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The Role of Fibroblasts in Dystrophic Epidermolysis Bullosa Pathogenesis and Current Treatment Approaches
Pub Date : 2025-02-04 DOI: 10.1016/j.xjidi.2025.100353
Alexander Nyström , Celine Pattaroni , Johannes S. Kern
Dystrophic epidermolysis bullosa (DEB) is a hereditary skin fragility disease characterized by the loss or dysfunction of collagen VII, predisposing patients to dermal–epidermal separation. This disease is highly associated with the development of progressive fibrosis of the skin and other organs and the occurrence of lethal cutaneous squamous cell carcinomas (cSCCs). These are not only caused by chronic wounding but also by collagen VII deficiency, which may directly alter cellular responses. This review focuses on the role of fibroblasts in DEB pathogenesis. In addition to keratinocytes, fibroblasts contribute to collagen VII production. Fibroblasts in injured DEB skin are activated and profibrotic and have a propensity to alter tissue homeostasis. Disease progression in DEB follows the trajectory of cancer injury through inflammation and fibrosis. Fibroblast activation and extracellular matrix remodeling that occur in advancing DEB may be directly linked to the aggressive biological behavior of DEB cSCCs. In contrast, the mechanisms underlying chronic itching and pain in DEB and the potential contribution of fibroblasts to these symptoms are only partially understood. The first therapies for DEB recently received regulatory approval, which is a major milestone toward a cure. However, to successfully treat DEB, systemic therapies to mitigate chronic inflammation and fibrosis are likely required, in addition to local collagen VII replacement.
{"title":"The Role of Fibroblasts in Dystrophic Epidermolysis Bullosa Pathogenesis and Current Treatment Approaches","authors":"Alexander Nyström ,&nbsp;Celine Pattaroni ,&nbsp;Johannes S. Kern","doi":"10.1016/j.xjidi.2025.100353","DOIUrl":"10.1016/j.xjidi.2025.100353","url":null,"abstract":"<div><div>Dystrophic epidermolysis bullosa (DEB) is a hereditary skin fragility disease characterized by the loss or dysfunction of collagen VII, predisposing patients to dermal–epidermal separation. This disease is highly associated with the development of progressive fibrosis of the skin and other organs and the occurrence of lethal cutaneous squamous cell carcinomas (cSCCs). These are not only caused by chronic wounding but also by collagen VII deficiency, which may directly alter cellular responses. This review focuses on the role of fibroblasts in DEB pathogenesis. In addition to keratinocytes, fibroblasts contribute to collagen VII production. Fibroblasts in injured DEB skin are activated and profibrotic and have a propensity to alter tissue homeostasis. Disease progression in DEB follows the trajectory of cancer injury through inflammation and fibrosis. Fibroblast activation and extracellular matrix remodeling that occur in advancing DEB may be directly linked to the aggressive biological behavior of DEB cSCCs. In contrast, the mechanisms underlying chronic itching and pain in DEB and the potential contribution of fibroblasts to these symptoms are only partially understood. The first therapies for DEB recently received regulatory approval, which is a major milestone toward a cure. However, to successfully treat DEB, systemic therapies to mitigate chronic inflammation and fibrosis are likely required, in addition to local collagen VII replacement.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100353"},"PeriodicalIF":0.0,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Unpacking the Itch Score: A Critical Examination of Routine Itch Measurement in Dermatology Practice
Pub Date : 2025-01-21 DOI: 10.1016/j.xjidi.2025.100351
Serene Majid , Steven R. Feldman
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引用次数: 0
Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity
Pub Date : 2025-01-21 DOI: 10.1016/j.xjidi.2025.100350
Nicole Vecin , Nathan C. Balukoff , Marita Yaghi , Tammy Gonzalez , Andrew P. Sawaya , Natasa Strbo , Marjana Tomic-Canic , Hadar Lev-Tov , Irena Pastar
Hidradenitis suppurativa tunnel structures lined with epithelium within the dermis are unique features of advanced disease stages that significantly impair patients’ QOL. The presence of hidradenitis suppurativa tunnels is associated with a decreased likelihood of achieving a clinical response, even when receiving biological therapy. The cellular and molecular mechanisms underlying tunnel formation and pathology are only partially understood, which hampers the development of more effective targeted therapies. Tunnels create a unique microenvironment that drives a vicious cycle of hidradenitis suppurativa inflammation, with tunnel keratinocytes exhibiting an activated phenotype characterized by distinct gene expression signatures. In this review, we summarize the current literature and discuss aspects of the pathophysiology of tunnels, including the role of hair follicle epidermal stem cells in tunnel formation, potential role of fibroblast-mediated epithelial–mesenchymal transition, role of dermal papilla fibroblasts, and aberrant proinflammatory repair response contributing to the observed fibrosis and scarring. Finally, tunnel structures are characterized by unique microbial dysbiosis and an overabundance of Gram-negative anaerobes that are not targeted by current therapeutics. In addition to outlining the possible mechanisms of tunnel formation, we provide perspectives on the translation of current knowledge into more effective treatment approaches for patients with hidradenitis suppurativa tunnels.
{"title":"Hidradenitis Suppurativa Tunnels: Unveiling a Unique Disease Entity","authors":"Nicole Vecin ,&nbsp;Nathan C. Balukoff ,&nbsp;Marita Yaghi ,&nbsp;Tammy Gonzalez ,&nbsp;Andrew P. Sawaya ,&nbsp;Natasa Strbo ,&nbsp;Marjana Tomic-Canic ,&nbsp;Hadar Lev-Tov ,&nbsp;Irena Pastar","doi":"10.1016/j.xjidi.2025.100350","DOIUrl":"10.1016/j.xjidi.2025.100350","url":null,"abstract":"<div><div>Hidradenitis suppurativa tunnel structures lined with epithelium within the dermis are unique features of advanced disease stages that significantly impair patients’ QOL. The presence of hidradenitis suppurativa tunnels is associated with a decreased likelihood of achieving a clinical response, even when receiving biological therapy. The cellular and molecular mechanisms underlying tunnel formation and pathology are only partially understood, which hampers the development of more effective targeted therapies. Tunnels create a unique microenvironment that drives a vicious cycle of hidradenitis suppurativa inflammation, with tunnel keratinocytes exhibiting an activated phenotype characterized by distinct gene expression signatures. In this review, we summarize the current literature and discuss aspects of the pathophysiology of tunnels, including the role of hair follicle epidermal stem cells in tunnel formation, potential role of fibroblast-mediated epithelial–mesenchymal transition, role of dermal papilla fibroblasts, and aberrant proinflammatory repair response contributing to the observed fibrosis and scarring. Finally, tunnel structures are characterized by unique microbial dysbiosis and an overabundance of Gram-negative anaerobes that are not targeted by current therapeutics. In addition to outlining the possible mechanisms of tunnel formation, we provide perspectives on the translation of current knowledge into more effective treatment approaches for patients with hidradenitis suppurativa tunnels.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100350"},"PeriodicalIF":0.0,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Commentary on “Capture of patient itch scores in practice reveals disparate itch impact based upon age, gender and race: A cross-sectional survey analysis.”
Pub Date : 2025-01-21 DOI: 10.1016/j.xjidi.2025.100352
Suephy C. Chen
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引用次数: 0
Detection by Single-Cell RNA Sequencing of Virally Mediated Skin Diseases
Pub Date : 2025-01-11 DOI: 10.1016/j.xjidi.2025.100348
Linda Zhou , Thomas H. Leung
Viruses are well-documented agents of specific skin diseases. However, their role and precise mechanism of action in other skin diseases remain unknown. We describe a single-cell RNA-sequencing–based strategy to interrogate human skin biopsies for viral transcripts, permitting detection of viral infection within a sample, single-cell resolution of virally infected cells and identification of subsequent transcriptomic perturbations. We validate our pipeline with 100% sensitivity and specificity by (i) detecting Merkel cell polyomavirus in Merkel cell carcinoma samples, (ii) detecting specific human papillomavirus strains in known human papillomavirus–positive tumors, and (iii) detecting rubella virus transcripts in patients with known rubella-associated granulomas. We identify infection of known and previously unreported cell types and elucidate viral-mediated transcriptional perturbations. In rubella virus–infected cells, we discover macrophage-specific evolution of the rubella virus E1 capsid protein. Finally, we interrogate skin biopsies from many established nonvirally mediated inflammatory skin diseases and do not find consistent evidence of viral infection in any condition. Combining single-cell RNA-sequencing data with virome detection strategies represents a potentially powerful approach to investigate and elucidate virus-mediated gene regulation in health and disease.
{"title":"Detection by Single-Cell RNA Sequencing of Virally Mediated Skin Diseases","authors":"Linda Zhou ,&nbsp;Thomas H. Leung","doi":"10.1016/j.xjidi.2025.100348","DOIUrl":"10.1016/j.xjidi.2025.100348","url":null,"abstract":"<div><div>Viruses are well-documented agents of specific skin diseases. However, their role and precise mechanism of action in other skin diseases remain unknown. We describe a single-cell RNA-sequencing–based strategy to interrogate human skin biopsies for viral transcripts, permitting detection of viral infection within a sample, single-cell resolution of virally infected cells and identification of subsequent transcriptomic perturbations. We validate our pipeline with 100% sensitivity and specificity by (i) detecting Merkel cell polyomavirus in Merkel cell carcinoma samples, (ii) detecting specific human papillomavirus strains in known human papillomavirus–positive tumors, and (iii) detecting rubella virus transcripts in patients with known rubella-associated granulomas. We identify infection of known and previously unreported cell types and elucidate viral-mediated transcriptional perturbations. In rubella virus–infected cells, we discover macrophage-specific evolution of the rubella virus E1 capsid protein. Finally, we interrogate skin biopsies from many established nonvirally mediated inflammatory skin diseases and do not find consistent evidence of viral infection in any condition. Combining single-cell RNA-sequencing data with virome detection strategies represents a potentially powerful approach to investigate and elucidate virus-mediated gene regulation in health and disease.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100348"},"PeriodicalIF":0.0,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143377720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal with Leishmania braziliensis In Vitro and Affects Pathology In Vivo
Pub Date : 2025-01-08 DOI: 10.1016/j.xjidi.2025.100347
Rodrigo C.O. Sanches , Leonardo G. Vaz , Fabio V. Marinho , Erika S. Guimarães , Edgar M. Carvalho , Lucas P. Carvalho , Sergio C. Oliveira
Cutaneous leishmaniasis, caused by Leishmania braziliensis, still represents a serious health problem in Brazil, especially in the northeast region. Currently, to our knowledge, no report describes the role of hypoxia inducible factor-1α (HIF-1α) during L braziliensis infection. In this study, we demonstrated that the parasite induces HIF-1α expression and stabilization in bone marrow–derived macrophages only when added with exogenous IFN-γ plus lipopolysaccharide. Coherently, we did not find an enrichment in the glycolytic pathway upon bone marrow–derived macrophage infection. Evaluating the impact of HIF-1α absence during macrophage infection in vitro, we observed HIF-1α–knockout cells present at high levels of IL-10, reduced production of nitric oxide, and decreased expression of VEGF-A. As a result, parasite viability improves within HIF-1α–knockout cells. However, in vivo, the absence of myeloid cells expressing HIF-1α had no influence on nitric oxide at tissue levels and in parasite burden. Conversely, lack of HIF-1α significantly affects L braziliensis–induced pathology. Ear lesions induced in myeloid HIF-1α–knockout mice were thicker, presenting higher frequency of macrophages, neutrophils, CD4+, and CD8+ T cells as well as higher levels of IL-12, IL-1β, and IFN-γ, compared with those in wild-type mice. Moreover, draining lymph nodes from myeloid HIF-1α–knockout mice also harbored increased populations of T cells. Our data demonstrate that HIF-1α plays an important role during L braziliensis infection influencing skin pathology in vivo.
{"title":"Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal with Leishmania braziliensis In Vitro and Affects Pathology In Vivo","authors":"Rodrigo C.O. Sanches ,&nbsp;Leonardo G. Vaz ,&nbsp;Fabio V. Marinho ,&nbsp;Erika S. Guimarães ,&nbsp;Edgar M. Carvalho ,&nbsp;Lucas P. Carvalho ,&nbsp;Sergio C. Oliveira","doi":"10.1016/j.xjidi.2025.100347","DOIUrl":"10.1016/j.xjidi.2025.100347","url":null,"abstract":"<div><div>Cutaneous leishmaniasis, caused by <em>Leishmania braziliensis</em>, still represents a serious health problem in Brazil, especially in the northeast region. Currently, to our knowledge, no report describes the role of hypoxia inducible factor-1α (HIF-1α) during <em>L braziliensis</em> infection. In this study, we demonstrated that the parasite induces HIF-1α expression and stabilization in bone marrow–derived macrophages only when added with exogenous IFN-γ plus lipopolysaccharide. Coherently, we did not find an enrichment in the glycolytic pathway upon bone marrow–derived macrophage infection. Evaluating the impact of HIF-1α absence during macrophage infection in vitro, we observed HIF-1α–knockout cells present at high levels of IL-10, reduced production of nitric oxide, and decreased expression of VEGF-A. As a result, parasite viability improves within HIF-1α–knockout cells. However, in vivo, the absence of myeloid cells expressing HIF-1α had no influence on nitric oxide at tissue levels and in parasite burden. Conversely, lack of HIF-1α significantly affects <em>L braziliensis</em>–induced pathology. Ear lesions induced in myeloid HIF-1α–knockout mice were thicker, presenting higher frequency of macrophages, neutrophils, CD4<sup>+</sup>, and CD8<sup>+</sup> T cells as well as higher levels of IL-12, IL-1β, and IFN-γ, compared with those in wild-type mice. Moreover, draining lymph nodes from myeloid HIF-1α–knockout mice also harbored increased populations of T cells. Our data demonstrate that HIF-1α plays an important role during <em>L braziliensis</em> infection influencing skin pathology in vivo.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100347"},"PeriodicalIF":0.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143199481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Transcriptionally Active Human Papillomavirus in Male Genital Lichen Sclerosus, Penile Intraepithelial Neoplasia, and Penile Squamous Cell Carcinoma 转录活性人乳头瘤病毒在男性生殖器地衣硬化、阴茎上皮内瘤变和阴茎鳞状细胞癌中的作用。
Pub Date : 2025-01-01 DOI: 10.1016/j.xjidi.2024.100320
Georgios Kravvas , Boyu Xie , Aiman Haider , Michael Millar , Hussain M Alnajjar , Alex Freeman , Asif Muneer , Christopher B Bunker , Aamir Ahmed
Penile intraepithelial neoplasia (PeIN) and penile squamous cell carcinoma (PeSCC) are both thought to be associated with male genital lichen sclerosus and human papillomavirus (HPV) infection through dichotomous pathways: (i) undifferentiated PeIN and warty/basaloid PeSCC are thought to be HPV related, whereas (ii) differentiated PeIN and usual PeSCC are considered HPV independent. Tissue arrays were constructed from male genital lichen sclerosus, undifferentiated and differentiated PeIN, usual-type PeSCC, and unaffected tissues. Staining for p16 and for high-risk and low-risk HPV subtypes through RNAscope was performed. The expression of HPV RNA and p16 were quantified, and appropriate statistical comparisons were undertaken. High-risk HPV was prevalent in undifferentiated PeIN (77%) and less so in PeSCC (46%) and was exiguous or absent in all other tissues. LR HPV was only observed in 2 tissue cores. Strong p16 staining exhibited 96.15% sensitivity and 100% specificity for high-risk HPV. Transcriptionally active HPV is unlikely to be implicated in male genital lichen sclerosus and differentiated PeIN, although it is clearly important in undifferentiated PeIN. The high prevalence of high-risk HPV in usual PeSCC challenges the existing paradigm. Strong p16 positivity was a reliable surrogate marker for the detection of transcriptionally active high-risk HPV.
阴茎上皮内瘤变(PeIN)和阴茎鳞状细胞癌(PeSCC)都被认为与男性生殖器地衣硬化和人乳头瘤病毒(HPV)感染有关,通过两种途径:(i)未分化的PeIN和疣状/基底样PeSCC被认为与HPV相关,而(ii)分化的PeIN和普通PeSCC被认为与HPV无关。组织阵列由男性生殖器硬化地衣、未分化和分化的PeIN、通常型PeSCC和未受影响的组织构建。通过RNAscope对p16以及高危和低危HPV亚型进行染色。定量HPV RNA和p16的表达,并进行相应的统计比较。高危HPV在未分化的PeIN中普遍存在(77%),在PeSCC中较少(46%),在所有其他组织中罕见或不存在。LR型HPV仅在2个组织核中观察到。强p16染色对高危HPV的敏感性为96.15%,特异性为100%。转录活性HPV不太可能与男性生殖器硬化地衣和分化的PeIN有关,尽管它在未分化的PeIN中明显重要。在通常的PeSCC中,高危HPV的高流行率挑战了现有的范式。强p16阳性是检测转录活性高危HPV的可靠替代标志物。
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引用次数: 0
Efficient Dual Cas9 Nickase Correction of a Prevalent Pathogenic LAMB3 Variant for Junctional Epidermolysis Bullosa
Pub Date : 2024-12-24 DOI: 10.1016/j.xjidi.2024.100343
Alex du Rand , John Hunt , Daniel Verdon , Ben Buttle , P. Rod Dunbar , Diana Purvis , Vaughan Feisst , Hilary Sheppard
Gene editing facilitated by homology-directed repair represents a promising strategy for precisely correcting pathogenic variants underlying monogenic disorders, including the life-threatening skin blistering condition junctional epidermolysis bullosa (JEB). Frequent reports of unintended off-target genotoxicity associated with conventional Cas9 nuclease editing have increasingly led to the adoption of dual-Cas9 nickases (dual-Cas9n) owing to their improved safety profile. However, rates of precise repair obtained with such strategies remain low. In this study, we establish a dual-Cas9n approach targeting LAMB3, using electroporation to deliver Cas9-nickase ribonucleoproteins and modified single-stranded oligodeoxynucleotide repair templates into primary JEB keratinocytes. Targeting a hotspot pathogenic variant (c.1903C>T, p.R635∗), we report perfect correction efficiencies of up to 54% based on standard next-generation sequencing. Using a high-fidelity Cas9 nuclease, we also report perfect repair of up to 74% when using a small-molecule modulator of DNA repair. Dual-Cas9n–corrected JEB keratinocytes demonstrated restored laminin-332 expression and secretion in vitro, leading to improved cellular adhesion and accurate laminin-332 localization in engineered skin equivalents. This protocol represents a significant improvement in precision gene repair using Cas9 nickases for epidermolysis bullosa, with the potential to be applied to a large cohort of patients harboring this prevalent pathogenic variant.
{"title":"Efficient Dual Cas9 Nickase Correction of a Prevalent Pathogenic LAMB3 Variant for Junctional Epidermolysis Bullosa","authors":"Alex du Rand ,&nbsp;John Hunt ,&nbsp;Daniel Verdon ,&nbsp;Ben Buttle ,&nbsp;P. Rod Dunbar ,&nbsp;Diana Purvis ,&nbsp;Vaughan Feisst ,&nbsp;Hilary Sheppard","doi":"10.1016/j.xjidi.2024.100343","DOIUrl":"10.1016/j.xjidi.2024.100343","url":null,"abstract":"<div><div>Gene editing facilitated by homology-directed repair represents a promising strategy for precisely correcting pathogenic variants underlying monogenic disorders, including the life-threatening skin blistering condition junctional epidermolysis bullosa (JEB). Frequent reports of unintended off-target genotoxicity associated with conventional Cas9 nuclease editing have increasingly led to the adoption of dual-Cas9 nickases (dual-Cas9n) owing to their improved safety profile. However, rates of precise repair obtained with such strategies remain low. In this study, we establish a dual-Cas9n approach targeting <em>LAMB3</em>, using electroporation to deliver Cas9-nickase ribonucleoproteins and modified single-stranded oligodeoxynucleotide repair templates into primary JEB keratinocytes. Targeting a hotspot pathogenic variant (c.1903C&gt;T, p.R635∗), we report perfect correction efficiencies of up to 54% based on standard next-generation sequencing. Using a high-fidelity Cas9 nuclease, we also report perfect repair of up to 74% when using a small-molecule modulator of DNA repair. Dual-Cas9n–corrected JEB keratinocytes demonstrated restored laminin-332 expression and secretion <em>in vitro</em>, leading to improved cellular adhesion and accurate laminin-332 localization in engineered skin equivalents. This protocol represents a significant improvement in precision gene repair using Cas9 nickases for epidermolysis bullosa, with the potential to be applied to a large cohort of patients harboring this prevalent pathogenic variant.</div></div>","PeriodicalId":73548,"journal":{"name":"JID innovations : skin science from molecules to population health","volume":"5 3","pages":"Article 100343"},"PeriodicalIF":0.0,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143101038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meeting Report on “The International Congress on Autoimmune Pre-disease (2024)”
Pub Date : 2024-12-18 DOI: 10.1016/j.xjidi.2024.100342
Justus Ohmes , Afsaneh Mehrpouyan , Julia Wimmer-Groß , Abdul Razzaque Ahmed , Kyle T. Amber , Swayanka Biswas , Angela Christiano , Shirin Emtenani , Stephanie Goletz , Jennifer Elisabeth Hundt , Laura Kirchhoff , Khalaf Kridin , Julie Lasselin , Matthias Laudes , Wing Yu Lee , Ralf J. Ludwig , Sripriya Murthy , Sadegh Mousavi , Tamas Nemeth , Mareike Neumann , Sarah Stenger
The International Congress on Autoimmune Pre-Disease was organized by the German Research Foundation–founded Research Training Group “Autoimmune Pre-Disease” and took place at the University of Lübeck, Germany, on September 16–17, 2024. The event featured various talks and posters from young researchers and international experts and emphasized early interventions and prevention in autoimmune diseases with a focus on systemic rheumatic diseases, pemphigus, and pemphigoid diseases.
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引用次数: 0
Capture of Patient Itch Scores in Practice Reveals Disparate Itch Impact on the Basis of Age, Gender, and Race: A Cross-Sectional Survey Analysis
Pub Date : 2024-12-11 DOI: 10.1016/j.xjidi.2024.100338
Yin Li , Robert A. Swerlick

Background

Skin symptom burden, varying with patient populations, may not be readily observed by clinicians, resulting in incomplete appreciation of total skin disease burden.

Objective

The purpose of this study was to define patient itch burdens and associated health-related QOL affecting different patient demographics and to identify potential population health disparities.

Methods

This is a cross-sectional, secondary data analysis of data captured using an automated routine electronic previsit survey completed by patients who visited Emory Healthcare Dermatology clinic between March 2021 and October 2022 (6532 patient visits). Descriptive statistics and ordered logit regression analyses were used to examine the prevalence and intensity of itch and the impacts of itch on QOL.

Results

Overall itch burden increases as age increases; females and African Americans experienced more itch burden than males and other racial groups. Itch places significant symptom, emotional, and functional burdens on patients’ QOL, impacts that are independent of patients’ demographics.

Limitations

The data collected were from a single dermatology practice and may not be reflective of other practices or populations.

Conclusion

Dermatology previsit surveys are feasible in examining the significant pruritus burden, especially for older individuals, females, and African Americans with chronic skin conditions.
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引用次数: 0
期刊
JID innovations : skin science from molecules to population health
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