Water is absolutely essential for the normal functioning of the skin and especially the stratum corneum (SC). However, as the SC is continuously exposed to varying humidities, maintenance of water within the tissue is crucial. Under most circumstances water present within the SC will be derived from bodily water, being lost by transepidermal water loss, and is normally bound by proteins together with naturally occurring hygroscopic compounds found largely within, but also external to, the corneocytes. Small amounts of water escape through this slightly leaky barrier to hydrate the dehydrated outer layers of the SC, and this is key to maintaining SC flexibility, SC maturation and SC desquamation. The retention of water in the SC is dependent on three major mechanisms: (a) the intercellular lamellar lipids whose physical conformation, predominantly an orthorhombic gel phase, provides a tight and effective barrier to the passage of water through the tissue, (b) the presence of corneodesmosome-bound and ceramide-hydrophobed corneocytes which influence the tortuosity of the SC and thereby the diffusion path length of water and (c) the presence of both intracellular and extracellular SC natural moisturizing factors (NMF). The structure, biochemistry and function of the SC and the epidermis can however be disturbed upon environmental challenge, particularly by disruption of the SC barrier resulting in the precipitation of dry flaky skin conditions. The maintenance of barrier function and thereby SC hydration is central to the production and optimal functioning of the SC. Fluctuating atmospheric conditions (high and low dew points) influence the formation of the epidermal barrier lipids, NMF, corneocyte envelope phenotypes and the desquamatory enzymes and are thus an initiator of dry skin. At low atmospheric dew points, the reduced SC water content precipitates the dry skin phenotype. On perturbation of barrier function, a cycle of events begins initially with the superficial dehydration of the SC (leaking of extracellular lipids, disruption of lipid lamellar architecture, loss of water-soluble NMF), the release of inflammatory mediators, induction of hyperproliferation of epidermal keratinocytes resulting in disturbed epidermal differentiation leading to an inferior SC (enhanced production of sphingosine-containing ceramides relative to phytosphingosine-containing ceramides and reduced transglutaminase activity leading to retention of fragile corneocyte envelopes in the superficial layers of the SC that have reduced levels of covalently bound ceramides), together with a flaky skin condition (reduced desquamatory enzyme activities and reduced corneodesmolysis). In extreme cases when inflammation is present, increased levels of proteases are observed in the SC and reduced interleukin 1 (IL-1) levels with increased IL-1 receptor antagonist protein levels. If left untreated, these events will continuously cycle to produce an even poorer skin condition, and
{"title":"Dry Skin: Environmental Aspects","authors":"A. Rawlings","doi":"10.1159/000086156","DOIUrl":"https://doi.org/10.1159/000086156","url":null,"abstract":"Water is absolutely essential for the normal functioning of the skin and especially the stratum corneum (SC). However, as the SC is continuously exposed to varying humidities, maintenance of water within the tissue is crucial. Under most circumstances water present within the SC will be derived from bodily water, being lost by transepidermal water loss, and is normally bound by proteins together with naturally occurring hygroscopic compounds found largely within, but also external to, the corneocytes. Small amounts of water escape through this slightly leaky barrier to hydrate the dehydrated outer layers of the SC, and this is key to maintaining SC flexibility, SC maturation and SC desquamation. The retention of water in the SC is dependent on three major mechanisms: (a) the intercellular lamellar lipids whose physical conformation, predominantly an orthorhombic gel phase, provides a tight and effective barrier to the passage of water through the tissue, (b) the presence of corneodesmosome-bound and ceramide-hydrophobed corneocytes which influence the tortuosity of the SC and thereby the diffusion path length of water and (c) the presence of both intracellular and extracellular SC natural moisturizing factors (NMF). The structure, biochemistry and function of the SC and the epidermis can however be disturbed upon environmental challenge, particularly by disruption of the SC barrier resulting in the precipitation of dry flaky skin conditions. The maintenance of barrier function and thereby SC hydration is central to the production and optimal functioning of the SC. Fluctuating atmospheric conditions (high and low dew points) influence the formation of the epidermal barrier lipids, NMF, corneocyte envelope phenotypes and the desquamatory enzymes and are thus an initiator of dry skin. At low atmospheric dew points, the reduced SC water content precipitates the dry skin phenotype. On perturbation of barrier function, a cycle of events begins initially with the superficial dehydration of the SC (leaking of extracellular lipids, disruption of lipid lamellar architecture, loss of water-soluble NMF), the release of inflammatory mediators, induction of hyperproliferation of epidermal keratinocytes resulting in disturbed epidermal differentiation leading to an inferior SC (enhanced production of sphingosine-containing ceramides relative to phytosphingosine-containing ceramides and reduced transglutaminase activity leading to retention of fragile corneocyte envelopes in the superficial layers of the SC that have reduced levels of covalently bound ceramides), together with a flaky skin condition (reduced desquamatory enzyme activities and reduced corneodesmolysis). In extreme cases when inflammation is present, increased levels of proteases are observed in the SC and reduced interleukin 1 (IL-1) levels with increased IL-1 receptor antagonist protein levels. If left untreated, these events will continuously cycle to produce an even poorer skin condition, and ","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81919778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Dry skin is estimated to be present in about 75% of people aged 75 and over. It has been known for many years that this condition is more frequent in winter, in cold and dry weather conditions. With technological progress, people are now mostly exposed to multiple indoor and outdoor pollutants and environment parameters (air-conditioning, chemicals, noise) which can interact which each other and affect human health, and particularly the skin. All these phenomena are intensified with skin aging and can be aggravated by seasons, the way of life, habits (nutrition, dust, allergens, air-conditioning, noise, smoking, unadapted cosmetic use, some treatments) and working conditions (visual display unit, stress). In fact, this environment can be defined as the whole ensemble of external factors which could have an influence on a subject’s health. This means material (climate, geography), organical (biosphere, fauna, flora), physicocultural (techniques), biocultural (nutritional habits, hygiene, medical use) and psychocultural (stress) elements. The aim of this article is to make a review in order to check which of these elements have a major impact on dry skin, in particular among seasons, working/living conditions and cosmetic or hygienic products.
{"title":"Dry Skin and the Environment","authors":"S. Mac-Mary, J. Sainthillier, P. Humbert","doi":"10.1159/000086157","DOIUrl":"https://doi.org/10.1159/000086157","url":null,"abstract":"Dry skin is estimated to be present in about 75% of people aged 75 and over. It has been known for many years that this condition is more frequent in winter, in cold and dry weather conditions. With technological progress, people are now mostly exposed to multiple indoor and outdoor pollutants and environment parameters (air-conditioning, chemicals, noise) which can interact which each other and affect human health, and particularly the skin. All these phenomena are intensified with skin aging and can be aggravated by seasons, the way of life, habits (nutrition, dust, allergens, air-conditioning, noise, smoking, unadapted cosmetic use, some treatments) and working conditions (visual display unit, stress). In fact, this environment can be defined as the whole ensemble of external factors which could have an influence on a subject’s health. This means material (climate, geography), organical (biosphere, fauna, flora), physicocultural (techniques), biocultural (nutritional habits, hygiene, medical use) and psychocultural (stress) elements. The aim of this article is to make a review in order to check which of these elements have a major impact on dry skin, in particular among seasons, working/living conditions and cosmetic or hygienic products.","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74647870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In order to clarify the mechanisms underlying the surfactant-induced dehydration of the stratum corneum (SC), we first examined the constitutive water-holding function of the SC by removing intercellular lipids as well as hygroscopic materials from intact human SC. The dehydration of the SC can be easily induced by depletion of intercellular lipids, but was not affected by an additional water treatment, which releases a large amount of hygroscopic materials including amino acids. Consistent with this, the application of isolated intercellular lipids or their subfractions to the lipid-depleted and dehydrated SC rescues the decreased water content as well as marked scaling, although glycerine did not have such an effect. Parallel differential scanning calorimetry analysis revealed that lipid depletion causes the SC to reduce the nonfreezable bound water content and that application of isolated intercellular lipids recovered the bound water content up to the control level. On the other hand, the additional release of hygroscopic materials from lipid-depleted SC did not affect the bound water content. Based upon the above constitutive water-holding mechanism in the SC, we assessed the physicochemical mechanisms involved in surfactant-induced dehydration of the SC, leading to tight sensation and skin roughness. Similar to treatment with acetone/ether, treatment with surfactant releases a significant amount of intercellular lipids, the intensity of which varies among various surfactants but correlates well with the intensity of the induced dehydration of the SC leading to the tight skin sensation and skin roughness. Recovery or inhibition experiments revealed that the dehydration of the SC induced by surfactant treatment is significantly attenuated by the application of isolated intercellular lipids or by the addition of monoglyceride (MG) during the washing process, which results in a significant reduction in skin roughness. The latter study showed that whereas the release of sebum components and amino acids during surfactant treatment is not affected by the addition of MG, the removal of ceramides is significantly attenuated by the addition of MG, which suggests an essential role for ceramide depletion in the induction of the surfactant-induced dehydration of the SC. In conclusion, the above findings collectively suggest that the ceramide content in the SC is strongly associated with the regulation of SC hydration and that its deficiency due to surfactant treatment is essentially responsible for the surfactant-induced dehydration of the SC. This hypothesis is further strengthened by the fact that synthetic pseudoceramides are remarkably effective in preventing or abolishing the dehydration of the SC which is an intrinsic factor for inducing the tight sensation and roughness of the skin and which provides a pathological basis for atopic dry skin.
{"title":"Surfactant-Induced Depletion of Ceramides and Other Intercellular Lipids: Implication for the Mechanism Leading to Dehydration of the Stratum corneum","authors":"G. Imokawa","doi":"10.1159/000086158","DOIUrl":"https://doi.org/10.1159/000086158","url":null,"abstract":"In order to clarify the mechanisms underlying the surfactant-induced dehydration of the stratum corneum (SC), we first examined the constitutive water-holding function of the SC by removing intercellular lipids as well as hygroscopic materials from intact human SC. The dehydration of the SC can be easily induced by depletion of intercellular lipids, but was not affected by an additional water treatment, which releases a large amount of hygroscopic materials including amino acids. Consistent with this, the application of isolated intercellular lipids or their subfractions to the lipid-depleted and dehydrated SC rescues the decreased water content as well as marked scaling, although glycerine did not have such an effect. Parallel differential scanning calorimetry analysis revealed that lipid depletion causes the SC to reduce the nonfreezable bound water content and that application of isolated intercellular lipids recovered the bound water content up to the control level. On the other hand, the additional release of hygroscopic materials from lipid-depleted SC did not affect the bound water content. Based upon the above constitutive water-holding mechanism in the SC, we assessed the physicochemical mechanisms involved in surfactant-induced dehydration of the SC, leading to tight sensation and skin roughness. Similar to treatment with acetone/ether, treatment with surfactant releases a significant amount of intercellular lipids, the intensity of which varies among various surfactants but correlates well with the intensity of the induced dehydration of the SC leading to the tight skin sensation and skin roughness. Recovery or inhibition experiments revealed that the dehydration of the SC induced by surfactant treatment is significantly attenuated by the application of isolated intercellular lipids or by the addition of monoglyceride (MG) during the washing process, which results in a significant reduction in skin roughness. The latter study showed that whereas the release of sebum components and amino acids during surfactant treatment is not affected by the addition of MG, the removal of ceramides is significantly attenuated by the addition of MG, which suggests an essential role for ceramide depletion in the induction of the surfactant-induced dehydration of the SC. In conclusion, the above findings collectively suggest that the ceramide content in the SC is strongly associated with the regulation of SC hydration and that its deficiency due to surfactant treatment is essentially responsible for the surfactant-induced dehydration of the SC. This hypothesis is further strengthened by the fact that synthetic pseudoceramides are remarkably effective in preventing or abolishing the dehydration of the SC which is an intrinsic factor for inducing the tight sensation and roughness of the skin and which provides a pathological basis for atopic dry skin.","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75303929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lipids in the intercellular spaces of the stratum corneum provide the permeability barrier of the skin. The primary function of the barrier is to prevent water loss to the environment. Secondarily, the barrier limits or prevents the penetration of potentially toxic substances that may contact the skin surface. The main lipids comprising the barrier are ceramides, cholesterol and long-chain saturated fatty acids. The ceramides are structurally heterogenous. In the human, there are 9 series of ceramides. Three of these are acylceramides consisting of long ω-hydroxy acids amide-linked to a long-chain base and bearing linoleate ester-linked to the ω-hydroxyl group. The base component can be sphingosine, phytosphingosine or 6-hydroxysphingosine. The other ceramides contain normal or α-hydroxy acids amide-linked to one of these bases. Linoleate is an essential fatty acid, without which the barrier of the skin cannot be maintained. This is thought to be reflected in the roles of the acylceramides in barrier formation and function. The intercellular lipids of the stratum corneum are organized into elaborate multilamellar structures. Water molecules hydrogen bond to polar head groups of the lamellae; however, there is no free water between the lamellae. Most of the water in the stratum corneum is inside the corneocytes. In a variety of pathological conditions, the lipid composition and organization are altered, leading to a reduced capacity to hold water and increased transepidermal water loss.
{"title":"Stratum corneum Lipids and Water","authors":"P. Wertz","doi":"10.1159/000086155","DOIUrl":"https://doi.org/10.1159/000086155","url":null,"abstract":"Lipids in the intercellular spaces of the stratum corneum provide the permeability barrier of the skin. The primary function of the barrier is to prevent water loss to the environment. Secondarily, the barrier limits or prevents the penetration of potentially toxic substances that may contact the skin surface. The main lipids comprising the barrier are ceramides, cholesterol and long-chain saturated fatty acids. The ceramides are structurally heterogenous. In the human, there are 9 series of ceramides. Three of these are acylceramides consisting of long ω-hydroxy acids amide-linked to a long-chain base and bearing linoleate ester-linked to the ω-hydroxyl group. The base component can be sphingosine, phytosphingosine or 6-hydroxysphingosine. The other ceramides contain normal or α-hydroxy acids amide-linked to one of these bases. Linoleate is an essential fatty acid, without which the barrier of the skin cannot be maintained. This is thought to be reflected in the roles of the acylceramides in barrier formation and function. The intercellular lipids of the stratum corneum are organized into elaborate multilamellar structures. Water molecules hydrogen bond to polar head groups of the lamellae; however, there is no free water between the lamellae. Most of the water in the stratum corneum is inside the corneocytes. In a variety of pathological conditions, the lipid composition and organization are altered, leading to a reduced capacity to hold water and increased transepidermal water loss.","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79903665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
On the other hand, an increase in environmental humidity also induced abnormalities in permeability homeostasis [9] . In this issue of Exogenous Dermatology, environmental factors on dry skin are discussed by fi ve distinguished experts (or their groups) in this fi eld: Wertz (this issue) gives an integrated overview of the epidermal barrier function and their regional variations. His contribution focuses on lipids of the SC and the relationship of SC hydration and barrier function. Furthermore, the pathophysiological aspects of hyperproliferative epidermal conditions with a decreased SC water content, increased transepidermal water loss and an altered skin surface are discussed. Rawlings (this issue) reports about water and SC biomechanics. The state of SC hydration depends on the supplied water from deeper parts of the skin, the evaporation rate at the surface and the water-binding capacity of the SC. The desquamation and proliferation process is highly dependent on both enzyme activity and the integrity of the intercellular lipid matrix. At high humidity, the epidermal synthesis of lipids and natural moisturizing factor is switched off. The reduction in natural moisturizing factor levels together with lipid composition induces changes in the water content in the different layers of the SC. Subsequently this leads to local secretion of proinfl ammatory cytokines that can, either directly or indiIt is well documented that climatic changes infl uence skin conditions, e.g. epidermal structure and functions. A dry environment for example has an impact on epidermal parameters [1] . Improvement of the stratum corneum (SC) homeostasis can ameliorate skin damage induced by barrier disruption in a dry environment [2] . Furthermore, a dry environment directly increases the epidermal level of pro-infl ammatory cytokines [3] . Thus, epidermal homeostasis is very vulnerable when exposed to dry environmental conditions. Histamine H 1 and H 2 receptor antagonists accelerate skin barrier repair and prevent epidermal hyperplasia induced by barrier disruption in a dry environment [4] . Furthermore, a dry environment increases the epidermal mast cell number and histamine content [5] . A recent publication showed the modulation of gene expression induced in human epidermis by environmental stress [6] : the authors could show a general overexpression of MRP8 and MRP14 (both members of the S100 family) as markers for stressed skin being involved in epidermal repair pathways. Loeffl er and Happle [7] reported an increased susceptibility against irritant patch tests during cold climatic conditions during winter and spring. The climatic impact on epidermal functions could be prevented with the application of a moisturizing cream [8] . The daily treatment is effective in improving mild subclinical infl ammation that is induced on the facial skin by the winter environment [8] . Published online: June 30, 2005
{"title":"Dry Skin and the Environment","authors":"J. Fluhr","doi":"10.1159/000086154","DOIUrl":"https://doi.org/10.1159/000086154","url":null,"abstract":"On the other hand, an increase in environmental humidity also induced abnormalities in permeability homeostasis [9] . In this issue of Exogenous Dermatology, environmental factors on dry skin are discussed by fi ve distinguished experts (or their groups) in this fi eld: Wertz (this issue) gives an integrated overview of the epidermal barrier function and their regional variations. His contribution focuses on lipids of the SC and the relationship of SC hydration and barrier function. Furthermore, the pathophysiological aspects of hyperproliferative epidermal conditions with a decreased SC water content, increased transepidermal water loss and an altered skin surface are discussed. Rawlings (this issue) reports about water and SC biomechanics. The state of SC hydration depends on the supplied water from deeper parts of the skin, the evaporation rate at the surface and the water-binding capacity of the SC. The desquamation and proliferation process is highly dependent on both enzyme activity and the integrity of the intercellular lipid matrix. At high humidity, the epidermal synthesis of lipids and natural moisturizing factor is switched off. The reduction in natural moisturizing factor levels together with lipid composition induces changes in the water content in the different layers of the SC. Subsequently this leads to local secretion of proinfl ammatory cytokines that can, either directly or indiIt is well documented that climatic changes infl uence skin conditions, e.g. epidermal structure and functions. A dry environment for example has an impact on epidermal parameters [1] . Improvement of the stratum corneum (SC) homeostasis can ameliorate skin damage induced by barrier disruption in a dry environment [2] . Furthermore, a dry environment directly increases the epidermal level of pro-infl ammatory cytokines [3] . Thus, epidermal homeostasis is very vulnerable when exposed to dry environmental conditions. Histamine H 1 and H 2 receptor antagonists accelerate skin barrier repair and prevent epidermal hyperplasia induced by barrier disruption in a dry environment [4] . Furthermore, a dry environment increases the epidermal mast cell number and histamine content [5] . A recent publication showed the modulation of gene expression induced in human epidermis by environmental stress [6] : the authors could show a general overexpression of MRP8 and MRP14 (both members of the S100 family) as markers for stressed skin being involved in epidermal repair pathways. Loeffl er and Happle [7] reported an increased susceptibility against irritant patch tests during cold climatic conditions during winter and spring. The climatic impact on epidermal functions could be prevented with the application of a moisturizing cream [8] . The daily treatment is effective in improving mild subclinical infl ammation that is induced on the facial skin by the winter environment [8] . Published online: June 30, 2005","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88968656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Lóden, N. Kuzmina, M. Nyrén, F. Edlund, L. Emtestam
Patients with eczema and other dry skin conditions use moisturizers also when the skin appears healthy. However, moisturizers have been found to change skin barrier function, and it appears that certain combinations of ingredients increase the skin susceptibility to external agents. In the present randomized and single-blind study, the influence of a urea-containing cream on nickel susceptibility in 35 patients with known allergy to nickel was evaluated. Treatment of the volar forearm twice daily for 20 days with the urea cream reduced transepidermal water loss (TEWL). However, the susceptibility to nickel sulfate was not changed by the cream treatment. Clinical scoring of the skin reaction did not show any difference between the untreated and the cream-treated area. Furthermore, the increase in TEWL did not differ between the areas. The absence in correlation between TEWL and skin susceptibility to nickel suggests different penetration pathways through the skin of water and nickel. Measurement of the skin permeability to other substances than water is pertinent to the understanding of the influence of moisturizers on the skin permeability and, ultimately, to their therapeutic efficacy in the prevention of contact eczema due to exposure to harmful exogenous substances.
{"title":"Nickel Susceptibility and Skin Barrier Function to Water after Treatment with a Urea-Containing Moisturizer","authors":"M. Lóden, N. Kuzmina, M. Nyrén, F. Edlund, L. Emtestam","doi":"10.1159/000086159","DOIUrl":"https://doi.org/10.1159/000086159","url":null,"abstract":"Patients with eczema and other dry skin conditions use moisturizers also when the skin appears healthy. However, moisturizers have been found to change skin barrier function, and it appears that certain combinations of ingredients increase the skin susceptibility to external agents. In the present randomized and single-blind study, the influence of a urea-containing cream on nickel susceptibility in 35 patients with known allergy to nickel was evaluated. Treatment of the volar forearm twice daily for 20 days with the urea cream reduced transepidermal water loss (TEWL). However, the susceptibility to nickel sulfate was not changed by the cream treatment. Clinical scoring of the skin reaction did not show any difference between the untreated and the cream-treated area. Furthermore, the increase in TEWL did not differ between the areas. The absence in correlation between TEWL and skin susceptibility to nickel suggests different penetration pathways through the skin of water and nickel. Measurement of the skin permeability to other substances than water is pertinent to the understanding of the influence of moisturizers on the skin permeability and, ultimately, to their therapeutic efficacy in the prevention of contact eczema due to exposure to harmful exogenous substances.","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79330024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fifteen grapevine workers developed skin reactions resembling erythema multiforme (EM) and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) following exposure to Dormex, a plant growth regulator, the active ingredient of which is hydrogen cyanamide. Five patients needed hospitalization, and all recovered following treatment. Whether these were contact EM-like reactions due to hydrogen cyanamide or classical EM, SJS-TEN induced by this chemical remains elusive. An awareness regarding the safe use of agricultural chemicals is needed among the general population.
{"title":"Hydrogen-Cyanamide-Related Severe Cutaneous Reactions Simulating Erythema multiforme and Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis","authors":"A. Inamadar, A. Palit","doi":"10.1159/000084697","DOIUrl":"https://doi.org/10.1159/000084697","url":null,"abstract":"Fifteen grapevine workers developed skin reactions resembling erythema multiforme (EM) and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) following exposure to Dormex, a plant growth regulator, the active ingredient of which is hydrogen cyanamide. Five patients needed hospitalization, and all recovered following treatment. Whether these were contact EM-like reactions due to hydrogen cyanamide or classical EM, SJS-TEN induced by this chemical remains elusive. An awareness regarding the safe use of agricultural chemicals is needed among the general population.","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86514534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Certain ingredients in moisturizing creams may influence the skin susceptibility to irritants. One agent of particular interest is the well-known humectant urea. The present placebo-controlled study on 28 subjects was designed to evaluate the effects of urea treatment on three types of sodium lauryl sulphate (SLS) exposures: (1) repeated exposure to SLS for 15 days with concurrent cream treatment, (2) the skin susceptibility to SLS following prophylactic treatment with urea and (3) SLS exposure after recovery of the surfactant-damaged skin by urea treatment. Parameters measured were transepidermal water loss (TEWL) and skin blood flow. Repeated exposure to SLS induced a slight but significant barrier damage, measured as TEWL, and the difference between the treatments was almost significant (p = 0.06). Treatment of normal skin reduced TEWL in the urea-treated area, and the irritant reaction to SLS was significantly decreased. Treatment of surfactant-damaged skin promoted barrier recovery, and the second exposure to SLS induced a less pronounced reaction in the urea-treated area compared to the placebo-treated site. In conclusion, urea promotes barrier recovery in SLS-damaged skin and makes both normal and irritated skin less susceptible to irritation. The findings may be of clinical relevance in attempts to reduce contact dermatitis due to irritant stimuli.
{"title":"The Influence of Urea Treatment on Skin Susceptibility to Surfactant-Induced Irritation: A Placebo-Controlled and Randomized Study","authors":"M. Lóden, E. Bárány, Per Mandahl, C. Wessman","doi":"10.1159/000083462","DOIUrl":"https://doi.org/10.1159/000083462","url":null,"abstract":"Certain ingredients in moisturizing creams may influence the skin susceptibility to irritants. One agent of particular interest is the well-known humectant urea. The present placebo-controlled study on 28 subjects was designed to evaluate the effects of urea treatment on three types of sodium lauryl sulphate (SLS) exposures: (1) repeated exposure to SLS for 15 days with concurrent cream treatment, (2) the skin susceptibility to SLS following prophylactic treatment with urea and (3) SLS exposure after recovery of the surfactant-damaged skin by urea treatment. Parameters measured were transepidermal water loss (TEWL) and skin blood flow. Repeated exposure to SLS induced a slight but significant barrier damage, measured as TEWL, and the difference between the treatments was almost significant (p = 0.06). Treatment of normal skin reduced TEWL in the urea-treated area, and the irritant reaction to SLS was significantly decreased. Treatment of surfactant-damaged skin promoted barrier recovery, and the second exposure to SLS induced a less pronounced reaction in the urea-treated area compared to the placebo-treated site. In conclusion, urea promotes barrier recovery in SLS-damaged skin and makes both normal and irritated skin less susceptible to irritation. The findings may be of clinical relevance in attempts to reduce contact dermatitis due to irritant stimuli.","PeriodicalId":12086,"journal":{"name":"Exogenous Dermatology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81696359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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