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INTRODUCTION: Dermatoporosis is a chronic cutaneous fragility syndrome, characterized by skin atrophy, purpura and pseudo-cicatrices. OBJECTIVE: To determine factors associated with dermatoporosis in a sample of subjects aged ≥ 60 years. METHODS: Observational, cross-sectional, descriptive, analytical study of subjects aged ≥ 60 years who underwent history taking, physical examination and application of a self-administered dermatoporosis diagnostic questionnaire. To determine the associated factors, a multivariate logistic regression analysis was used. RESULTS: In 315 evaluated subjects, the prevalence of dermatoporosis was 29%; 70% were females. Associated risk factors were age > 75 years (p = 0.001), prolonged sun exposure (p = 0.002), use of anticoagulants/antiplatelet medications (p = 0.004), oral steroids (p = 0.03) and chronic kidney disease (p = 0.03), as well as maternal age > 40 years at last pregnancy (p = 0.02), breastfeeding for > 7 months per pregnancy and > 18 cumulative months (p = 0.01). Age < 20 years at first pregnancy and menopause after 45 years were related to dermatoporosis absence. The correlation between self-assessment and clinical diagnosis was considerably high (0.95, p < 0.001). CONCLUSIONS: The risk factors associated with dermatoporosis were similar to those previously reported.

INTRODUCCIÓN: La dermatoporosis es un síndrome crónico de fragilidad cutánea, caracterizado por atrofia, púrpura y pseudocicatrices en piel. OBJETIVO: Determinar los factores asociados a dermatoporosis en una muestra de sujetos ≥ 60 años. MÉTODOS: Estudio observacional, transversal, descriptivo y analítico de sujetos ≥ 60 años a quienes se realizó historia clínica, exploración física y aplicación de un autocuestionario diagnóstico de dermatoporosis. Para determinar los factores asociados se realizó análisis de regresión logística multivariado. RESULTADOS: En 315 sujetos, la prevalencia de dermatoporosis fue de 29 %; 70 % fue del sexo femenino. Los factores asociados fueron edad > 75 años (p = 0.001), exposición solar prolongada (p = 0.002), ingesta de anticoagulantes/antiplaquetarios (p = 0.004), esteroides orales (p = 0.03) y enfermedad renal crónica (p = 0.03); así como, edad materna > 40 años en el último parto (p = 0.02), lactancia > 7 meses por embarazo y lactancia acumulada > 18 meses (p = 0.01). Se relacionaron con su ausencia, edad < 20 años en el primer embarazo y menopausia después de los 45 años. La correlación entre la autovaloración y el diagnóstico clínico fue muy alta (0.95, p < 0.001). ­. CONCLUSIONES: Los factores de riesgo asociados a dermatoporosis fueron similares a los previamente reportados.

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Resumen Introducción: La dermatoporosis es un síndrome crónico de fragilidad cutánea, caracterizado por atrofia, púrpura y pseudocicatrices en piel. Objetivo: Determinar los factores asociados a dermatoporosis en una muestra de sujetos ≥ 60 años. Métodos: Estudio observacional, transversal, descriptivo y analítico de sujetos ≥ 60 años a quienes se realizó historia clínica, exploración física y aplicación de un autocuestionario diagnóstico de dermatoporosis. Para determinar los factores asociados se realizó análisis de regresión logística multivariado. Resultados: En 315 sujetos, la prevalencia de dermatoporosis fue de 29 %; 70 % fue del sexo femenino. Los factores asociados fueron edad > 75 años (p = 0.001), exposición solar prolongada (p = 0.002), ingesta de anticoagulantes/antiplaquetarios (p = 0.004), esteroides orales (p = 0.03) y enfermedad renal crónica (p = 0.03); así como, edad materna > 40 años en el último parto (p = 0.02), lactancia > 7 meses por embarazo y lactancia acumulada > 18 meses (p = 0.01). Se relacionaron con su ausencia, edad < 20 años en el primer embarazo y menopausia después de los 45 años. La correlación entre la autovaloración y el diagnóstico clínico fue muy alta (0.95, p < 0.001). Conclusiones: Los factores de riesgo asociados a dermatoporosis fueron similares a los previamente reportados.

Abstract Introduction: Dermatoporosis is a chronic cutaneous fragility syndrome, characterized by skin atrophy, purpura and pseudo-cicatrices. Objective: To determine factors associated with dermatoporosis in a sample of subjects aged ≥ 60 years. Methods: Observational, cross-sectional, descriptive, analytical study of subjects aged ≥ 60 years who underwent history taking, physical examination and application of a self-administered dermatoporosis diagnostic questionnaire. To determine the associated factors, a multivariate logistic regression analysis was used. Results: In 315 evaluated subjects, the prevalence of dermatoporosis was 29%; 70% were females. Associated risk factors were age > 75 years (p = 0.001), prolonged sun exposure (p = 0.002), use of anticoagulants/antiplatelet medications (p = 0.004), oral steroids (p = 0.03) and chronic kidney disease (p = 0.03); as well maternal age > 40 years at last pregnancy (p = 0.02), breastfeeding for > 7 months per pregnancy and > 18 cumulative months (p = 0.01). Age < 20 years at first pregnancy and menopause after 45 years were related to dermatoporosis absence. The correlation between self-assessment and clinical diagnosis was considerably high (0.95, p < 0.001). Conclusions: The risk factors associated with dermatoporosis were similar to those previously reported.

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BACKGROUND: The use of soap for skin cleansing is common among the population. However, it is possible that it causes damage to skin cells and disrupts the skin barrier. OBJECTIVE: To determine the cytotoxic effect of soaps on in vitro-cultured keratinocytes and to correlate it with clinical irritation. METHOD: A survey was conducted to find out the most widely used commercial soaps and their number. Subsequently, their cytotoxicity was evaluated in human keratinocyte cultures using the resazurin assay. The soaps with the highest and lowest cytotoxicity were applied to the skin of healthy volunteers to assess their effect on the skin barrier using colorimetry and transepidermal water loss (TEWL) assays. RESULTS: Of the analyzed soaps, 37 % were shown to be toxic to keratinocytes in vitro. The soap with the highest toxicity induced the highest rate of erythema and TEWL, in comparison with the least toxic soap and the vehicle used as the control solution. CONCLUSION: Soaps marketed for skin cleansing can contain chemical ingredients that damage human keratinocytes and cause skin barrier subclinical irritation. Their use can worsen preexisting dermatoses, generate xerotic or irritant contact dermatitis, and cause atrophy and dermatoporosis.

INTRODUCCIÓN: El jabón para el aseo cutáneo es de empleo común entre la población, sin embargo, es posible que cause daño a las células de la piel y modifique la barrera cutánea. OBJETIVO: Determinar el efecto citotóxico de los jabones en queratinocitos cultivados in vitro y correlacionarlo con la irritación clínica. MÉTODO: Se realizó una encuesta para conocer los jabones comerciales más utilizados y su cantidad; posteriormente, se evaluó su citotoxicidad en cultivos de queratinocitos humanos mediante el método de resazurina. Los jabones con mayor y menor citotoxicidad se aplicaron en piel de voluntarios sanos para evaluar su efecto en la barrera cutánea mediante ensayos de colorimetría y pérdida transepidérmica de agua. RESULTADOS: De los jabones analizados, 37 % demostró ser tóxico para los queratinocitos in vitro. El jabón con mayor toxicidad indujo el mayor índice de eritema y pérdida transepidérmica de agua, en comparación con el jabón menos tóxico y el vehículo empleado como solución control. CONCLUSIÓN: Los jabones comercializados para el aseo cutáneo pueden incluir ingredientes químicos que dañan los queratinocitos humanos y causan irritación subclínica de la barrera cutánea. Su utilización puede agravar dermatosis preexistentes, generar dermatitis xerósica o de contacto irritativa y causar atrofia y dermatoporosis.

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Resumen Introducción: El jabón para el aseo cutáneo es de empleo común entre la población, sin embargo, es posible que cause daño a las células de la piel y modifique la barrera cutánea. Objetivo: Determinar el efecto citotóxico de los jabones en queratinocitos cultivados in vitro y correlacionarlo con la irritación clínica. Método: Se realizó una encuesta para conocer los jabones comerciales más utilizados y su cantidad; posteriormente, se evaluó su citotoxicidad en cultivos de queratinocitos humanos mediante el método de resazurina. Los jabones con mayor y menor citotoxicidad se aplicaron en piel de voluntarios sanos para evaluar su efecto en la barrera cutánea mediante ensayos de colorimetría y pérdida transepidérmica de agua. Resultados: De los jabones analizados, 37 % demostró ser tóxico para los queratinocitos in vitro. El jabón con mayor toxicidad indujo el mayor índice de eritema y pérdida transepidérmica de agua, en comparación con el jabón menos tóxico y el vehículo empleado como solución control. Conclusión: Los jabones comercializados para el aseo cutáneo pueden incluir ingredientes químicos que dañan los queratinocitos humanos y causan irritación subclínica de la barrera cutánea. Su utilización puede agravar dermatosis preexistentes, generar dermatitis xerósica o de contacto irritativa y causar atrofia y dermatoporosis.

Abstract Introduction: The use of soap for skin cleansing is common among the population. However, it is possible that it causes damage to skin cells and disrupts the skin barrier. Objective: To determine the cytotoxic effect of soaps on in vitro-cultured keratinocytes and to correlate it with clinical irritation. Method: A survey was conducted to find out the most widely used commercial soaps and their number. Subsequently, their cytotoxicity was evaluated in human keratinocyte cultures using the resazurin assay. The soaps with the highest and lowest cytotoxicity were applied to the skin of healthy volunteers to assess their effect on the skin barrier using colorimetry and transepidermal water loss (TEWL) assays. Results: Of the analyzed soaps, 37 % were shown to be toxic to keratinocytes in vitro. The soap with the highest toxicity induced the highest rate of erythema and TEWL, in comparison with the least toxic soap and the vehicle used as the control solution. Conclusion: Soaps marketed for skin cleansing can contain chemical ingredients that damage human keratinocytes and cause skin barrier subclinical irritation. Their use can worsen preexisting dermatoses, generate xerotic or irritant contact dermatitis, and cause atrophy and dermatoporosis.

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BACKGROUND: The misfolding and prion-like propagation of the protein α-synuclein (α-syn) is the leading molecular signature in Parkinson's disease (PD). There is a significant coincidence of PD and melanoma that may suggest a shared pathophysiology. This study compared the presence of α-syn in neural crest-derived tissues, such as nevi, melanoma, skin tags, and skin biopsies from patients with PD and healthy controls. METHODS: Biopsies from participants with PD were obtained from patients from a tertiary referral center for dermatology and neurology in Mexico and a private dermatopathology center in Florida between January 2015 and March 2016. Biopsies from 7 patients with melanoma, 15 with nevi, 9 with skin tags, 8 with PD, and 9 skin biopsies from healthy volunteers were analyzed for immunohistochemical determination of α-syn and tyrosinase. All analyses were performed by pathologists who were blinded with respect to the clinical diagnosis. RESULTS: In healthy controls, positive α-syn status was restricted to scattered cells in the basal layer of the epidermis and accounted for 1 ± 0.8% of the analyzed area. In patients with PD, there was increased staining for α-syn PD (3.3 ± 2.3%), with a higher percentage of positive cells in nevi (7.7 ± 5.5%) and melanoma (13.6 ± 3.5%). There was no increased staining in skin tags compared with healthy controls. CONCLUSION: Patients with PD and melanoma have increased staining for α-syn in their skin. The authors propose that neurons and melanocytes, both derived from neuroectodermal cells, may share protein synthesis and regulation pathways that become dysfunctional in PD and melanoma.

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The pathogenesis of melasma has not been clearly elucidated. Using Fontana Masson; diastase-resistant periodic acid-Schiff stains; and immunohistochemistry to stem cell factor (SCF), its receptor c-kit, anti-mast cell tryptase, and anti-collagen type IV antibody, we evaluated melasma lesions and compared them with perilesional skin and photoprotected skin. Samples were taken from lesional and photoprotected nonlesional skin in 24 patients. In other 24 patients, we took biopsies of lesional and perilesional skin. With Fontana Masson, we observed many pigmented basal cells protruding into the dermis of the melasma skin. Periodic acid-Schiff stain and anti-collagen type IV showed damage on the basal membrane in 95.5% and 83%, respectively, in melasma lesion. The immunoreactivity of SCF and the prevalence of mast cells were increased in the dermis of melasma compared with perilesional dermis. The expression of c-kit was significantly increased at lesional epidermis; a frequent protrusion of c-kit-positive basal cells into the dermis was evident in 70% versus that in 29% of perilesional skin. The expression of c-kit was increased at lesional dermis of melasma compared with perilesional skin. We found a low correlation between c-kit expression and prevalence of mast cells; these were increased in melasma skin. The results may suggest a role of SCF, c-kit, and mast cells in the pathogenesis of melasma. We were surprised by the unexpected evidence of damage to basal membrane (BM), which could facilitate the fall or the migration of active melanocytes and melanin into the dermis allowing the constant hyperpigmentation in melasma.

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Melasma is an abnormal acquired hyperpigmentation of the face of unknown origin, it is considered a single disease and very little has been found regarding its pathogenesis. It is usually assumed that melasma is due to excessive melanin production, but excessive retention or abnormal metabolism of this molecule has not yet been considered. In order to search for an alternate explanation for the excessive pigmentation in melasma the molecular structure and concentration of melanin in the stratum corneum of patients with melasma was analyzed using Raman spectroscopy and optical transmission spectroscopy, respectively. From this study it became apparent that in melasma melanin is concentrated in the deeper layers of the skin but its exteriorization remains the same as for healthy skin. Raman spectroscopy measurements showed degraded molecules of melanin in some subjects, which may help explain the variable success rate of the standard therapy.

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