Sun exposure, a relevant exposome factor in acne patients and how photoprotection can improve outcomes.

BACKGROUND: Acne pathophysiology includes a complex interaction among inflammatory mediators, hyperseborrhea, alteration of keratinization and follicular colonization by Propionibacterium acnes. AIMS: To describe the impact of the exposome on acne and how photoprotection can improve outcomes. METHODS: A narrative review of the literature was carried out; searches with Google Scholar and Pubmed from January 1992 to November 2022 were performed. The keywords used were "acne," "sunscreens," "photoprotection," "cosmetics," "cosmeceuticals," "pathogenesis," "etiology," "exposome," "sunlight," "stress," "lack of sleep," "diet," "postinflammatory hyperpigmentation," "pollution," "exposome," "ultraviolet radiation," and "visible light." RESULTS: Environmental factors such as solar radiation, air pollution, tobacco consumption, psychological stress, diverse microorganisms, nutrition, among others, can trigger or worsen acne. Solar radiation can temporarily improve lesions. However, it can induce proinflammatory and profibrotic responses, and produce post-inflammatory hyperpigmentation and/or post-inflammatory erythema. While photoprotection is widely recommended to acne patients, only four relevant studies were found. Sunscreens can significantly improve symptomatology or enhance treatment and can prevent post-inflammatory hyperpigmentation. Furthermore, they can provide camouflage and improve quality of life. Based on acne pathogenesis, optimal sunscreens should have emollient, antioxidant and sebum controlling properties. CONCLUSIONS: The exposome and solar radiation can trigger or worsen acne. UV light can induce post-inflammatory hyperpigmentation/erythema, and can initiate flares. The use of specifically formulated sunscreens could enhance adherence to topical or systemic therapy, camouflage lesions (tinted sunscreens), decrease inflammation, and reduce the incidence of post-inflammatory hyperpigmentation/erythema.

Granulomas in Dermatopathology: Principal Diagnoses - Part 1. / Granulomas en dermatopatología: principales entidades. Parte I.

This series of 2 articles on dermatopathologic diagnoses reviews conditions in which granulomas form. Part 1 clarifies concepts, discusses the presentation of different types of granulomas and giant cells, and considers a large variety of noninfectious diseases. Some granulomatous diseases have a metabolic origin, as in necrobiosis lipoidica. Others, such as granulomatous mycosis fungoides, are related to lymphomas. Still others, such as rosacea, are so common that dermatologists see them nearly daily in clinical practice.

Granulomas in Dermatopathology: Principal Diagnoses - Part 2. / Granulomas en dermatopatología: principales entidades. Parte II.

Part 2 of this series on granulomatous diseases focuses on skin biopsy findings. Whereas the first part treated noninfectious conditions (metabolic disorders and tumors, among other conditions), this part mainly deals with various types of infectious disease along with other conditions seen fairly often by clinical dermatologists.

Dermatopatología de la oclusión intraluminal vascular: parteII (coagulopatías, émbolos y miscelánea) / Clinical and Histopathologic Characteristics of the Main Causes of Vascular Occusion - Part II: Coagulation Disorders, Emboli, and Other

La patología vascular oclusiva es causante de diversas y variadas manifestaciones clínicas, algunas de ellas con catastróficas consecuencias para el paciente. Dado que las causas de tal oclusión son muy variadas, hemos abordado en un artículo previo reciente en esta misma revista las causas trombóticas. En el presente artículo recopilamos diversas causas adicionales de oclusión intravascular

Vascular occlusion has multiple, diverse clinical manifestations, some of which can have grave consequences for patients. It also has a wide variety of causes, including thrombi, which we recently addressed in part I of this review. In this second part, we look at additional causes of vascular occlusion

Dermatopatología de la oclusión intraluminal vascular: parte I (trombos) / Clinical and Histopathologic Characteristics of the Main Causes of Vascular Occlusion - Part I: Thrombi

La patplogía vascular oclusiva es causante de diversas y variadas manifestaciones clínicas, algunas de las cuales son de catastróficas consecuencias para el paciente. Sin embargo, las causas de tal oclusión son muy variadas, extendiéndose desde trombos por acción descontrolada de los mecanismos de coagulación, hasta anomalías de los endotelios de los vasos u oclusión por materiales extrínsecos. En una serie de dos artículos hacemos una revisión de las principales causas de oclusión vascular, resumiendo sus manifestaciones clínicas principales y los hallazgos histopatológicos fundamentales. Esta primera parte corresponde a las oclusiones vasculares que cursan con trombos

Vascular occlusion has multiple, diverse clinical manifestations, some of which can have grave consequences for patients. The causes of vascular occlusion are also highly variable, ranging from thrombi triggered by the uncontrolled activation of coagulation mechanisms, on the one hand, to endothelial dysfunction or occlusion by material extrinsic to the coagulation system on the other. In a 2-part review, we look at the main causes of vascular occlusion and the key clinical and histopathologic findings. In this first part, we focus on vascular occlusion involving thrombi

Clinical and Histopathologic Characteristics of the Main Causes of Vascular Occlusion - Part I: Thrombi. / Dermatopatología de la oclusión intraluminal vascular: parte I (trombos).

Vascular occlusion has multiple, diverse clinical manifestations, some of which can have grave consequences for patients. The causes of vascular occlusion are also highly variable, ranging from thrombi triggered by the uncontrolled activation of coagulation mechanisms, on the one hand, to endothelial dysfunction or occlusion by material extrinsic to the coagulation system on the other. In a 2-part review, we look at the main causes of vascular occlusion and the key clinical and histopathologic findings. In this first part, we focus on vascular occlusion involving thrombi.

Clinical and Histopathologic Characteristics of the Main Causes of Vascular Occusion - Part II: Coagulation Disorders, Emboli, and Other. / Dermatopatología de la oclusión intraluminal vascular: parteII (coagulopatías, émbolos y miscelánea).

Vascular occlusion has multiple, diverse clinical manifestations, some of which can have grave consequences for patients. It also has a wide variety of causes, including thrombi, which we recently addressed in partI of this review. In this second part, we look at additional causes of vascular occlusion.

Placas anulares en el tronco de un adolescente / Annular Plaques on the Trunk of a Teenage Boy

No disponible

Carcinoma en coraza / Carcinoma en Cuirasse

No disponible

Nódulo brillante en la frente de un adulto / A Shiny Nodule on the Forehead of a Man

No disponible

La efectividad del tratamiento con omalizumab en la vida real es menor en pacientes con urticaria crónica de más de 18 meses de evolución y tratamiento inmunosupresor previo / The Effectiveness of Omalizumab Treatment in Real-Life is Lower in Patients with Chronic Urticaria Longer than 18 Months’ Evolution and Prior Immunosuppressive Treatment

Antecedentes: Aunque la eficacia del omalizumab en el tratamiento de la urticaria crónica espontánea está demostrada en ensayos clínicos de fase iii, la información disponible sobre la efectividad en la vida real utilizando la puntuación de actividad urticarial semanal (UAS7) es escasa. El objetivo del estudio fue evaluar la respuesta clínica (UAS7 ≤ 6) y la respuesta completa (UAS7 = 0) en las semanas 12 y 24 en una cohorte de la vida real e identificar posibles predictores de respuesta al omalizumab. Métodos: Se llevó a cabo una revisión retrospectiva de los registros clínicos de pacientes consecutivos con urticaria crónica espontánea de moderada a grave (UAS≥16) tratados con omalizumab en el Servicio de Dermatología de un hospital universitario en Barcelona, España, desde febrero de 2014 a septiembre de 2017. Se evaluaron los valores de UAS7 y la evolución siguiendo un protocolo predefinido. El análisis estadístico de los datos se realizó utilizando el paquete estadístico SPSS 18 (SPSS 18 Inc., Chicago, IL, EE. UU.). Resultados: Se incluyeron en el estudio 48 pacientes, que completaron 24 semanas de seguimiento. Las tasas de respuesta clínica (UAS7 < 6) y completa (UAS7 = 0) fueron del 70,8% y del 47,9% a la semana 12 y del 64,6% y del 52,1% a la semana 24. Los pacientes con urticaria de larga duración (≥ 18 meses) tuvieron menor probabilidad de lograr una respuesta clínica en la semana 12 (odds ratio: 0,25; intervalo de confianza del 95%: 0,06-0,96). El tratamiento inmunosupresor previo tendía a asociarse con una menor probabilidad de respuesta completa en la semana 12 (odds ratio: 0,27; intervalo de confianza del 95%: 0,07-1,02). El tratamiento con antihistamínicos H1 se asoció con una menor probabilidad de respuesta a la semana 24 (odds ratio: 0,1; intervalo de confianza del 95%: 0,01-0,88). Conclusiones: La eficiencia y la seguridad del omalizumab en la vida real son similares a la eficacia y la seguridad en los ensayos clínicos. La duración de la enfermedad, la terapia inmunosupresora previa y el requerimiento de tratamiento concomitante con antihistamínicos H1 pueden ayudar a predecir la respuesta al tratamiento con omalizumab

Background: The efficacy of omalizumab in the treatment of chronic spontaneous urticaria has been demonstrated in phase iii clinical trials, but limited information is available regarding real-life effectiveness using the weekly Urticarial Activity Score (UAS7). The aim of the study was to assess clinical response (UAS7 ≤ 6) and complete response (UAS7 = 0) rates at weeks 12 and 24 in a real-life cohort and to identify possible predictors of response to omalizumab. Methods: Clinical records of consecutive patients with moderate-to-severe chronic spontaneous urticaria (UAS ≥ 16) treated with omalizumab at a university-affiliated reference dermatology department in Barcelona, Spain, from February 2014 to September 2017 were retrospectively reviewed. UAS7 values and patients’ evolution were assessed according to a predefined protocol. Statistical analysis of data was done using SPSS 18 statistical package (SPSS 18 Inc., Chicago, IL, USA) software. Results: Forty-eight patients were included in the study. All of them completed at least 24-weeks of treatment and follow-up. At week 12, clinical response rates (UAS7 < 6) were 70.8% and complete response rates (UAS7 = 0) were 47.9%. At week 24, clinical response rates were 64.6% and complete response rates were 52.1%. Patients: with long-term urticaria (≥ 18 months’ duration) were less likely to achieve a clinical response at week 12 (odds ratio: 0.25; 95% confidence interval 0.06-0.96). Previous immunosuppressive treatment tended to be associated with a lower probability of complete response at week 12 (odds ratio: 0.27 95% confidence interval: 0.07-1.02). H1-antihistamine treatment was associated with lower probability of response at week 24 (odds ratio: 0.1 95% 95% confidence interval: 0.01-0.88) Conclusions: The effectiveness and safety of omalizumab in real life are similar to efficacy and safety in clinical trials. Duration of disease, previous immunosuppressive therapy and requirement for concomitant H1-antihistamine treatment may be helpful in predicting response to omalizumab treatment