry atmosphere. The delipidated and thinner cornea1 layer with scaling keratinocytes becomes permeable to irritants and allergens, even large proteins of fungi and Dermatophagoides, and granular keratinocytes produce cytokines, like IL-la and p, IL-8, GM - CSF and TNF-cr, which initiate cutaneous inflammation and T-cell migration. So, these patients get dry skin or xerosis, mainly in the dorsum of their hands or their anterior shins, and, as a next step, they develop chappy erythematous pruritic skin or an annular vesiculous eczema - erythema or eczema craquelee or aestheatotic eczema. On histology it may correspond to a spongiotic eczematous dermatitis and it needs treatment with topical corticosteroids, emollients and avoidance of environmental aggressive factors.
I SO56 Atopic dermatitis - An environmental
disease based on data from patch testing
K. Turjanmaa. Department University
Hospital,
of Dermatology,
Tampere,
I SO58 The ozone depletion and the skin J.-P. Ortonne. U385 INSERM, Faculte’ de Mkdecine,
Tampere
Finland
Since the observation of C. Bruynzeel-Koomen in 1986 that IgE molecules are present on epidermal Langerhans’ cells in atopic dermatitis, a lot of effort has been put on studying the mechanism and the consequences of this discovery. Under patch test cups, house dust mites and birch pollen have been found to produce eczematous skin reactions confirming that not only rhinitis and asthma are attributed to these aeroallergens. It has been shown that aeroallergens bind to allergen-specific IgE on Langerhans’ cells and are then presented to T lymphocytes. Allergen-specific T cells, mainly Th2 cells, are found in positive protein patch test (PPT) reactions. They are capable of secreting IL-4, leading to an inflammation similar to the delayed-type immune reaction. Aeroallergens have been shown to alter the epidermal barrier function which further facilitates the allergen penetration of the skin and keeps the eczema going on. These basic observations give us new insight into the pathomechanism of airborne contact dermatitis caused by protein allergens. In addition to mites and pollens, animal dander, flours in bakeries and milk products in dairies may cause even occupational problems. PPT has recently been used also for the diagnosis of delayed-type food allergy in children. Contact with food takes place via the gastrointestinal tract, but there is an increasing amount of information suggesting that atopic eczema caused by ingested food could be reliably diagnosed by patch testing with the allergenic food. For the time being, PPTs need to be standardized, including confirmation of clinical relevance by challenge tests. ElSO57 Environmental dry skin. From xerosis to
eczema
Margarida Goncalo. Clinica Vniversidade
P-3000,
de Dermatologia,
Hospital
da
Portugal
Cornea1 keratinocytes and epidermal lipids form a skin barrier which has its own reparative mechanisms, namely proliferating keratinocytes and enzymes like HMG-CoA reductase and serine palmitoyl transferase that regulate cholesterol and ceramide synthesis. When there are intrinsic defects on its constitution or reparative mechanisms, like in atopics or in old age, skin barrier may be easily disrupted by environmental factors, like con-
Dermatologie,
H6pital
de l’Archet,
Nice,
Service
de
France
Stratospheric ozone depletion (SOD) due to chlorofluorocarbons has long been predicted, Recent investigations demonstrate that the ozone layer shows definite thinning. Estimates suggest that ozone destruction will be enhanced for at least the next 70 years. SOD threatens to increase exposure to ultraviolet radiation in the range from 290-320 nm (UVB) reaching the surface of the earth, which is known to be a factor in a number of diseases including skin abnormalities: photoaging, photocarcinogenesis, alteration of the immune system of the skin. There is little doubt that cumulative exposure to UV-radiations is important in the aetiology of non-melanoma skin cancers. Evidence is also strong for a link with cutaneous malignant melanoma, also here it appears to be intermittent intense exposure that is most damaging. There is therefore great concern about the possible exacerbation of these impacts as a result of increased exposure of UV-radiation associated with SOD. Attemps are made to estimate these additional future risks for the development of skin cancer. The combination of predictions for changes in atmospheric ozone and effective UV with dynamic models for skin cancer induction allow full scenario studies. A recent report estimates for Northwest Europe the excess skin cancer cases due to SOD around the year 2100 at 550,000 (+315%) per year if the use of CFCs is not restricted (Slaper H et al, Nature 1996; 384: 256-258). As a consequence of international restrictions on the production of ozone-depleting substances recommended by the Copenhagen Amendments, the figure would be reduced at 4,000 (+2%) per year. Even if this latter scenario is fully implemented, the calculated number of excess cases caused by SOD would be 14,000 per year in Northwest Europe around the year 2050. These data demonstrate the importance of the restricitons protocols specified by recent international conventions. Dermatologists may play a key-role in this major public health problem by monitoring the incidence, mortality and morbidity of UV-exposure caused by current and future SOD and by evaluating prevention and early detection measures of photocarcinogenesis.