{"title":"Editor’s Picks October 2025","authors":"","doi":"10.1111/jdv.70004","DOIUrl":"10.1111/jdv.70004","url":null,"abstract":"<p></p><p>Emek Kocatürk</p><p>Tan et al. reviewed the environmental and health impacts of plastics, focusing on microplastics in dermatological products, which are essentially indestructible and difficult to remove from ecosystems. Their use — especially single-use items — continues to drive fossil fuel extraction and chemical exposure. Plastics and microplastics also pose significant environmental and health risks due to their persistent and pervasive nature.</p><p>This article highlights the plastic lifecycle, exposure routes, associated health risks and provides helpful recommendations based on guidelines from professional societies and health organizations, aiming to reduce plastic's environmental impact in dermatology (Figure 1).</p><p>Tan E, Saha S, Niebel D. Plastics in dermatology: A review and solutions. <i>J Eur Acad Dermatol Venereol</i> 2025; <b>39</b>: 1715–1724. https://doi.org/10.1111/jdv.20537.</p><p>This meta-analysis investigates the risk of heart failure (HF) associated with tumour necrosis factor inhibitors (TNFis) in patients with immune-mediated inflammatory diseases (IMIDs), addressing current guidelines that often contraindicate TNFi use in advanced HF and highlight potential risks for new-onset HF.</p><p>The meta-analysis did not show increased risk of de novo HF in TNFi-treated groups compared to controls. While TNFis are safe concerning the risk of new-onset HF in IMID patients and guidelines should be revised accordingly, more data are needed on their effect on worsening HF (Figure 2).</p><p>Galajda NÁ, Meznerics FA, Mátrai P, et al. Evaluation of the risk of heart failure with tumour necrosis factor inhibitors: A large-scale meta-analysis in immune-mediated inflammatory diseases. <i>J Eur Acad Dermatol Venereol</i> 2025; <b>39</b>: 1760–1772. https://doi.org/10.1111/jdv.20786.</p><p>This study aimed to characterize the prevalence, treatment patterns, disease profile and negative burden of chronic spontaneous urticaria (CSU) in adult patients from five European countries (Figure 3).</p><p>According to the study, CSU patients are inadequately treated, with nearly three-fourths suffering from poorly controlled urticaria, even among those receiving treatment. Moreover, CSU negatively impacts patients' lives, with reported worse mean scores for mental and physical health compared to the control population. The study highlights the multifaceted burden of CSU on patients' lives in real-world settings and the need for comprehensive and personalized care.</p><p>Balp MM, Krupsky K, Gupta S, et al. Prevalence, treatment and burden of chronic spontaneous urticaria in five European countries. <i>J Eur Acad Dermatol Venereol</i> 2025; <b>39</b>: 1806–1817. https://doi.org/ 0.1111/jdv.20772.</p><p>Tanasov et al. highlight several key conclusions regarding the association between dermatologic and venereological conditions and erectile dysfunction (ED), a common yet underdiagnosed condition, emphasizing the importance of a holistic ap","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 10","pages":"1701-1702"},"PeriodicalIF":8.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Scratching the surface: NK-1 inhibitors for chronic itch—Promise or placebo?","authors":"Gil Yosipovitch","doi":"10.1111/jdv.20859","DOIUrl":"10.1111/jdv.20859","url":null,"abstract":"<p>Chronic pruritus (CP) remains a significant therapeutic challenge across dermatologic and systemic diseases. The neuropeptide substance P and its receptor, neurokinin-1 receptor (NK1R), have emerged as pivotal mediators in the pathogenesis of itch.<span><sup>1</sup></span> The meta-analysis by Ho et al.<span><sup>2</sup></span> provides a timely and comprehensive synthesis of the current clinical evidence supporting the efficacy of systemic NK1R antagonists—particularly serlopitant and aprepitant—in alleviating CP. The authors conducted a rigorous literature review spanning multiple databases and clinical trial registries. Their final analysis incorporated 20 studies (13 RCTs, 2 non-RCTs, and 5 grey literature reports) with a total of 2876 patients. This broad inclusion enhances the generalizability of the findings and reflects the real-world application of NK1R-targeting therapies. However, the pooled analysis revealed a modest albeit statistically significant reduction in pruritus scores with systemic NK1R antagonists compared to placebo (SMD: −0.44; <i>p</i> = 0.002). Importantly, the odds of achieving a clinically meaningful 4-point improvement in itch severity were higher in the treatment 33.9% of patients meeting this threshold, compared to 24.7% in the placebo arm. These results are significantly less impressive than those of other anti-pruritic drugs that are not biologics or JAK inhibitors, where we expect higher itch reductions. For example, Kappa opioid difelikefalin, approved in the United States and Europe, achieved a 4-point NRS reduction in studies ranging from 42% to 64%.<span><sup>3, 4</sup></span></p><p>Subgroup analyses offer important insights for clinical practice. Notably, serlopitant and aprepitant demonstrated superior antipruritic effects compared to placebo, with aprepitant exhibiting a larger effect size (SMD: −1.55). However, the wide confidence interval suggests considerable variability and potential heterogeneity in the studies examining aprepitant. Interestingly, although initially the use of aprepitant was recommended for malignancy-associated pruritus, the analysis found greater efficacy in nonmalignant dermatologic inflammatory conditions. These findings echo the pathophysiological understanding that substance P, released from sensory neurons, contributes to neurogenic inflammation and directly activates mast cells and keratinocytes—both of which are key contributors to itch propagation in the skin. Blocking NK1R, antagonists may disrupt this cascade and provide symptom relief.</p><p>Although the authors suggest that NK-1 inhibitors are effective, the overall effect sizes, while statistically significant, are modest. This may reflect heterogeneity in study populations, treatment durations, and disease etiologies. Second, the inclusion of grey literature—while helpful in reducing publication bias—introduces variability in study quality. Additionally, the duration of treatment and sustainability of antipruritic ","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 10","pages":"1703-1704"},"PeriodicalIF":8.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20859","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prurigo nodularis is a Th-2-mediated immune disease","authors":"Adam Reich, Artur Kuboszek","doi":"10.1111/jdv.70010","DOIUrl":"https://doi.org/10.1111/jdv.70010","url":null,"abstract":"<p>Prurigo nodularis (PN), being a subtype of chronic prurigo, is defined as a chronic skin disorder characterized by the presence of highly pruritic, hyperkeratotic nodules that occur due to neuronal sensitization to itch and the development of an itch-scratch-itch cycle.<span><sup>1</sup></span> The pathogenesis of PN remains unclear, but the involvement of T-helper (Th) 1, Th2, Th17 and Th22 pathways has been implicated.<span><sup>2, 3</sup></span> Data from clinical trials on the efficacy of biological drugs blocking interleukin (IL) 4, IL-13 and IL-31,<span><sup>4</sup></span> that is, cytokines associated with the Th2 axis, strengthens the role of Th2-related inflammation as a key factor in evoking itch, pruriginous skin lesions and maintaining the vicious itch-scratch cycle.</p><p>To further elaborate the role of Th2-related cytokines in the pathogenesis of PN, Ständer et al.<span><sup>5</sup></span> conducted a longitudinal, observational study across multiple international centres to provide an in-depth analysis of gene expression profiles of PN patients in relation to histological features and clinical parameters. The core scientific advance of this study is the subdivision of PN into two Th2-skewed immune signature groups.</p><p>The study identifies elevated expression of IL-31, IL-31 receptor A (IL-31RA), oncostatin M (OSM) and OSMRß in lesional PN skin compared to non-lesional and healthy controls, both at the mRNA and protein levels. Importantly, two Th2 subclusters were revealed: cluster 1 contained <i>IL4R, CCL17, CCL22</i> and was associated with barrier-related and regulatory genes (e.g. FOXP3, LOR), while cluster 2 contained <i>IL13, IL10</i> and <i>CCL18</i>, associated with markers of general inflammation and Th17/Th22 pathways.<span><sup>5</sup></span> This bifurcation suggests distinct immunopathogenic mechanisms within PN and could help tailor biologic therapies to each immune signature group. The study by Stander et al.<span><sup>5</sup></span> reinforces the role of the IL-31/OSM axis as key mediators of pruritus in PN. While the correlation between IL-31 expression and itch severity was modest, the finding is still important. It points to a complex regulatory role for IL-31, not limited to direct pruritogenic activity but possibly involving neuronal sensitization and neuroinflammation. The authors propose that OSM, derived not only from T cells but also monocytes (a novel observation), contributes to both neuroimmune signalling and dermal remodelling. The distinction between the two Th2 immune signatures has immediate translational potential. Therapies targeting IL-4/IL-13 (e.g. dupilumab) or IL-31 (e.g. nemolizumab) may benefit different patient subsets.</p><p>Interestingly, Parthasarathy et al.<span><sup>3</sup></span> also found that PN is not a uniform disease but is comprised of distinct immunologic endotypes, with practical implications for precision medicine in the era of targeted biologics. They further supporte","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 10","pages":"1705-1706"},"PeriodicalIF":8.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.70010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"MAPK activity as a surrogate of acral melanoma immunogenicity?","authors":"Rastine Merat","doi":"10.1111/jdv.20878","DOIUrl":"10.1111/jdv.20878","url":null,"abstract":"<p>While acral melanoma, and particularly its dominant histological subtype, acral lentiginous melanoma (ALM), represents only a minor subset of melanomas in Caucasian populations, it is arguably the most universally occurring form of melanoma, affecting individuals regardless of skin phototype. Interestingly, and contrary to intuitive assumptions, the biological divergence observed in acral melanoma and more specifically in ALM, characterized by a distinct genomic trajectory,<span><sup>1</sup></span> including delayed MAPK pathway dependence<span><sup>2</sup></span> and an immunosuppressive tumour microenvironment,<span><sup>3</sup></span> may also extend, at least in part, to other histological subtypes arising at acral sites, particularly the nodular subtype.</p><p>This possibility of an atypical, delayed MAPK activation pattern, in contrast to the canonical evolutionary trajectory of non-acral melanomas, compels us to adopt a more nuanced framework for understanding acral and other non-UV-driven melanomas. Such a framework should move beyond the traditional dichotomy of <i>BRAFV600</i>-mutant versus non-mutant melanomas and instead evaluate MAPK pathway activity itself as a potential biological surrogate for tumour immunogenicity.</p><p>As an initial step towards this more refined stratification of acral melanoma, spatial transcriptomic technologies applied to a limited number of samples offer a valuable starting point. This approach can help determine whether, within a spatially heterogeneous tumour microenvironment, MAPK activity in malignant cells correlates with a specific immune infiltration profile. In the context of acral melanoma, such findings would be consistent with observations previously described in melanoma more broadly, where MAPK pathway activation has been associated with an immunosuppressive tumour microenvironment.<span><sup>4</sup></span></p><p>This is precisely one of the key focuses of the study by Yang et al.,<span><sup>5</sup></span> reported in this issue of <i>JEADV</i>. Spatial transcriptomic analysis was performed on a selected number of samples extracted from a larger cohort of acral melanoma patients to assess the immune landscape in relation to <i>BRAF</i> expression levels. The authors used transcriptomic profiling to analyse both the CD3-positive lymphocytic microenvironment and the gene expression profiles of malignant melanocytes, stratified by <i>BRAF</i> expression level. Their findings indicate that, in acral melanomas, high <i>BRAF</i> expression is associated with an immunosuppressive microenvironment. In the ‘BRAF-high group’, this was evident at the cellular level through neutrophil enrichment identified by cell-type deconvolution and a reduced presence of activated natural killer cells, specifically revealed using the CIBERSORT algorithm. At the transcriptomic level, this was further supported by the downregulation, among others, of pathways related to antigen presentation.</p><p>Assuming, mainly ba","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 10","pages":"1713-1714"},"PeriodicalIF":8.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20878","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"When TNF-α becomes a matter of the heart","authors":"Wolf-Henning Boehncke","doi":"10.1111/jdv.20866","DOIUrl":"10.1111/jdv.20866","url":null,"abstract":"<p>Physicians across several specialties are aware of guidelines recommending avoidance of TNF-α inhibitors (TNF-i) when treating patients for immune-mediated inflammatory diseases (IMIDs) who also suffer from advanced heart failure (HF). This is primarily based on an FDA report on early post-marketing surveillance data<span><sup>1</sup></span> and clinical trials failing to show a clinical benefit in HF.<span><sup>2</sup></span> Remarkably, the meta-analysis by Galajda et al. published in this issue of the JEADV indicates that TNF-i-treated IMID patients neither have an increased risk for developing de novo HF, nor a statistically significant risk enhancement for worsening HF.<span><sup>3</sup></span></p><p>The evidence generated by Galajda et al. is strong: Methodologically solid, they distinguish between worsening and de novo HF, considering randomized trials as well as non-randomized observational studies. Of note, another meta-analysis showed even a (statistically non-significant) risk-reducing effect of TNF-i therapy.<span><sup>4</sup></span> It is confusing that companies invested heavily to study TNF-i for the treatment of HF only to learn from the FDA that this may be harmful, which in the end may not be the case.</p><p>A closer look at what is generally accepted regarding the role of TNF-α in HF helps to better understand the discussion<span><sup>5</sup></span>: HF is a condition in which the heart either cannot pump enough blood or can do so only at the cost of increased filling pressures. It is triggered by a wide range of pathophysiologic changes, including infarction, pressure or volume overload, or metabolic dysregulation. Regardless of the underlying aetiology, inflammatory signalling cascades are activated which promote dysfunction and progressive remodelling of the myocardium. The best-studied cytokine in this context is TNF-α. Increased myocardial expression of TNF-α has been consistently documented in experimental models and in patients, with several lines of evidence pointing towards a causative role. TNF-α-mediated adverse remodelling and HF progression may involve effects on cardiomyocytes, macrophages, the extracellular matrix and endothelial cells; but it may also exert protective actions on injured or stressed cardiomyocytes (Table 1). It has been suggested that deleterious and beneficial effects may be mediated through distinct receptors (TNFR1 and TNFR2, respectively).</p><p>Taken together, TNF-α has both negative and protective effects in HF. Besides, the trials studying etanercept for HF were stopped prematurely due to lack of clinical benefit, which is not the same as adverse events (although an infliximab trial showed increased HF hospitalizations). Finally, the above-mentioned FDA report is based on relatively weak evidence. It is therefore not too surprising that two meta-analyses do not support the guideline recommendations. The latter, however, refer to patients with ‘advanced’ HF only, in whom TNF-i may well b","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 10","pages":"1707-1708"},"PeriodicalIF":8.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The burden of chronic spontaneous urticaria in Europe: Call for action","authors":"Emek Kocatürk, Simon Francis Thomsen","doi":"10.1111/jdv.20893","DOIUrl":"10.1111/jdv.20893","url":null,"abstract":"<p>Chronic spontaneous urticaria (CSU) is a highly burdensome inflammatory condition that manifests with sudden onset of itch, wheals and angioedema, which causes patients to feel a loss of control and suffer from emotional distress, including anxiety, embarrassment and self-consciousness.<span><sup>1</sup></span> These symptoms significantly impair sleep, sexual function, social life and performance in school or work, and are commonly accompanied by psychiatric comorbidities such as depression and anxiety.<span><sup>2</sup></span> Despite the high burden and the need for comprehensive care including effective treatment and regular follow-up, many patients remain undertreated—for instance, a study from Germany found that 60% of CU patients were not receiving any treatment.<span><sup>3</sup></span></p><p>In their recent paper, Balp et al.<span><sup>4</sup></span> delve into the investigation of the prevalence, treatment approaches and overall impact of CSU in five European countries, including France, Germany, the UK, Italy and Spain. The prevalence of diagnosed CSU was 0.92%, varying by country—from the lowest in France to the highest in Italy—with a mean age of 42.4 years and 58% female predominance. The primary diagnosis was most frequently made by a primary care physician (35%), a dermatologist (35%) and an allergologist (27%). Interestingly, more than half of the patients did not report receiving any treatment for their CSU, and more than 70% reported poorly controlled urticaria even when they received treatment. The frequency of biologic treatment was <1%. This study also highlighted the significant impairment in health-related quality of life (HRQoL) among patients, as evidenced by markedly reduced scores on different HRQoL scales, with particularly severe impacts observed in the UK. Patients showed significantly higher rates of anxiety, depression and work productivity impairment compared to the general population, with consistent findings across all countries studied. The burden was most pronounced in the UK, where CSU patients reported the highest levels of anxiety, depression, absenteeism, presenteeism and overall activity impairment. Furthermore, CSU patients utilized significantly more healthcare resources than the general population—including higher rates of emergency room visits, hospitalizations and more frequent consultations with healthcare providers—particularly specialists such as dermatologists and allergists.</p><p>The study reinforces the profound psychosocial toll of CSU, including anxiety, depression and work impairment, underscoring the need for integrated care models that address both physical and mental health. The particularly severe burden observed in the UK raises questions about country-specific healthcare system differences, patient access to care or socio-cultural factors influencing disease perception and management outcomes.</p><p>These findings highlight a major gap between high disease burden and under-trea","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 10","pages":"1711-1712"},"PeriodicalIF":8.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20893","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Moles and melanomas on tattoos: Where we are in 2025","authors":"Nicolas Kluger","doi":"10.1111/jdv.20820","DOIUrl":"https://doi.org/10.1111/jdv.20820","url":null,"abstract":"<p>The recent letter by Kruczek et al. published in the Journal about melanomas on tattoos<span><sup>1</sup></span> brings further comments regarding the current state of knowledge on that specific topic.</p><p>First, the occurrence of a melanoma within a tattoo is still considered as a fortuitous event. The low number of case reports compared to the millions of tattooed individuals worldwide, the lack of cases of multiple melanomas arising within one tattoo and a mouse model showing that UV-induced skin cancers develop outside of black tattoos<span><sup>2</sup></span> are currently arguments against a direct link. It is important to remind that currently the sun exposure and sun protection habits of tattooed individuals have been rarely evaluated and disserve further large studies.<span><sup>3</sup></span></p><p>Individuals with risks factors for melanoma such as personal or familial history of melanoma, numerous moles, atypical mole syndromes etc. should have a proper mapping of preexisting moles before tattooing and discuss which location may suit best according to mole density. The EADV Tattoo and body art task force has published a patient leaflet on that topic and is accessible on the EADV website. However, only 20% of melanomas on tattoos arise from preexisting moles.<span><sup>4</sup></span></p><p>The challenges of moles and other pigmented lesions surveillance within tattoos are well known. A tattooed individual may not notice the arising of a new mole within a tattoo or neglect subtle clinical changes of a pigmented lesion. Dermatoscopy may be more difficult due to tattoo pigments deposition in the dermis, but it is far from being impossible (Figure 1). Kruczek et al. suggested the use of new tools such as reflectance confocal microscopy.<span><sup>1</sup></span> The cost benefits for the patient and the health care system compared to (unnecessary) excisions should be evaluated by clinical studies. Regular follow-up with clinical and dermatoscopy pictures followed by surgical excision whenever it appears necessary is the simplest course of action. Follow-up with medical skin imaging systems can be handy, nevertheless, the performance of artificial intelligence devices and apps when it comes to analysing pigmented lesions on tattoos has not been evaluated to my knowledge. Untrained AI apps that are available on the market for the public may ‘choose’ the worse diagnostic in doubt raising unnecessary stress for the app user. Scarring and distortion of the tattoo after excision remain secondary when it comes to suspicion of malignancy. A skilled dermatologic surgeon will try to conceal the surgical scar with the tattoo design if possible. However, a tattooed patient will understand the necessity of sacrificing the tattoo in this context.</p><p>Virtually any tattooed individual does have tattoo pigments in the draining lymph node of their tattoos. If macroscopically a tattooed ‘black’ lymph node appears greyish, the pathologist will distingu","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 9","pages":"1535-1536"},"PeriodicalIF":8.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20820","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sodium intake: An emerging dietary target in psoriasis","authors":"Stephen Chu-Sung Hu, Hung-Pin Tu, Jason Shourick","doi":"10.1111/jdv.20834","DOIUrl":"https://doi.org/10.1111/jdv.20834","url":null,"abstract":"<p>Psoriasis is a chronic immune-mediated skin disease primarily driven by overactivation of the Th17 immune pathway. Emerging evidence indicates that dietary factors may influence the development and exacerbation of psoriasis. Limited studies have suggested that a low-calorie, low-fat diet, along with dietary supplementation with omega-3 polyunsaturated fatty acids and vitamin D, may improve the severity of psoriasis. Additionally, reduced alcohol consumption and a gluten-free diet may be beneficial in selected patients.<span><sup>1</sup></span></p><p>Dietary sodium intake is a recognized risk factor for cardiometabolic disorders, including hypertension, ischaemic heart disease and chronic renal disease. It is also known that sodium from the diet can be stored in the skin. Previous studies have demonstrated increased sodium concentrations in the skin lesions of patients with atopic dermatitis.<span><sup>2</sup></span> More recently, noninvasive sodium-23 magnetic resonance imaging has shown elevated skin sodium content in patients with psoriasis (PASI >5) compared to healthy controls.<span><sup>3</sup></span> Prior research suggests that high sodium concentrations may contribute to immune dysregulation by activating the Th17 immune pathway, offering a potential mechanism for the role of sodium in psoriasis pathogenesis.<span><sup>4</sup></span> However, the association between dietary sodium intake and psoriasis has rarely been explored in epidemiological studies at the population level.</p><p>In this issue of the journal, Chattopadhyay et al. performed a cross-sectional, population-based epidemiological study using data from the UK Biobank and the US National Health and Nutrition Examination Survey (NHANES), and found that higher dietary sodium intake was associated with an increased risk of psoriasis.<span><sup>5</sup></span> The primary analysis was performed using the UK Biobank database, which included 468,913 participants with and without psoriasis. Dietary sodium intake was assessed by measuring spot urine sodium concentration, and 24-h urinary sodium was estimated using the INTERSALT equation. The results showed that each 1 g increase in estimated 24-h urinary sodium was associated with an 18% higher risk of psoriasis. These findings were further validated using the NHANES database, which included 2393 participants with and without psoriasis, and also demonstrated a significant positive association between dietary sodium intake (assessed via self-report) and psoriasis risk.</p><p>This study provides valuable insights into the role of dietary factors in the development of psoriasis. By utilizing two separate population-based databases from different countries (the United Kingdom and the United States), it offers strong epidemiological evidence for an association between dietary sodium intake and psoriasis. Moreover, the study complements and supports previous smaller-scale investigations that demonstrated increased skin sodium content ","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 9","pages":"1529-1530"},"PeriodicalIF":8.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20834","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Bridging the gap: Treatment of atopic dermatitis with dupilumab during pregnancy","authors":"Christian Vestergaard, Mette Deleuran","doi":"10.1111/jdv.20832","DOIUrl":"https://doi.org/10.1111/jdv.20832","url":null,"abstract":"<p>In this issue of the <i>JEADV</i>, two papers address a previously unmet need—providing evidence for the use of dupilumab in the treatment of atopic dermatitis (AD) during pregnancy.</p><p>Atopic dermatitis affects individuals of all ages and sexes and persists into adulthood in approximately 5–10% of cases. These cases often require active treatment in women of childbearing potential and during pregnancy.<span><sup>1</sup></span> However, women with moderate to severe AD—or with other conditions requiring systemic treatment—have frequently been left in a therapeutic limbo. Due to limited safety data, physicians often advise stopping systemic treatment before and during pregnancy to avoid any risk to the fetus.</p><p>In 2019, the European Task Force on Atopic Dermatitis published a position statement on treating conceiving, pregnant and lactating women with AD.<span><sup>2</sup></span> At that time, there was a significant lack of evidence regarding both topical and systemic treatments during pregnancy. Most recommendations for systemic immunosuppressants were extrapolated from data on other patient populations, particularly organ transplant recipients and women with connective tissue diseases. Notably, there was no available evidence on the safety of dupilumab use in pregnant AD patients. Since then, several Delphi exercises have attempted to refine these guidelines, though consensus has generally been limited to treatments already in use—most notably, cyclosporine.<span><sup>3</sup></span></p><p>In the first paper, Preuss et al.<span><sup>4</sup></span> utilize the US-based collaborative network TriNetX, which provides real-time access to up to 110 million electronic health records.<span><sup>4</sup></span> From this vast dataset, they identified 293 women who had been exposed to dupilumab during pregnancy. Remarkably, the study found no increased risk of adverse pregnancy outcomes. In fact, the data suggested a reduced risk of preterm labour among dupilumab-exposed women.</p><p>The second paper, by S. Gregoriou et al.<span><sup>5</sup></span> presents a systematic review of published case reports involving dupilumab use during pregnancy.<span><sup>5</sup></span> The authors identified 14 publications, encompassing 61 pregnancies and 2 cases of breastfeeding. While 28 of the women discontinued dupilumab upon learning they were pregnant, fetal exposure had already occurred during some of the most critical periods of gestation. Even so, the study reported no adverse pregnancy outcomes among the cases reviewed.</p><p>Together, these two studies offer reassuring evidence for dermatologists managing moderate to severe AD in pregnant patients. The findings suggest that dupilumab does not increase the risk of adverse pregnancy outcomes and may even offer some benefits. Based on the data presented in this issue of the <i>JEADV</i>, it may be reasonable to consider continuing dupilumab in selected patients with moderate to severe, uncontrolled AD—esp","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 9","pages":"1527-1528"},"PeriodicalIF":8.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20832","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Beyond skin: Integrating the cardiovascular impact of psoriasis therapies into disease management","authors":"Tiago Torres","doi":"10.1111/jdv.20828","DOIUrl":"https://doi.org/10.1111/jdv.20828","url":null,"abstract":"<p>The association between moderate-to-severe psoriasis and increased cardiovascular morbidity and mortality is well established, with chronic systemic inflammation recognized as a central pathogenic mechanism.<span><sup>1</sup></span> Nevertheless, a patient's cardiovascular risk and the impact of psoriasis therapies on cardiovascular outcomes have not yet been fully integrated into the therapeutic algorithms that guide the selection of systemic treatments for psoriasis. In this context, the prospective, registry-based study by Lluch-Galcerá et al. offers clinically meaningful data and raises important considerations for future treatment recommendations and clinical decision-making.<span><sup>2</sup></span></p><p>Drawing on more than 21,000 person-years of follow-up from 5622 patients across 11,368 treatment cycles from the BIOBADADERM registry—a well-established Spanish prospective multicentre cohort of patients with psoriasis treated with systemic therapies in routine clinical practice—the authors report differential incidence rates of major adverse cardiovascular events (MACE) across therapeutic classes. Notably, apremilast and IL-17 inhibitors were associated with a statistically significant lower risk of MACE compared to methotrexate, whereas cyclosporine was linked to an increased risk. Other therapeutic classes, including IL-12/23, IL-23 and TNF inhibitors, showed no significant difference versus methotrexate in adjusted models.</p><p>These findings merit attention on several levels. First, they provide real-world evidence (RWE) in a therapeutic area where data on the cardiovascular impact of psoriasis therapies remain scarce and are largely extrapolated from other immune-mediated inflammatory diseases.<span><sup>3</sup></span> Moreover, randomized controlled trials (RCTs) in psoriasis are often underpowered and lack long-term follow-up, limiting their ability to detect rare events such as MACE. Thus, the present data fill a critical gap by evaluating cardiovascular outcomes in a large, representative cohort of patients with psoriasis treated in routine clinical practice.</p><p>Second, the observed protective association with apremilast and IL-17 inhibitors, although observational, is biologically plausible. Previous mechanistic and clinical studies have reported favourable effects of both drug classes on surrogate markers of cardiovascular risk, including lipid profiles, insulin sensitivity and inflammatory biomarkers. In particular, IL-17A blockade has been shown to attenuate vascular inflammation and endothelial dysfunction,<span><sup>4</sup></span> while apremilast may exert cardioprotective effects via modulation of cAMP-mediated anti-inflammatory pathways.<span><sup>5</sup></span> While causality cannot be inferred, these findings may signal a class effect with potential cardiometabolic relevance, particularly in patients with multiple risk factors.</p><p>Conversely, the increased cardiovascular risk associated with cyclosporine rei","PeriodicalId":17351,"journal":{"name":"Journal of the European Academy of Dermatology and Venereology","volume":"39 9","pages":"1531-1532"},"PeriodicalIF":8.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jdv.20828","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}