BACKGROUND:Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease frequently associated with metabolic alterations. Conventional methods of measurement, such as BMI, do not adequately capture these differences in body composition. OBJECTIVES:To assess body composition in HS using bioimpedance analysis, compare findings with psoriasis and healthy controls and explore HS phenotypes based on metabolic and clinical profiles. METHODS:In this cross-sectional study, body composition was measured using the InBody 770. HS severity was assessed using Hurley staging and IHS4. K-means clustering was applied to identify HS subtypes. RESULTS:The study included 109 HS patients, 106 psoriasis patients and 106 healthy controls. HS patients had a significantly higher BMI than psoriasis patients and controls (median 32.3 vs. 28.6 and 27.0 kg/m2; both p < 0.001). Body fat mass was also highest in HS (36.0 kg vs. 26.6 kg and 24.5 kg; p < 0.001), as was visceral fat area (171.8 cm2 vs. 130.6 cm2 and 114.0 cm2; p < 0.01). After multivariable adjustment, HS remained associated with increased adiposity, including higher body fat mass, percentage body fat, visceral fat area and obesity degree compared with both control groups. Lower physical activity was significantly associated with higher IHS4 scores (p = 0.030). Multivariable adjustment showed no significant association between Hurley stage or IHS4 and body composition parameters (p > 0.05). CONCLUSIONS:HS showed a markedly altered body composition, with higher BMI, body fat mass and visceral fat area than both psoriasis patients and healthy controls. These findings support the use of bioelectrical impedance analysis as an additional clinical tool beyond BMI to better characterize metabolic risk in HS.

BackgroundDietary factors have been suggested to influence inflammatory skin diseases; however, their role in the pathogenesis and clinical course of hidradenitis suppurativa (HS) remains insufficiently understood. Increasing evidence suggests that HS is a systemic immunometabolic disease characterized by chronic low-grade inflammation and metabolic comorbidities such as obesity, insulin resistance, and metabolic syndrome. Dietary patterns may therefore influence HS activity through metabolic and inflammatory pathways.ObjectiveTo systematically evaluate available evidence on dietary patterns, nutritional interventions, and micronutrient status in hidradenitis suppurativa and to assess their associations with disease onset, disease severity, and underlying metabolic and inflammatory mechanisms.MethodsA systematic search was conducted in PubMed/Medline for studies published between 1985 and 2026, following PRISMA guidelines. Eligible study types included observational studies, interventional trials, and case-control or cross-sectional studies investigating dietary exposures or nutritional interventions in HS. Reference lists were screened for additional records.ResultsEleven studies met the inclusion criteria. Across observational cohorts, lower adherence to Mediterranean-style dietary patterns, higher glycaemic dietary patterns, and micronutrient deficiencies, particularly vitamin D and zinc, were generally associated with greater HS disease severity. Interventional evidence was limited. A small pilot study reported clinical improvement following a very low-calorie ketogenic diet, and yeast-exclusion diets were associated with symptom improvement in small patient cohorts. Evidence from bariatric surgery cohorts suggested that malabsorptive procedures and persistent micronutrient deficiencies may be associated with worsening HS in some patients. Overall, the available studies suggest potential links between diet and HS through metabolic, inflammatory, and microbiome-related pathways, although the evidence remains limited and heterogeneous.ConclusionCurrent evidence suggests that dietary habits and nutritional status may influence hidradenitis suppurativa through metabolic and inflammatory mechanisms. Although data remain heterogeneous and largely observational, promoting anti-inflammatory dietary patterns, optimizing micronutrient intake, and addressing obesity may offer supportive benefits alongside standard HS therapies. Further controlled studies are needed to establish causality.

Atopic dermatitis (AD) is a chronic, relapsing inflammatory disease, significantly impacting a patient’s quality of life. To date, a substantial proportion of patients present an insufficient response to available treatment options. Lebrikizumab, a monoclonal antibody targeting interleukin 13, has shown a promising clinical benefit in phase 3 trials, however, real-world data on the effectiveness and safety of lebrikizumab for atopic dermatitis (AD) are limited and mostly restricted to Asian populations. Aim of this study was to evaluate the real-world effectiveness and safety of lebrikizumab in patients with AD. This retrospective study included 35 patients from a largely homogenous Central European population with moderate to severe Atopic Dermatitis treated with lebrikizumab at the Dermatology Department of the St. Josef-Hospital in Bochum between December 2023 and April 2025. Eczema area and severity index (EASI), SCORing Atopic Dermatitis (SCORAD), peak-pruritus (PP)-numerical rating scale (NRS) and dermatology life quality index (DLQI) were assessed during the treatment. Lebrikizumab reduced all clinical indices by week 4, with improvements maintained through week 16. At week 24, the achievement rates for EASI-50 (50

Actinic keratosis (AK) is a prevalent, chronic skin condition and a precursor to cutaneous squamous cell carcinoma. Effective, patient-friendly therapies that target both visible and subclinical lesions are essential. Tirbanibulin, a topical microtubule inhibitor, is the latest treatment approved in the USA and European Union (EU) for treating non-hyperkeratotic, non-hypertrophic AK on the face and scalp. This study aimed to assess the overall value of tirbanibulin for treating AK on the face or scalp across Germany, Italy, and Spain and to identify key value drivers using a multi-stakeholder perspective. This study used a multi-criteria decision analysis (MCDA) to assess the holistic value of tirbanibulin compared with 5-fluorouracil 4

BACKGROUND:The anti-PD1 antibody (PD1i) cemiplimab is approved as second-line treatment for locally advanced or metastatic basal cell carcinoma (BCC), resulting in an ORR of 20-30 %. This study aimed to investigate the efficacy of cemiplimab as first-line or second-line treatment of BCC in a German real-world patient cohort. METHODS:Patients with histologically confirmed locally advanced or metastatic BCC who were treated with cemiplimab were retrospectively identified from the prospective multicenter real-world skin cancer registry ADOREG. Study endpoints were overall response rate (ORR), progression-free survival (PFS), and overall survival (OS). Therapy outcome was compared between patients receiving first-line cemiplimab and patients treated with cemiplimab in second-line. RESULTS:37 patients from 17 skin cancer centers were identified who received cemiplimab. The median follow-up after start of any first-line treatment was 37.1 months, and 17.9 months after initiation of any cemiplimab treatment. Patients who received first-line cemiplimab (n = 8) had an ORR of 62.5 %, compared to an ORR of 31.0 % for patients who received second-line cemiplimab (n = 29); Median PFS was 19.8 months for first-line cemiplimab and 5.3 months for second-line cemiplimab. Reinduction with HHIs after progression on second-line cemiplimab resulted in an ORR of 20.0 % and a median PFS of 3.8 months. CONCLUSION:We demonstrate a comparable outcome for cemiplimab as second-line treatment of BCC in our real-world patient cohort as reported in previous registration studies. Additionally, we found a trend for a more favorable outcome in first-line therapy, suggesting a rationale to further investigate cemiplimab as first-line treatment of advanced BCC.

This guideline was developed in close collaboration with multidisciplinary experts from the European Association of Dermato-Oncology (EADO), the European Dermatology Forum (EDF) and the European Organization for Research and Treatment of Cancer (EORTC). Recommendations for the diagnosis and treatment of melanoma were developed on the basis of systematic literature research and consensus conferences. Cutaneous melanoma (CM) is the most dangerous form of skin tumor and accounts for 90% of skin cancer mortality. The diagnosis of melanoma can be made clinically and must always be confirmed by dermoscopy. If melanoma is suspected, a histopathological examination is always required. Sequential digital dermoscopy and whole-body photography can be used in high-risk patients to improve the detection of early-stage melanoma. If available, confocal reflectance microscopy can also improve the clinical diagnosis in special cases. Melanoma is classified according to the 8th version of the American Joint Committee on Cancer classification. For thin melanomas up to a tumor thickness of 0.8 mm, no further diagnostic imaging is required. From stage IB, lymph node sonography is recommended, but no further imaging examinations. From stage IIB/C, whole-body examinations with computed tomography or positron emission tomography CT in combination with magnetic resonance imaging of the brain are recommended. From stage IIB/C and higher, a mutation test is recommended, especially for the BRAF V600 mutation. It is important to perform a structured follow-up to detect relapses and secondary primary melanomas as early as possible. A stage-based follow-up regimen is proposed, which in the experience of the guideline group covers the optimal requirements, although further studies may be considered. This guideline is valid until the end of 2026.

Approximately 30% of patients with hidradenitis suppurativa (HS) report a positive family history of the disease. Currently, there are limited data available on familial HS. To address this gap, we conducted a retrospective analysis at our centre to identify differences between patients with and without a positive family history of HS.

Background: Meta-inflammation is a hallmark of hidradenitis suppurativa (HS). Research on meta-inflammation in HS is growing, but there is still no research on haptoglobin as an inflammatory protein in lesional HS skin. This study examines the relationship between haptoglobin expression in HS skin lesions and clinical parameters. Methods: An examination was performed on 44 skin samples from HS patients and 10 healthy skin samples. Clinical parameters were then compared with haptoglobin expression. Results: Median haptoglobin expression was significantly higher in the Hurley stage III lesions compared with milder stages (H-score: 37.6 versus 17.1, p = 0.028). High haptoglobin expression (≥30.8% positive cells) was associated with advanced disease (Hurley stage III: 80% versus 41.7%, p = 0.01), active smoking (80% versus 50%, p = 0.039), increased pain (visual analogue scale: 5 versus 1.5, p = 0.03), and a higher prevalence of diabetes (35% versus 8.3%, p = 0.029) and hypertension (55% versus 25%, p = 0.042). No significant associations were found with the BMI, disease duration, or CRP levels. Conclusions: High haptoglobin expression (positive cells ≥ 30.8%) in a skin lesion is associated with higher HS severity, active smoking, more pain and the comorbidities of diabetes mellitus and arterial hypertension in HS patients.

BACKGROUND:Haptoglobin (Hp) is an acute-phase protein and an independent marker for hidradenitis suppurativa (HS) severity. The different Hp genotypes (Hp 1-1, Hp 1-2, and Hp 2-2) differ in their antioxidant and anti-inflammatory functions. Hp genotypes have never been investigated in HS patients. OBJECTIVE:Our aim was to characterize and determine the frequency of Hp genotypes in HS patients. Additionally, the characteristics of the different Hp genotypes are analyzed for differences in personal, disease-specific, and laboratory parameters. METHODS:Genomic DNA was extracted from peripheral blood leukocytes using the Maxwell RSC Blood DNA Kit. Polymerase chain reaction (PCR) products were separated and analyzed using 0.7% agarose gels for genotyping. The chi-square test, Kruskal-Wallis test, and/or post hoc analysis with the Dunn-Bonferroni test were used to determine differences between the different genotypes and HS characteristics. We compared the genotype distribution in HS with 69 randomly selected, unmatched, and healthy control patients. RESULTS:A total of 72 patients with HS were included in this study, including 29 women (40.3%) and 43 men (59.7%). A positive family history of HS was reported by 29.2% of patients (n = 21). Hp genotype 1-1 was present in 20.8%, Hp 1-2 in 33.3%, and Hp 2-2 in 45.8% of HS patients. The control group had a similar Hp distribution with 18.8%, 37.7%, and 43.5%, respectively. A positive family history of HS was significantly more frequent in Hp 2-2 (42.4%) compared to Hp 1-1 (6.7%) and Hp 1-2 (25%) (p = 0.035). The number of HS flares in the last 4 weeks was significantly higher in Hp 2-2 patients compared to Hp 1-2 patients (p = 0.006). CONCLUSION:Hp genotype 2-2 and the Hp2 allele were significantly more associated with familial HS than the other genotypes. In addition, HS patients with genotypes 2-2 had more frequent flare-ups than those with the different genotypes.

Background: Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory dermatosis with substantial quality-of-life impact. HS frequently co-exists with obesity and metabolic comorbidities. Cigarette smoking is highly prevalent and has been linked to heightened inflammatory activity and impaired wound healing. The role of cumulative tobacco exposure (packyears) in relation to metabolic comorbidities in HS is less well defined. We therefore investigated whether lifetime pack-years relate to laboratory parameters and the presence of comorbidities in HS. Methods: We conducted a retrospective, single-center study involving 131 patients with HS. We collected clinical data, including disease severity scores and quality of life indices, along with laboratory markers such as complete blood count and C-reactive protein. Smoking status and cumulative exposure (pack-years) were assessed based on patient history. To compare laboratory parameters between smoking subgroups, we used Mann–Whitney U tests. Additionally, we performed logistic regression analyses to evaluate the association between cumulative cigarette exposure and the presence of comorbidities. Results: Among the cohort, 63.4% were active smokers with a median of 15 pack-years. Smokers had significantly higher leukocyte, neutrophil, lymphocyte, monocyte, eosinophil, and basophil counts, indicating elevated systemic inflammation. Hematocrit, hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin were also significantly higher in smokers, while C-reactive protein levels did not differ notably between groups. Subgroup analysis revealed that patients with arterial hypertension, diabetes mellitus, and hypercholesterolemia had significantly more pack-years than those without these conditions. These comorbidities, components of metabolic syndrome, were strongly associated with higher lifetime tobacco exposure in HS patients. Conclusions: Smoking contributes not only to heightened inflammatory activity in HS but is also significantly associated with the presence of metabolic comorbidities. These findings underscore the importance of early interdisciplinary intervention and structured smoking cessation programs to improve outcomes in HS patients.

BACKGROUND:Hidradenitis suppurativa (HS) is a chronic inflammatory disease with a complex immune response. Given the considerable heterogeneity of the clinical phenotype of HS, this study aimed to analyse the immunohistochemical pattern of interstitial inflammation. METHODS:Immunohistochemical analysis was performed on skin samples from 49 patients with HS. The immunohistochemical markers CD3, CD4 and CD8 for T-cells, CD20 for B-cells, CD138 for plasma cells and CD30, CD56, Bcl-2 and Bcl-6 were stained on lesional skin. RESULTS:The analysis of immune cell dominance in patients with HS revealed that 33.3% of the cohort exhibited B-cell dominance, defined as a ratio of the sum of CD20+ and CD138+ cells to CD3+ cells greater than 1, while the majority (66.7%) demonstrated T-cell dominance, defined as a ratio of CD3+ cells to the sum of CD20+ and CD138+ cells greater than 1. B-cell-dominant HS is associated with a significantly elevated probability of mammary involvement (13.3% vs. 0%; p = 0.041). T-cell-dominant HS patients tended to demonstrate a higher mean tobacco consumption, but not significantly (20 vs. 5 tobacco pack-years; p = 0.06). CD4-dominant HS patients exhibited a significantly greater involvement of the mons pubis (62.5% vs. 28.6%, p = 0.023) compared to CD8-dominant patients, who demonstrated a significantly higher number of abscesses (p = 0.027). CONCLUSIONS:For the first time, we describe the clinical and immunohistochemical characteristics of T-cell- and B-cell-dominant HS. Although HS seems to be more dominated by T-cells, a B-cell dominance was found in 33% of cases.

Sehr geehrte Herausgeber, Das bullöse Pemphigoid (BP) gehört zur Gruppe der bullösen Autoimmunerkrankungen. Es ist durch subepidermale Blasenbildung und Autoantikörper gegen hemidesmosomale Proteine gekennzeichnet.1-3 In der Literatur wird das BP mit fortgeschrittenem Alter, neurologischen Erkrankungen, Medikamenten, paraneoplastischen Syndromen, genetischer Prädisposition und ultraviolettem Licht in Verbindung gebracht.4, 5 In einigen Berichten wurde eine Assoziation zwischen BP und bakteriellen Krankheitserregern beobachtet.6 Nach unserem Kenntnisstand stellen wir die ersten beiden Fälle vor, in denen nach der Eradikation von Helicobacter (H.) pylori eine vollständige Remission des BP beobachtet wurde. Eine 83-jährige Patientin stellte sich mit neu aufgetretenen prallen Blasen und starkem Juckreiz am ganzen Körper vor. Die Patientin nahm keine Medikamente ein und es wurden keine Vorerkrankungen angegeben. Die Laboruntersuchungen ergaben Leukozytose, Eosinophilie, erhöhte LDH und erhöhtes CRP. Chronische Infektionserkrankungen (HIV, Hepatitis, Borreliose, Syphilis, Toxoplasmose) wurden ausgeschlossen. Die histologische Untersuchung des entnommenen Gewebes zeigte subepidermale, nicht akantholytische Blasen mit einer Infiltration von eosinophilen Granulozyten. Die direkte Immunfluoreszenz (DIF) zeigte lineare Ablagerungen von C3 an der dermo-epidermalen Junktionszone. Die indirekte Immunfluoreszenz (IIF) mit NaCl-separierter Spalthaut zeigte lineare Antikörperablagerungen im Blasendach. Die IIF-Diagnostik unter Verwendung des BIOCHIPs (Dermatology Mosaic 7, EUROIMMUN, Lübeck, Deutschland) ergab eine Reaktivität für BP180 und BP230. Nach klinisch-pathologischer Korrelation wurde ein bullöses Pemphigoid diagnostiziert. Eine Gastroskopie und eine Koloskopie wurden aufgrund von Sodbrennen und okkultem Blut im Stuhl durchgeführt. Die Gastroskopie ergab eine leichte Refluxösophagitis und eine Atrophie der Magenschleimhaut. In der biopsierten Magenschleimhaut konnte eine aktive H.-pylori-Infektion nachgewiesen und durch einen fäkalen Antigentest bestätigt werden. Die Koloskopie war unauffällig. Zur Behandlung der akuten Exazerbation des BP wurde eine topische Therapie mit Clobetasol (1–2 x täglich) und systemische Therapie mit Prednisolon (anfänglich 1 mg/kg Körpergewicht [KG]) begonnen. Die Tagesdosis von Prednisolon wurde nach der ersten Woche schrittweise um 25 % pro Woche reduziert. Nach Erreichen einer Tagesdosis von weniger als 20 mg wurde die Dosis alle 2 Wochen schrittweise reduziert. Zusätzlich wurde eine H.-pylori-Eradikationstherapie mit Amoxicillin (1000 mg 2 x täglich), Pantoprazol (40 mg 2 x täglich) und Clarithromycin (500 mg 2 x täglich) über 14 Tage eingeleitet. Die Haut verbesserte sich unter dieser Therapie deutlich. Die erfolgreiche Eradikation wurde durch einen negativen HP-Antigentest im Stuhl nach 6 Wochen bestätigt. Eine komplette Remission des BP wurde nach 12 Wochen erreicht. Prednisolon und Clobetasol wurden auf Wunsch der Patientin abgesetzt. Innerhalb von 24 Monaten trat das BP nicht wieder auf. Eine topische oder systemische Behandlung des BP war in diesem Zeitraum nicht erforderlich. Der zweite Fall betraf eine 89-jährige Patientin mit einer Exazerbation eines bereits bekannten BP. In den letzten 6 Jahren traten etwa zwei BP-Schübe pro Jahr auf. Die Diagnose eines BP wurde aufgrund der typischen Hautveränderungen und der Befunde (DIF und IIF) bei der aktuellen Vorstellung erneut bestätigt. An der dermo-epidermalen Junktionszone zeigten sich in der DIF lineare Ablagerungen von IgG und C3. In der IIF wurden lineare Antikörperablagerungen im Blasendach nachgewiesen (Substrat: NaCl-separierte Spalthaut). Mit dem BIOCHIP-Mosaik wurden Anti-BP180- und Anti-BP230-Antikörper im Serum nachgewiesen. Als Vorerkrankungen waren arterielle Hypertonie, Herzinsuffizienz und leichte Demenz bekannt. Laborchemisch lag ebenfalls eine Eosinophilie vor. Die Behandlung des BP mit verschiedenen Medikamenten, darunter Azathioprin, Dapson und Doxycyclin, war bei der Patientin in der Vergangenheit erfolglos. Die Behandlung mit topischen (Clobetasol 1–2 x täglich) und systemischen Glukokortikoiden (Prednisolon in einer Anfangsdosis von 1 mg/kg KG) brachte in der Vergangenheit eine vorübergehende Besserung, so dass wir diese Therapie wieder einleiteten. Ein positiver Stuhltest auf das H.-pylori-Antigen und ein 13C-Harnstoff-Atemtest bestätigten auch in diesem Fall eine aktive H.-pylori-Infektion. Bei der zweiten Patientin wurde H. pylori ebenfalls erfolgreich mit Amoxicillin (1000 mg 2 x täglich), Pantoprazol (40 mg 2 x täglich) und Clarithromycin (500 mg 2 x täglich) über 14 Tage eliminiert. Die Eradikation wurde nach 4 Wochen durch einen negativen Stuhltest auf das H.-pylori-Antigen bestätigt. Im zweiten Fall wurde nach 16 Wochen eine komplette Remission des BP erreicht und Prednisolon abgesetzt. Ab diesem Zeitpunkt sollte Clobetasol nur noch bei neu aufgetretenen Hautveränderungen eingesetzt werden. Eine Nachuntersuchung nach 15 Monaten zeigte eine anhaltende komplette Remission. Eine lokale oder systemische Therapie war während der gesamten Nachbeobachtungszeit nicht erforderlich. Die genaue Pathogenese des BP ist noch nicht vollständig geklärt. In beiden Fällen war das BP nach Beseitigung der H.-pylori-Infektion unter Kontrolle, so dass keine langfristige BP-Behandlung erforderlich war. Dieser zeitliche Zusammenhang deutet darauf hin, dass HP-Infektionen als Provokationsfaktor für das BP diskutiert werden sollten. Chronische H.-pylori-Infektionen sind in der Regel asymptomatisch und bleiben daher lange Zeit unentdeckt. H.-pylori-Antigene können kreuzreaktive T-Zellen aktivieren und die Produktion von Autoantikörpern induzieren.7 Eine ständige Interaktion zwischen bakteriellen Antigenen und dem Immunsystem könnte die autoimmune Verbindung zwischen BP und H. pylori erklären.8 In unseren beiden Fällen könnte die vermutlich schon länger bestehende H.-pylori-Infektion die Bildung von BP180- und BP230-Antikörpern ausgelöst haben, die zu den subepidermalen Blasen in der Haut geführt haben. Jedoch bleibt der genaue Autoimmunmechanismus hypothetisch und sollte weiter untersucht werden. Unsere Annahme wird auch durch die deutlich erhöhte Prävalenz von Antikörpern gegen HBV, HCV, H. pylori, Toxoplasma gondii und CMV bei Patienten mit Pemphigus oder bullösem Pemphigoid unterstützt. Die erhöhten Antikörper könnten auf eine anhaltende Aktivierung des Immunsystems zurückzuführen sein, unabhängig vom bakteriellen oder viralen Erreger. In der Studie von Sagi et al. wiesen Patienten mit bullösen Autoimmunerkrankungen eine höhere Prävalenz von erhöhter IgG-Titer gegen H. pylori auf (90 % vs. 31 %; im Vergleich zu Kontrollpersonen), was auf eine wichtige immunologische Wirkung von H. pylori bei bullösen Autoimmunerkrankungen hindeuten könnte.9 Ein Zusammenhang zwischen H. pylori und bullösen Autoimmundermatosen (BAID) wurde auch für Pemphigus vulgaris und lineare bullöse IgA-Dermatosen beschrieben.10, 11 Diese Daten deuten darauf hin, dass unsere Beobachtung auch für andere BAID von Interesse sein könnte. Mortazavi et al. fanden eine signifikant höhere Prävalenz von erhöhter IgG-Antikörper gegen H. pylori bei unbehandeltem Pemphigus vulgaris im Vergleich zu gesunden Kontrollpersonen (79,3% vs. 59,5%).10 Matsuo et al. berichteten über eine lineare bullöse IgA-Dermatose vom Sublamina-densa-Typ, die nach der Eradikation von HP vollständig verschwand.11 Die möglichen Auswirkungen von Infektionen auf verschiedene bullöse Autoimmunerkrankungen sind uneinheitlich. Eine retrospektive Studie zeigte einen Zusammenhang zwischen BP und Leukozytose.12 Leukozytosen treten am häufigsten im Rahmen von akuten oder chronischen Infektionen auf. Leukozytosen treten im Vergleich zu H.-pylori-negativen Kontrollen bei chronischen H.-pylori-Infektionen signifikant häufiger auf.13, 14 Es lässt sich nicht abschließend beurteilen, ob dieser beobachtete Zusammenhang zwischen Leukozytose, H. pylori und BP in einem kausalen Zusammenhang steht. Die wichtige Rolle der eosinophilen Granulozyten beim BP ist hingegen weitgehend unbestritten.15, 16 Bei unseren beiden Patienten war auch eine Eosinophilie im Gewebe und im Blut nachweisbar. Metaanalysen haben gezeigt, dass die Prävalenz von H.-pylori-Infektionen in Entwicklungsländern am höchsten ist. In Afrika beispielsweise ist die Prävalenz von H.-pylori-Infektionen mit 70,1 % doppelt so hoch wie in Westeuropa.17 Die unterschiedlichen Hygienestandards könnten eine wichtige Ursache für den großen Unterschied sein. In der Literatur konnten wir keine Daten zur erhöhten Prävalenz des BP in Afrika finden. Lu et al. berichteten über eine geringere Prävalenz von BP in Afrika im Vergleich zu Europa, was im Widerspruch zu unserer Hypothese steht.18 Eine mögliche Ursache für diese Diskrepanz könnte in der Unterdiagnose vom BP in Afrika liegen. Die Diskrepanz könnte auch darauf zurückzuführen sein, dass das BP eine multifaktorielle Erkrankung ist und beispielsweise auch andere Umweltfaktoren, Lebensstilfaktoren und genetische Faktoren eine Rolle spielen könnten. Wir gehen davon aus, dass die Dunkelziffer der H.-pylori-Infektionen bei BP höher ist als erwartet. Größere Studien sind erforderlich, um den Zusammenhang zwischen BP und H.-pylori-Infektion zu bestätigen. Zusammenfassend ist der zeitliche Zusammenhang zwischen der Eradikation von H. pylori und der Stabilisierung des BP eine wichtige Beobachtung. In beiden Fällen kam es zu einer Langzeitremission, so dass eine Langzeittherapie des BP nicht erforderlich war. Diese beiden Fälle zeigen, dass HP-Infektionen als Provokationsfaktor für BP diskutiert werden sollten. Open access Veröffentlichung ermöglicht und organisiert durch Projekt DEAL. Keiner.

Background Skin cancer prevention remains a critical public health challenge, particularly in fair-skinned populations in Europe, the United States and Australia, where incidence rates of keratinocyte skin cancer and melanoma continue to rise despite decades of public education on ultraviolet-radiation (UVR) protection. Although progress has been observed in Oceania, the overall effectiveness of current prevention strategies remains insufficient. This paper aims to refine and disseminate more effective UVR protection messages by developing an evidence-based, internationally adaptable public education leaflet.Methods The development of this educational material followed the current guidelines for the development of health promotion materials and effective public education. Based on the scientific evidence, a plain-language message has been drafted. It was subsequently revised through multiple rounds of multi-stakeholder feedback from dermato-oncology, epidemiology, public health experts, patient organizations representatives and NGOs involved in prevention and health promotion.Results The final educational leaflet emphasizes three core messages: avoiding intentional sun exposure and tanning, utilizing shade and protective clothing as primary UV protection strategies and using sunscreen as a supplementary protective measure. Additional recommendations address childhood sun protection, the dangers of tanning beds and the importance of monitoring skin for early signs of cancer. Common concerns such as vitamin D synthesis and sunscreen safety are also addressed with evidence-based responses.Discussion This initiative highlights the necessity of shifting public attitudes towards UVR exposure and developing tailored, culturally sensitive communication strategies. The freely available leaflet will be distributed through professional associations and online platforms. Future efforts should involve policymakers in implementing structural changes, such as enhancing public shade availability and regulating tanning facilities, to promote long-term behavioural shifts in UV protection.