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.

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.

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.

The Effectiveness of Omalizumab Treatment in Real-Life is Lower in Patients with Chronic Urticaria Longer than 18 Months' Evolution and Prior Immunosuppressive Treatment. / 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.

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.

Algorithm for Treatment of Chronic Spontaneous Urticaria with Omalizumab. / Algoritmo de tratamiento con omalizumab en urticaria crónica espontánea.

BACKGROUND AND OBJECTIVE: Pivotal trials with omalizumab for treatment of chronic spontaneous urticaria (CSU) are generally run over 12 to 24weeks. However, in clinical practice, many patients need longer treatment. In this article, we present an algorithm for treatment with omalizumab. MATERIAL AND METHODS: The consensus document we present is the result of a series of meetings by the CSU working group of "Xarxa d'Urticària Catalana i Balear" (XUrCB) at which data from the recent literature were presented, discussed, compared, and agreed upon. RESULTS: Treatment with omalizumab should be initiated at the authorized dose, and is adjusted at 3-monthly intervals according to the Urticaria Activity Score Over 7days, the Urticaria Control Test, or both. CONCLUSIONS: The algorithm proposed is designed to provide guidance on how to adjust omalizumab doses, how and when to discontinue the drug, and how to reintroduce it in cases of relapse.

Allergic Contact Dermatitis by Anatomical Regions: Diagnostic Clues. / Dermatitis de contacto alérgica por regiones anatómicas. Claves diagnósticas.

Allergic contact dermatitis (ACD) is a common disease in daily clinical practice, and its prevalence has increased in recent years. It is characterized clinically by varying degrees of erythema, vesiculation, flaking, and lichenification, though these signs can also be present in other eczematous diseases. Patch testing is the main diagnostic tool to confirm ACD, but its accurate interpretation requires correct correlation with the medical history (details of exposure) and physical examination. We provide a practical and instructive description of the most common clinical patters of ACD depending on the area affected. Knowledge of these patterns will not only help the clinician reach the diagnosis but will suggest possible allergens and forms of contact.