14 results on '"Roenneberg S"'
Search Results
2. Pityriasis rubra pilaris: algorithms for diagnosis and treatment.
- Author
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Roenneberg, S. and Biedermann, T.
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SKIN disease diagnosis , *IMMUNOSUPPRESSIVE agents , *MEDICAL protocols , *PSYCHOLOGICAL stress , *INDIVIDUALIZED medicine - Abstract
Abstract: Pityriasis rubra pilaris (PRP) is a rare inflammatory skin disease that affects men and women of all ages and also children. The clinical appearance of PRP is highly variable, as is the individual prognosis. Therefore, stratifying PRP into six disease subtypes represents a first step to personalized medicine for this rare inflammatory skin disease. The next step should be to associate specific therapeutic strategies with these subtypes of PRP. However, no randomized, controlled trials on the treatment of PRP have been performed. Consequently, the actual treatment algorithm for PRP will be based on clinical experience, small case series and case reports. The majority of published evidence is on type I PRP, whereas the treatment experience for other clinical types of PRP is still sparse and has to be gained. Nevertheless, it is now time to start developing valid algorithms as a basis for the diagnosis and treatment of PRP based on the data available. This review makes use of algorithms developed in psoriasis and atopic eczema and puts together recent insights into the pathogenesis, diagnosis and treatment experience of PRP. The innovative intention of this appraisal is to develop a structured algorithm for PRP treatment that should be further developed going forward. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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3. 360 Interface Dermatitis is characterized by a type I immune response and an epidermal reaction to IFN-γ and TNF-α
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Lauffer, F., Jargosch, M., Krause, L., Garzorz-Stark, N., Franz, R., Roenneberg, S., Biedermann, T., Theis, F., Schmidt-Weber, C., Eyerich, S., and Eyerich, K.
- Published
- 2017
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4. Histology-based classifier to distinguish early mycosis fungoides from atopic dermatitis.
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Roenneberg S, Braun SA, Garzorz-Stark N, Stark SP, Muresan AM, Schmidle P, Biedermann T, Guenova E, and Eyerich K
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- Humans, Epidermis pathology, Dermatitis, Atopic diagnosis, Dermatitis, Atopic pathology, Skin Neoplasms diagnosis, Skin Neoplasms pathology, Mycosis Fungoides diagnosis, Mycosis Fungoides pathology
- Abstract
Background: Histopathological differentiation of early mycosis fungoides (MF) from benign chronic inflammatory dermatoses remains difficult and often impossible, despite the inclusion of all available diagnostic parameters., Objective: To identify the most impactful histological criteria for a predictive diagnostic model to discriminate MF from atopic dermatitis (AD)., Methods: In this multicentre study, two cohorts of patients with either unequivocal AD or MF were evaluated by two independent dermatopathologists. Based on 32 histological attributes, a hypothesis-free prediction model was developed and validated on an independent patient's cohort., Results: A reduced set of two histological features (presence of atypical lymphocytes in either epidermis or dermis) was trained. In an independent validation cohort, this model showed high predictive power (95% sensitivity and 100% specificity) to differentiate MF from AD and robustness against inter-individual investigator differences., Limitations: The study investigated a limited number of cases and the classifier is based on subjectively evaluated histological criteria., Conclusion: Aiming at distinguishing early MF from AD, the proposed binary classifier performed well in an independent cohort and across observers. Combining this histological classifier with immunohistochemical and/or molecular techniques (such as clonality analysis or molecular classifiers) could further promote differentiation of early MF and AD., (© 2023 The Authors. Journal of the European Academy of Dermatology and Venereology published by John Wiley & Sons Ltd on behalf of European Academy of Dermatology and Venereology.)
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- 2023
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5. Gene Expression-Based Molecular Test as Diagnostic Aid for the Differential Diagnosis of Psoriasis and Eczema in Formalin-Fixed and Paraffin-Embedded Tissue, Microbiopsies, and Tape Strips.
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Fischer F, Doll A, Uereyener D, Roenneberg S, Hillig C, Weber L, Hackert V, Meinel M, Farnoud A, Seiringer P, Thomas J, Anand P, Graner L, Schlenker F, Zengerle R, Jonsson P, Jargosch M, Theis FJ, Schmidt-Weber CB, Biedermann T, Howell M, Reich K, Eyerich K, Menden M, Garzorz-Stark N, Lauffer F, and Eyerich S
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- Humans, Formaldehyde, Tissue Fixation methods, Diagnosis, Differential, Paraffin Embedding, Gene Expression, Psoriasis diagnosis, Psoriasis genetics, Psoriasis metabolism, Eczema diagnosis, Eczema genetics
- Abstract
Highly effective targeted therapies are available to treat noncommunicable chronic inflammatory skin diseases. In contrast, the exact diagnosis of noncommunicable chronic inflammatory skin diseases is complicated by its complex pathogenesis and clinical and histological overlap. Particularly, the differential diagnosis of psoriasis and eczema can be challenging in some cases, and molecular diagnostic tools need to be developed to support a gold standard diagnosis. The aim of this work was to develop a real-time PCR-based molecular classifier to distinguish psoriasis from eczema in formalin-fixed and paraffin-embedded-fixed skin samples and to evaluate the use of minimally invasive microbiopsies and tape strips for molecular diagnosis. In this study, we present a formalin-fixed and paraffin-embedded-based molecular classifier that determines the probability for psoriasis with a sensitivity/specificity of 92%/100%, respectively, and an area under the curve of 0.97, delivering comparable results to our previous published RNAprotect-based molecular classifier. The psoriasis probability, as well as levels of NOS2 expression, positively correlated with the disease hallmarks of psoriasis and negatively with eczema hallmarks. Furthermore, minimally invasive tape strips and microbiopsies were effectively used to differentiate psoriasis from eczema. In summary, the molecular classifier offers broad usage in pathology laboratories as well as outpatient settings and can support the differential diagnosis of noncommunicable chronic inflammatory skin diseases on a molecular level using formalin-fixed and paraffin-embedded tissue, microbiopsies, and tape strips., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2023
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6. The neglected twin: Nummular eczema is a variant of atopic dermatitis with codominant T H 2/T H 17 immune response.
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Böhner A, Jargosch M, Müller NS, Garzorz-Stark N, Pilz C, Lauffer F, Wang R, Roenneberg S, Zink A, Thomas J, Theis FJ, Biedermann T, Eyerich S, and Eyerich K
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- Humans, Skin, Cytokines metabolism, Immunity, Dermatitis, Atopic, Eczema pathology, Psoriasis
- Abstract
Background: Nummular eczema (NE) is a common chronic inflammatory skin disease characterized by multiple, pruritic, discoid-shaped lesions. Since the underlying immune mechanisms are not fully understood, it is unclear whether NE should be regarded as variant of atopic dermatitis (AD) or a distinct disease., Objective: We compared the clinical, histopathologic, and molecular signatures of NE with that of type 2 and type 3 skin diseases., Methods: We performed bulk RNA sequencing as well as histologic and clinical studies in lesional and nonlesional skin biopsy specimens from NE (n = 50), AD (n = 47), and psoriasis (n = 90) patients., Results: NE displayed typical hallmarks of AD, such as an impaired epidermal barrier, microbial colonization, spongiosis, and eosinophil infiltration, but also aspects of psoriasis, including increased epidermal thickness, number of Ki-67
+ cells, and neutrophilic infiltration. At the gene expression level, neutrophil-attracting cytokines (IL19, CXCL8, CXCL5) were upregulated, whereas TH 2-related cytokines (IL13, CCL17, CCL18, CCL26, CCL27) were similarly expressed in NE compared to AD. Principal component analysis of transcriptome data from lesional skin showed that AD and NE cluster together distinct of psoriasis. In line with this, an established molecular classifier identified NE as AD rather than psoriasis. Finally, we demonstrated clinical and molecular efficacy of dupilumab treatment in NE., Conclusion: NE shows overlapping type 2 and type 3 immune signatures, while type 2 immunity predominates and should be the primary target of specific therapeutic interventions. This supports the view of NE as a variant of AD., (Copyright © 2023 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)- Published
- 2023
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7. Drug-induced Linear IgA Bullous Dermatosis: A Case Report and Review of the Literature.
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Lammer J, Hein R, Roenneberg S, Biedermann T, and Volz T
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- Aged, Diagnosis, Differential, Drug Eruptions drug therapy, Drug Eruptions pathology, Humans, Linear IgA Bullous Dermatosis drug therapy, Linear IgA Bullous Dermatosis pathology, Male, Anti-Bacterial Agents adverse effects, Drug Eruptions diagnosis, Drug Eruptions etiology, Linear IgA Bullous Dermatosis chemically induced, Linear IgA Bullous Dermatosis diagnosis, Vancomycin adverse effects
- Abstract
Linear IgA bullous dermatosis (LABD) is a rare subepidermal autoimmune blistering disease characterized by linear deposition of IgA along the basement membrane zone. Although most reported cases are idiopathic, there is a subset of patients with drug-induced LABD. Various drugs have been associated with the drug-induced form of the disease. This paper reviews the literature on drugs reported to elicit linear IgA dermatosis and its specific clinical presentation. In addition, a case report of a 77-year-old male patient with linear IgA dermatosis induced by vancomycin is described. The aim of this paper is to emphasize the need to include this differential diagnosis in cases of suspected adverse drug reactions, as well as to highlight the role of drugs in LABD.
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- 2019
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8. Type I Immune Response Induces Keratinocyte Necroptosis and Is Associated with Interface Dermatitis.
- Author
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Lauffer F, Jargosch M, Krause L, Garzorz-Stark N, Franz R, Roenneberg S, Böhner A, Mueller NS, Theis FJ, Schmidt-Weber CB, Biedermann T, Eyerich S, and Eyerich K
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- Adolescent, Adult, Aged, Apoptosis immunology, Biopsy, Dermatitis, Atopic genetics, Dermatitis, Atopic pathology, Female, Gene Expression Profiling, Gene Knockdown Techniques, Humans, Keratinocytes immunology, Lichen Planus genetics, Lichen Planus pathology, Lupus Erythematosus, Cutaneous genetics, Lupus Erythematosus, Cutaneous pathology, Male, Middle Aged, Necrosis immunology, Psoriasis genetics, Psoriasis pathology, RNA, Small Interfering metabolism, Receptor-Interacting Protein Serine-Threonine Kinases genetics, Receptor-Interacting Protein Serine-Threonine Kinases immunology, Skin cytology, Skin immunology, Skin pathology, Transcriptome immunology, Dermatitis, Atopic immunology, Keratinocytes pathology, Lichen Planus immunology, Lupus Erythematosus, Cutaneous immunology, Psoriasis immunology
- Abstract
Interface dermatitis is a characteristic histological pattern that occurs in autoimmune and chronic inflammatory skin diseases. It is unknown whether a common mechanism orchestrates this distinct type of skin inflammation. Here we investigated the overlap of two different interface dermatitis positive skin diseases, lichen planus and lupus erythematosus. The shared transcriptome signature pointed toward a strong type I immune response, and biopsy-derived T cells were dominated by IFN-γ and tumor necrosis factor alpha (TNF-α) positive cells. The transcriptome of keratinocytes stimulated with IFN-γ and TNF-α correlated significantly with the shared gene regulations of lichen planus and lupus erythematosus. IFN-γ, TNF-α, or mixed supernatant of lesional T cells induced signs of keratinocyte cell death in three-dimensional skin equivalents. We detected a significantly enhanced epidermal expression of receptor-interacting-protein-kinase 3, a key regulator of necroptosis, in interface dermatitis. Phosphorylation of receptor-interacting-protein-kinase 3 and mixed lineage kinase domain like pseudokinase was induced in keratinocytes on stimulation with T-cell supernatant-an effect that was dependent on the presence of either IFN-γ or TNF-α in the T-cell supernatant. Small hairpin RNA knockdown of receptor-interacting-protein-kinase 3 prevented cell death of keratinocytes on stimulation with IFN-γ or TNF-α. In conclusion, type I immunity is associated with lichen planus and lupus erythematosus and induces keratinocyte necroptosis. These two mechanisms are potentially involved in interface dermatitis., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2018
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9. Ixekizumab gegen die Acrodermatitis continua.
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Pilz AC, Roenneberg S, Biedermann T, and Eyerich K
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- 2018
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10. Ixekizumab for acrodermatitis continua.
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Pilz AC, Roenneberg S, Biedermann T, and Eyerich K
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- Acrodermatitis pathology, Female, Humans, Middle Aged, Acrodermatitis drug therapy, Antibodies, Monoclonal, Humanized therapeutic use, Dermatologic Agents therapeutic use
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- 2018
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11. Toll-like receptor 7/8 agonists stimulate plasmacytoid dendritic cells to initiate T H 17-deviated acute contact dermatitis in human subjects.
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Garzorz-Stark N, Lauffer F, Krause L, Thomas J, Atenhan A, Franz R, Roenneberg S, Boehner A, Jargosch M, Batra R, Mueller NS, Haak S, Groß C, Groß O, Traidl-Hoffmann C, Theis FJ, Schmidt-Weber CB, Biedermann T, Eyerich S, and Eyerich K
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- Administration, Cutaneous, Adult, Aged, Biomarkers metabolism, Case-Control Studies, Dermatitis, Contact pathology, Female, Flow Cytometry, Humans, Imiquimod administration & dosage, Immunohistochemistry, Male, Middle Aged, Psoriasis pathology, Real-Time Polymerase Chain Reaction, Toll-Like Receptor 8 agonists, Dendritic Cells metabolism, Dermatitis, Contact metabolism, Imiquimod adverse effects, Models, Biological, Psoriasis metabolism, Th17 Cells metabolism, Toll-Like Receptor 7 agonists
- Abstract
Background: A standardized human model to study early pathogenic events in patients with psoriasis is missing. Activation of Toll-like receptor 7/8 by means of topical application of imiquimod is the most commonly used mouse model of psoriasis., Objective: We sought to investigate the potential of a human imiquimod patch test model to resemble human psoriasis., Methods: Imiquimod (Aldara 5% cream; 3M Pharmaceuticals, St Paul, Minn) was applied twice a week to the backs of volunteers (n = 18), and development of skin lesions was monitored over a period of 4 weeks. Consecutive biopsy specimens were taken for whole-genome expression analysis, histology, and T-cell isolation. Plasmacytoid dendritic cells (pDCs) were isolated from whole blood, stimulated with Toll-like receptor 7 agonist, and analyzed by means of extracellular flux analysis and real-time PCR., Results: We demonstrate that imiquimod induces a monomorphic and self-limited inflammatory response in healthy subjects, as well as patients with psoriasis or eczema. The clinical and histologic phenotype, as well as the transcriptome, of imiquimod-induced inflammation in human skin resembles acute contact dermatitis rather than psoriasis. Nevertheless, the imiquimod model mimics the hallmarks of psoriasis. In contrast to classical contact dermatitis, in which myeloid dendritic cells sense haptens, pDCs are primary sensors of imiquimod. They respond with production of proinflammatory and T
H 17-skewing cytokines, resulting in a TH 17 immune response with IL-23 as a key driver. In a proof-of-concept setting systemic treatment with ustekinumab diminished imiquimod-induced inflammation., Conclusion: In human subjects imiquimod induces contact dermatitis with the distinctive feature that pDCs are the primary sensors, leading to an IL-23/TH 17 deviation. Despite these shortcomings, the human imiquimod model might be useful to investigate early pathogenic events and prove molecular concepts in patients with psoriasis., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2018
- Full Text
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12. Dome-shaped Papules on the Left Flank: A Quiz. Cutaneous Rosai-Dorfman Disease (sinus histiocytosis with massive lymphadenopathy.
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Roenneberg S, Hegyi I, Kempf W, Kerl K, and Guenova E
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- Administration, Cutaneous, Biopsy, Female, Histiocytosis, Sinus immunology, Histiocytosis, Sinus pathology, Histiocytosis, Sinus therapy, Humans, Middle Aged, Radiotherapy Dosage, Skin drug effects, Skin immunology, Skin radiation effects, Skin Diseases immunology, Skin Diseases pathology, Skin Diseases therapy, Steroids administration & dosage, Histiocytosis, Sinus diagnosis, Skin pathology, Skin Diseases diagnosis
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- 2018
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13. α-Gal-a new clue for anaphylaxis in mastocytosis.
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Roenneberg S, Böhner A, Brockow K, Arnold A, Darsow U, Eberlein B, and Biedermann T
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- Humans, Male, Middle Aged, Patient Care Management, Recurrence, Skin Tests methods, Anaphylaxis complications, Anaphylaxis diagnosis, Anaphylaxis etiology, Anaphylaxis therapy, Food Hypersensitivity complications, Food Hypersensitivity diagnosis, Food Hypersensitivity immunology, Galactose immunology, Mastocytosis, Systemic complications, Mastocytosis, Systemic diagnosis, Mastocytosis, Systemic immunology
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- 2016
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14. Acute Generalized Pustular Psoriasis Treated With the IL-17A Antibody Secukinumab.
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Böhner A, Roenneberg S, Eyerich K, Eberlein B, and Biedermann T
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- Acute Disease, Antibodies, Monoclonal pharmacology, Antibodies, Monoclonal, Humanized, Dermatologic Agents pharmacology, Humans, Male, Middle Aged, Psoriasis immunology, Psoriasis pathology, Treatment Outcome, Antibodies, Monoclonal therapeutic use, Dermatologic Agents therapeutic use, Interleukin-17 antagonists & inhibitors, Psoriasis drug therapy
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- 2016
- Full Text
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