{"title":"British Society for Allergy and Immunology Abstracts From the 2024 Annual Conference","authors":"","doi":"10.1111/cea.14576","DOIUrl":"10.1111/cea.14576","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 10","pages":"781-847"},"PeriodicalIF":6.3,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142388511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thierry Batard, Camille Taillé, Laurent Guilleminault, Andrzej Bozek, Véronique Bordas-Le Floch, Oliver Pfaar, Walter G. Canonica, Cezmi Akdis, Mohamed H. Shamji, Laurent Mascarell
Allergic asthma is the predominant phenotype among asthmatics. Although conventional pharmacotherapy is a central component in the management of asthma, it does not enable control of asthma symptoms in all patients. In recent decades, some uncontrolled asthmatic patients, especially those with allergic asthma, have benefited from biological therapies. However, biologics do not address all the unmet needs left by conventional pharmacotherapy. Furthermore, it is noteworthy that neither conventional pharmacotherapy nor biological therapies have disease-modifying properties. In this context, allergen immunotherapy (AIT) represents an indispensable component of the therapeutic arsenal against allergic asthma, due to its disease-modifying immunological effects. In this review article, funded by an AIT manufacturer, we find clinical trials support AIT as the only treatment option able both to improve allergic asthma symptoms and to prevent the onset and worsening of the condition. For patients with severe asthma or other safety concerns, the combination of AIT and biologics offers very promising new treatment modalities for the management of allergic asthma.
{"title":"Allergen Immunotherapy for the Prevention and Treatment of Asthma","authors":"Thierry Batard, Camille Taillé, Laurent Guilleminault, Andrzej Bozek, Véronique Bordas-Le Floch, Oliver Pfaar, Walter G. Canonica, Cezmi Akdis, Mohamed H. Shamji, Laurent Mascarell","doi":"10.1111/cea.14575","DOIUrl":"10.1111/cea.14575","url":null,"abstract":"<p>Allergic asthma is the predominant phenotype among asthmatics. Although conventional pharmacotherapy is a central component in the management of asthma, it does not enable control of asthma symptoms in all patients. In recent decades, some uncontrolled asthmatic patients, especially those with allergic asthma, have benefited from biological therapies. However, biologics do not address all the unmet needs left by conventional pharmacotherapy. Furthermore, it is noteworthy that neither conventional pharmacotherapy nor biological therapies have disease-modifying properties. In this context, allergen immunotherapy (AIT) represents an indispensable component of the therapeutic arsenal against allergic asthma, due to its disease-modifying immunological effects. In this review article, funded by an AIT manufacturer, we find clinical trials support AIT as the only treatment option able both to improve allergic asthma symptoms and to prevent the onset and worsening of the condition. For patients with severe asthma or other safety concerns, the combination of AIT and biologics offers very promising new treatment modalities for the management of allergic asthma.</p><p><b>Trial Registration:</b> clinicaltrials.gov identifier: NCT06027073</p>","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"55 2","pages":"111-141"},"PeriodicalIF":6.3,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14575","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371132","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}
Petra Staubach, Raffi Tachdjian, H. Henry Li, Roman Hakl, Emel Aygören-Pürsün, Lolis Wieman, John-Philip Lawo, Timothy J. Craig
<p>Hereditary angioedema (HAE) is a rare, autosomal dominant disease characterised by recurrent, unpredictable, painful, debilitating and potentially life-threatening attacks [<span>1-3</span>]. HAE imparts a substantial disease burden that impacts daily activities and extends beyond symptoms directly attributable to HAE attacks, encompassing mental health (anxiety and depression) and psychosocial impacts associated with unpredictable attack recurrence [<span>1, 3</span>].</p><p>Per World Allergy Organization (WAO)/European Academy of Allergy and Clinical Immunology (EAACI) guidelines, the goal of HAE treatment is complete disease control and normalisation of patients' lives [<span>2</span>]. This can only be achieved with effective long-term prophylactic (LTP) therapy [<span>2</span>]. Early onset of efficacy and durability of protection are critical attributes of LTP therapies to optimise HAE disease control and establish clinician and patient confidence in the treatment. Despite the availability of approved LTP therapies, there is still an unmet need for treatments with a rapid onset and improved durability of protection against HAE attacks [<span>2, 4</span>].</p><p>Activated factor XII (FXIIa) is the principal initiator of the kallikrein–kinin system, leading to production of bradykinin, the key inflammatory mediator responsible for vasodilation and vascular permeability [<span>2, 5, 6</span>]. C1 inhibitor (C1INH) regulates FXIIa in healthy individuals [<span>5, 6</span>]. In HAE, most patients have C1INH deficiency (HAE-C1INH-Type1) or dysfunction (HAE-C1INH-Type2), leading to uncontrolled activation of FXII. The subsequent dysregulation of the kallikrein–kinin system results in overproduction of bradykinin, ultimately leading to HAE attacks [<span>2, 5, 6</span>].</p><p>Garadacimab is a first-in-class, fully human, potent, anti-activated FXII monoclonal antibody under clinical evaluation as an LTP therapy for HAE attacks [<span>7, 8</span>]. Garadacimab has high affinity and specificity for FXIIa, with in vitro data demonstrating decreased bradykinin production [<span>8</span>]. In the 6-month pivotal Phase 3 (VANGUARD) study (NCT04656418), patients aged ≥ 12 years with HAE with C1INH deficiency or dysfunction and an average attack rate of ≥ 3 attacks in the 3 months preceding study initiation were randomised (3:2) to receive garadacimab 200 mg subcutaneous once monthly after an initial 400 mg loading dose (<i>n</i> = 39) or volume-matched placebo (<i>n</i> = 25). Garadacimab significantly reduced monthly number of attacks versus placebo (mean: 0.27 vs. 2.01, respectively; <i>p</i> < 0.0001 and median [interquartile range] 0.00 [0.00–0.31] vs. 1.35 [1.00–3.20], respectively). Throughout the study, 62% of patients treated with garadacimab remained attack free, demonstrating durable protection against HAE attacks [<span>7</span>].</p><p>In this post hoc analysis of the pivotal Phase 3 (VANGUARD) study, the onset of protection against HAE
{"title":"Timing of Onset of Garadacimab for Preventing Hereditary Angioedema Attacks","authors":"Petra Staubach, Raffi Tachdjian, H. Henry Li, Roman Hakl, Emel Aygören-Pürsün, Lolis Wieman, John-Philip Lawo, Timothy J. Craig","doi":"10.1111/cea.14568","DOIUrl":"10.1111/cea.14568","url":null,"abstract":"<p>Hereditary angioedema (HAE) is a rare, autosomal dominant disease characterised by recurrent, unpredictable, painful, debilitating and potentially life-threatening attacks [<span>1-3</span>]. HAE imparts a substantial disease burden that impacts daily activities and extends beyond symptoms directly attributable to HAE attacks, encompassing mental health (anxiety and depression) and psychosocial impacts associated with unpredictable attack recurrence [<span>1, 3</span>].</p><p>Per World Allergy Organization (WAO)/European Academy of Allergy and Clinical Immunology (EAACI) guidelines, the goal of HAE treatment is complete disease control and normalisation of patients' lives [<span>2</span>]. This can only be achieved with effective long-term prophylactic (LTP) therapy [<span>2</span>]. Early onset of efficacy and durability of protection are critical attributes of LTP therapies to optimise HAE disease control and establish clinician and patient confidence in the treatment. Despite the availability of approved LTP therapies, there is still an unmet need for treatments with a rapid onset and improved durability of protection against HAE attacks [<span>2, 4</span>].</p><p>Activated factor XII (FXIIa) is the principal initiator of the kallikrein–kinin system, leading to production of bradykinin, the key inflammatory mediator responsible for vasodilation and vascular permeability [<span>2, 5, 6</span>]. C1 inhibitor (C1INH) regulates FXIIa in healthy individuals [<span>5, 6</span>]. In HAE, most patients have C1INH deficiency (HAE-C1INH-Type1) or dysfunction (HAE-C1INH-Type2), leading to uncontrolled activation of FXII. The subsequent dysregulation of the kallikrein–kinin system results in overproduction of bradykinin, ultimately leading to HAE attacks [<span>2, 5, 6</span>].</p><p>Garadacimab is a first-in-class, fully human, potent, anti-activated FXII monoclonal antibody under clinical evaluation as an LTP therapy for HAE attacks [<span>7, 8</span>]. Garadacimab has high affinity and specificity for FXIIa, with in vitro data demonstrating decreased bradykinin production [<span>8</span>]. In the 6-month pivotal Phase 3 (VANGUARD) study (NCT04656418), patients aged ≥ 12 years with HAE with C1INH deficiency or dysfunction and an average attack rate of ≥ 3 attacks in the 3 months preceding study initiation were randomised (3:2) to receive garadacimab 200 mg subcutaneous once monthly after an initial 400 mg loading dose (<i>n</i> = 39) or volume-matched placebo (<i>n</i> = 25). Garadacimab significantly reduced monthly number of attacks versus placebo (mean: 0.27 vs. 2.01, respectively; <i>p</i> < 0.0001 and median [interquartile range] 0.00 [0.00–0.31] vs. 1.35 [1.00–3.20], respectively). Throughout the study, 62% of patients treated with garadacimab remained attack free, demonstrating durable protection against HAE attacks [<span>7</span>].</p><p>In this post hoc analysis of the pivotal Phase 3 (VANGUARD) study, the onset of protection against HAE","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 12","pages":"1020-1023"},"PeriodicalIF":6.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364619","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":"Rethinking Blood Biomarkers in Autoimmune Urticaria: A Response to Recent Findings","authors":"Sukhdeep Singh, Hitaishi Mehta, Muthu Sendhil Kumaran","doi":"10.1111/cea.14571","DOIUrl":"10.1111/cea.14571","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 12","pages":"1027-1028"},"PeriodicalIF":6.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alba Camino-Mera, Jacobo Pardo-Seco, Xabier Bello, Laura Argiz, Robert J. Boyle, Adnan Custovic, Jethro Herberg, Myrsini Kaforou, Stefania Arasi, Alessandro Fiocchi, Valentina Pecora, Simona Barni, Francesca Mori, Teresa Bracamonte, Luis Echeverria, Virginia O'Valle-Aísa, Noelia Lara Hernández-Martínez, Iria Carballeira, Emilio García, Carlos Garcia-Magan, José Domingo Moure-González, Purificación Gonzalez-Delgado, Teresa Garriga-Baraut, Sonsoles Infante, Gabriela Zambrano-Ibarra, Margarita Tomás-Pérez, Adrianna Machinena, Mariona Pascal, Ana Prieto, Sonia Vázquez-Cortes, Montserrat Fernández-Rivas, Leticia Vila, Laia Alsina, María José Torres, Giusi Mangone, Santiago Quirce, Federico Martinón-Torres, Marta Vázquez-Ortiz, Alberto Gómez-Carballa, Antonio Salas
Background
Food protein-induced enterocolitis syndrome (FPIES) is a food allergy primarily affecting infants, often leading to vomiting and shock. Due to its poorly understood pathophysiology and lack of specific biomarkers, diagnosis is frequently delayed. Understanding FPIES genetics can shed light on disease susceptibility and pathophysiology—key to developing diagnostic, prognostic, preventive and therapeutic strategies. Using a well-characterised cohort of patients we explored the potential genome-wide susceptibility factors underlying FPIES.
Methods
Blood samples from 41 patients with oral food challenge-proven FPIES were collected for a comprehensive whole exome sequencing association study.
Results
Notable genetic variants, including rs872786 (RBM8A), rs2241880 (ATG16L1) and rs2289477 (ATG16L1), were identified as significant findings in FPIES. A weighted SKAT model identified six other associated genes including DGKZ and SIRPA. DGKZ induces TGF-β signalling, crucial for epithelial barrier integrity and IgA production; RBM8A is associated with thrombocytopenia absent radius syndrome, frequently associated with cow's milk allergy; SIRPA is associated with increased neutrophils/monocytes in inflamed tissues as often observed in FPIES; ATG16L1 is associated with inflammatory bowel disease. Coexpression correlation analysis revealed a functional correlation between RBM8A and filaggrin gene (FLG) in stomach and intestine tissue, with filaggrin being a known key pathogenic and risk factor for IgE-mediated food allergy. A transcriptome-wide association study suggested genetic variability in patients impacted gene expression of RBM8A (stomach and pancreas) and ATG16L1 (transverse colon).
Conclusions
This study represents the first case–control exome association study of FPIES patients and marks a crucial step towards unravelling genetic susceptibility factors underpinning the syndrome. Our findings highlight potential factors and pathways contributing to FPIES, including epithelial barrier dysfunction and immune dysregulation. While these results are novel, they are preliminary and need further validation in a second cohort of patients.
{"title":"Whole Exome Sequencing Identifies Epithelial and Immune Dysfunction-Related Biomarkers in Food Protein-Induced Enterocolitis Syndrome","authors":"Alba Camino-Mera, Jacobo Pardo-Seco, Xabier Bello, Laura Argiz, Robert J. Boyle, Adnan Custovic, Jethro Herberg, Myrsini Kaforou, Stefania Arasi, Alessandro Fiocchi, Valentina Pecora, Simona Barni, Francesca Mori, Teresa Bracamonte, Luis Echeverria, Virginia O'Valle-Aísa, Noelia Lara Hernández-Martínez, Iria Carballeira, Emilio García, Carlos Garcia-Magan, José Domingo Moure-González, Purificación Gonzalez-Delgado, Teresa Garriga-Baraut, Sonsoles Infante, Gabriela Zambrano-Ibarra, Margarita Tomás-Pérez, Adrianna Machinena, Mariona Pascal, Ana Prieto, Sonia Vázquez-Cortes, Montserrat Fernández-Rivas, Leticia Vila, Laia Alsina, María José Torres, Giusi Mangone, Santiago Quirce, Federico Martinón-Torres, Marta Vázquez-Ortiz, Alberto Gómez-Carballa, Antonio Salas","doi":"10.1111/cea.14564","DOIUrl":"10.1111/cea.14564","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Food protein-induced enterocolitis syndrome (FPIES) is a food allergy primarily affecting infants, often leading to vomiting and shock. Due to its poorly understood pathophysiology and lack of specific biomarkers, diagnosis is frequently delayed. Understanding FPIES genetics can shed light on disease susceptibility and pathophysiology—key to developing diagnostic, prognostic, preventive and therapeutic strategies. Using a well-characterised cohort of patients we explored the potential genome-wide susceptibility factors underlying FPIES.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Blood samples from 41 patients with oral food challenge-proven FPIES were collected for a comprehensive whole exome sequencing association study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Notable genetic variants, including rs872786 (<i>RBM8A</i>), rs2241880 (<i>ATG16L1</i>) and rs2289477 (<i>ATG16L1</i>), were identified as significant findings in FPIES. A weighted SKAT model identified six other associated genes including <i>DGKZ</i> and <i>SIRPA</i>. DGKZ induces TGF-β signalling, crucial for epithelial barrier integrity and IgA production; <i>RBM8A</i> is associated with thrombocytopenia absent radius syndrome, frequently associated with cow's milk allergy; <i>SIRPA</i> is associated with increased neutrophils/monocytes in inflamed tissues as often observed in FPIES; <i>ATG16L1</i> is associated with inflammatory bowel disease. Coexpression correlation analysis revealed a functional correlation between <i>RBM8A</i> and filaggrin gene (<i>FLG</i>) in stomach and intestine tissue, with filaggrin being a known key pathogenic and risk factor for IgE-mediated food allergy. A transcriptome-wide association study suggested genetic variability in patients impacted gene expression of <i>RBM8A</i> (stomach and pancreas) and <i>ATG16L1</i> (transverse colon).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study represents the first case–control exome association study of FPIES patients and marks a crucial step towards unravelling genetic susceptibility factors underpinning the syndrome. Our findings highlight potential factors and pathways contributing to FPIES, including epithelial barrier dysfunction and immune dysregulation. While these results are novel, they are preliminary and need further validation in a second cohort of patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 11","pages":"919-929"},"PeriodicalIF":6.3,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14564","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342723","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}
Shambo Samrat Samajdar, Saibal Moitra, Sougata Sarkar, Santanu K. Tripathi
{"title":"Efficacy and Safety of Subcutaneous vs. Sublingual Immunotherapy in Allergic Rhinitis: A Systematic Review and Meta-Analysis","authors":"Shambo Samrat Samajdar, Saibal Moitra, Sougata Sarkar, Santanu K. Tripathi","doi":"10.1111/cea.14574","DOIUrl":"10.1111/cea.14574","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"55 2","pages":"199-201"},"PeriodicalIF":6.3,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Karen H. T. Li, Olivia Wing, Hilary I. Allen, Timothy D. H. Smith, Frank Moriarty, Robert J. Boyle
Background
Cow's milk allergy (CMA) overdiagnosis appears to be increasing and is associated with excessive low-allergy formula prescription. We evaluated recent trends and regional variation in low-allergy formula prescribing for CMA in England, and assessed potential risk factors for higher prescribing rates.
Methods
Data on national and regional prescribing of low-allergy formulas were extracted from England's electronic prescription database using R. Region-level factors were evaluated for potential associations with regional low-allergy formula prescription rates using multivariate linear regression. Analysis of national prescribing trends covered 2007–2023, analysis of regional variation and region-level factors examined 2017–2019, prior to a re-organisation of the regional healthcare structure in England.
Results
Low-allergy formula prescribing increased from 6.1 to 23.3 L per birth nationally, between 2007 and 2023. Regional prescribing rate varied from 0.8 to 47.6 L per birth in 2017–2019. We found significant associations between regional low-allergy formula prescribing rate and regional prescribing rates for milk feed thickeners Gaviscon Infant and Carobel Instant (β = 0.10, p < 0.01), and for other anti-reflux medications used in young children (β = 0.89 p < 0.01). Inconsistent associations were seen with prescribing junior adrenaline auto-injectors and oral antibiotics. A model including these four variables accounted for 37% of regional variation in low-allergy formula prescribing rate. Region-level socio-economic deprivation, CMA guideline recommendations and paediatric allergy service provision were not associated with low-allergy formula prescribing.
Conclusions
Low-allergy formula prescribing in England is increasing, varies significantly by region and is consistently associated with prescribing rates for milk feed thickeners and other anti-reflux medication for young children. Community prescribing behaviours may be important determinants of CMA overdiagnosis.
{"title":"Time Trends, Regional Variation and Associations of Low-Allergy Formula Prescribing in England","authors":"Karen H. T. Li, Olivia Wing, Hilary I. Allen, Timothy D. H. Smith, Frank Moriarty, Robert J. Boyle","doi":"10.1111/cea.14570","DOIUrl":"10.1111/cea.14570","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cow's milk allergy (CMA) overdiagnosis appears to be increasing and is associated with excessive low-allergy formula prescription. We evaluated recent trends and regional variation in low-allergy formula prescribing for CMA in England, and assessed potential risk factors for higher prescribing rates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data on national and regional prescribing of low-allergy formulas were extracted from England's electronic prescription database using R. Region-level factors were evaluated for potential associations with regional low-allergy formula prescription rates using multivariate linear regression. Analysis of national prescribing trends covered 2007–2023, analysis of regional variation and region-level factors examined 2017–2019, prior to a re-organisation of the regional healthcare structure in England.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Low-allergy formula prescribing increased from 6.1 to 23.3 L per birth nationally, between 2007 and 2023. Regional prescribing rate varied from 0.8 to 47.6 L per birth in 2017–2019. We found significant associations between regional low-allergy formula prescribing rate and regional prescribing rates for milk feed thickeners Gaviscon Infant and Carobel Instant (<i>β</i> = 0.10, <i>p</i> < 0.01), and for other anti-reflux medications used in young children (<i>β</i> = 0.89 <i>p</i> < 0.01). Inconsistent associations were seen with prescribing junior adrenaline auto-injectors and oral antibiotics. A model including these four variables accounted for 37% of regional variation in low-allergy formula prescribing rate. Region-level socio-economic deprivation, CMA guideline recommendations and paediatric allergy service provision were not associated with low-allergy formula prescribing.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Low-allergy formula prescribing in England is increasing, varies significantly by region and is consistently associated with prescribing rates for milk feed thickeners and other anti-reflux medication for young children. Community prescribing behaviours may be important determinants of CMA overdiagnosis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 11","pages":"909-918"},"PeriodicalIF":6.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14570","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342722","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}
Caroline Beutner, Stephan Traidl, Martin Wagenmann, Moritz Maximilian Hollstein, Dirk Beutner, Michael Peter Schön, Timo Buhl
{"title":"Dupilumab Improves Clinical Symptoms and Biomarkers in Comorbid Seasonal Timothy Grass Pollen Allergic Rhinitis in Patients With CRSwNP","authors":"Caroline Beutner, Stephan Traidl, Martin Wagenmann, Moritz Maximilian Hollstein, Dirk Beutner, Michael Peter Schön, Timo Buhl","doi":"10.1111/cea.14572","DOIUrl":"10.1111/cea.14572","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"55 2","pages":"196-198"},"PeriodicalIF":6.3,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tamar Landau, Keren Gamrasni, Alex Levin, Yotam Barlev, Oliver Sanders, Shira Benor, Michael Brandwein
<p>Atopic dermatitis (AD), is a common, complex and heterogeneous inflammatory skin disease [<span>1</span>]. Many patients develop AD by 5 years, directly affecting quality of life [<span>2</span>], and increasing risk for other comorbidities, including asthma, allergic rhinitis, and food allergies [<span>3</span>]. Filaggrin mutations and family history of atopy are important risk factors for AD development [<span>1, 4</span>]. Each provides poor predictive value when used independently to stratify risk, yet family history of atopy has been used in the research setting [<span>5, 6</span>] and is the current standard of care (SOC). A prognostic AD clinical risk score can empower clinicians to diagnose AD earlier on. It can also be employed by the clinical trialist to enrich birth cohorts with a priori screening for at-risk patients. We aimed to develop a clinical risk score using information available in the prenatal period, with consideration to explainability and applicability, and validate it on an external, geographically independent dataset.</p><p>The training dataset included the electronic medical records (EMR) of all infant-mother dyads captured in the Leumit Health Services (Leumit) EMR between 2010 and 2019 with a recorded AD diagnosis before the age of three (<i>n</i> = 7370) and a random sample of infant-mother dyads selected from the Leumit EMR whereby AD was not diagnosed in the child's EMR (<i>n</i> = 63,852). Leumit is one of four national health providers and its EMR captures routine data from all medical consultations, procedures, and prescriptions, along with relevant sociodemographic data. The US-based Infant Feeding Practices Study 2 (IFPS2) was used as a validation dataset [<span>7</span>]. The cohort included a nationally distributed panel of 1807 infants born between 2005 and 2007, of which 389 (21.5%) reported a doctor's diagnosis of AD by the age of one. Additional information about study methods and findings are available in the online repository (https://github.com/tami-myor/AD-Score/tree/main).</p><p>The scoring method is designed to generate a value from 0 to 1, representing the probable risk in probabilistic terms, and can be effectively calculated if some variables are missing. Patients were divided into high (> 0.5), medium (0.35–0.5) and low-risk groups (< 0.35) There was a significant difference in means among the risk groups in relation to the actual cases of atopic dermatitis (ANOVA, <i>p</i> < 0.001) for both train and validation set. When compared to the SOC, individuals in the low-risk group were less likely to develop AD than those without a parental history of atopy and individuals in the high-risk group were more likely to develop AD than those with a parental history of atopy for both train and validation set. The OR in a univariate logistic regression model for developing AD was 2.30 (CI 2.15–2.46, <i>p</i> < 0.001) for the medium-risk group and 4.06 (CI 3.80–4.34, <i>p</i> < 0.001) for
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