Introduction. Atopic dermatitis (AD) is the most prevalent inflammatory dermatological disorder, affecting a significant percentage of the global population. This chronic disease has a multifactorial and intricate pathogenesis, influenced by genetic predisposition, skin barrier dysfunction, immune dysregulation, neuroimmune mechanisms, and alterations in the skin microbiome, among other factors. Methods. The treatment of AD has faced significant clinical challenges due to the ineffectiveness of conventional therapies. However, recent advances in understanding its pathophysiology have led to the introduction of new therapeutic options. Recently, the OX40 receptor has been identified as a key factor in the development of AD. Recent studies have demonstrated that blocking the OX40 ligand with monoclonal antibodies significantly and sustainably improves the signs and symptoms of moderate to severe AD. Results. A comprehensive review of the available literature on anti-OX40 treatments in atopic dermatitis that evaluates their mechanism of action, their clinical efficacy, and the prospects of this promising therapeutic option for improving AD management is provided. Conclusions. Anti-OX40 and anti-OX40L blockers are a promising therapeutic alternative for the management of moderate–severe atopic dermatitis. Prospective analytical studies are needed to determine whether this new therapeutic target represents a qualitative advance in modifying the progression of the disease.

Background/Objectives: Teledermatology has transformed access to dermatologic care, yet its association with melanoma prognostic parameters and diagnostic pathways in tertiary settings remains incompletely characterized. To compare the clinicopathologic profile of melanomas diagnosed under face-to-face consultation (2019) versus teledermatology-based referral (teleconsultation) (2022). Methods: A retrospective observational study comparing two patient cohorts: those diagnosed with melanoma via in-person consultation in 2019, and those diagnosed through teleconsultation in 2022. These years were selected to reflect the structural shift in care delivery models before and after the COVID-19 pandemic, during which teledermatology was formally implemented. Sociodemographic, clinical, and histopathological variables were collected. A multivariable logistic regression model assessed variables associated with being diagnosed in the 2022 teledermatology cohort versus the 2019 face-to-face cohort. Statistical analyses were performed using R (v. 4.4.3). Results: A total of 151 patients were included (89 in-person in 2019, 62 via teleconsultation in 2022). Multivariable analysis identified three variables independently associated with being diagnosed via teleconsultation. Increasing Breslow thickness was inversely associated with teleconsultation diagnosis (OR 0.60 per 1 mm increase; 95% CI 0.40–0.91; p= 0.017). Similarly, the presence of histologic regression (OR 0.28; 95% CI 0.09–0.90; p = 0.032) and immunosuppression (OR 0.08; 95% CI 0.008–0.86; p = 0.037) were inversely associated with teleconsultation diagnosis. No significant associations were found for sex, age, tumor location, ulceration, mitosis, or clinical stage. Conclusions: In this retrospective single-center comparison of two care models, melanomas diagnosed through teleconsultation in 2022 were associated with a more favorable clinicopathologic profile at diagnosis than those diagnosed via face-to-face consultation in 2019. These findings support the role of teledermatology-based referral pathways in facilitating timely melanoma assessment, although causal inference is limited by the observational design.

Background: Patients diagnosed with melanoma are at increased risk of developing multiple primary melanomas (MPMs). Identifying clinical and genetic factors associated with MPM is critical for implementing personalized surveillance strategies. This study aims to describe the clinical, histopathological, and genetic characteristics of patients with MPM managed in a tertiary hospital and to contextualize findings within the current literature. Methods: We conducted a retrospective review of patients diagnosed with two or more primary melanomas between 2010 and 2023 at a tertiary dermatology unit. Demographic data, personal and family cancer history, phototype, melanoma characteristics, genetic testing, staging, treatments, and outcomes were collected. These data were compared with findings from the recent literature. Results: Thirteen patients (ten males, three females; median age: 59 years) were found to have a total of 33 melanomas. Most patients had Fitzpatrick phototype II and no immunosuppression. The number of melanomas per patient ranged from two to five. Synchronous lesions were observed in two patients. Common locations included the trunk and extremities. Histologically, 57% were in situ melanomas, and subsequent melanomas were generally thinner than the index lesion. Two patients showed progression to advanced disease. One patient was positive for MC1R mutation; the rest were negative or inconclusive. Additional phenotypic and environmental risk factors were extracted from patient records and are summarized as follows: Ten patients (76.9%) had Fitzpatrick skin phototype II, and three (23.1%) had phototype III. Chronic occupational sun exposure was reported in four patients (30.8%), while five (38.5%) recalled having suffered multiple sunburns during childhood or adolescence. Eight patients (61.5%) presented with a total nevus count exceeding 50, and five (38.5%) exhibited clinically atypical nevi. None of the patients reported use of tanning beds. Conclusions: Our findings are consistent with the existing literature indicating that patients with MPM often present with thinner subsequent melanomas and require long-term dermatologic follow-up. The inclusion of genetic testing and phenotypic risk factors enables stratified surveillance and supports the application of personalized medicine in melanoma management.

Background: Psoriasis is a chronic inflammatory skin disease linked to systemic comorbidities, including metabolic, cardiovascular, and autoimmune disorders. Thyroid dysfunction, particularly hypothyroidism, has been observed in patients with moderate-to-severe psoriasis, suggesting possible shared inflammatory pathways. Objectives: This study aims to explore the relationship between psoriasis and thyroid dysfunction in adults with moderate-to-severe psoriasis undergoing biologic therapy to determine whether psoriasis predisposes individuals to thyroid disorders and to identify demographic or clinical factors influencing this association. Materials and Methods: A cross-sectional study included adult patients with moderate-to-severe psoriasis receiving biologic therapy, recruited from the Psoriasis Unit at the Dermatology Department of Hospital Universitario San Cecilio in Granada, Spain, from 2017 to 2023. Patients with mild psoriasis or those treated with conventional systemic therapies were excluded. The data collected included demographics and clinical characteristics, such as age, sex, BMI (body mass index), and psoriasis severity (psoriasis severity was evaluated using the Psoriasis Area Severity Index (PASI), body surface area (BSA) involvement, Investigator’s Global Assessment (IGA), pruritus severity using the Numerical Rating Scale (NRS), and impact on quality of life through the Dermatology Life Quality Index (DLQI)). Thyroid dysfunction, including hypothyroidism and subclinical hypothyroidism, was assessed based on records from the Endocrinology Department. Results: Thyroid dysfunction was found in 4.2% of patients, all classified as hypothyroidism, primarily subclinical. The affected patients were generally older, with a mean age of 57.4 years. No significant differences in psoriasis severity (PASI, BSA) or treatment response were observed between patients with and without thyroid dysfunction. Conclusion: Our findings suggest hypothyroidism is the main thyroid dysfunction in psoriatic patients, independent of psoriasis severity. The lack of impact on psoriasis severity suggests hypothyroidism may be an independent comorbidity, warranting further research into shared inflammatory mechanisms.