Airway and esophageal eosinophils in children with severe uncontrolled asthma

Erkman, Jessica; Vaynblat, Allen; Thomas, Kristen; Levine, Jeremiah; Moy, Libia; Greifer, Melanie; Giusti, Robert; Shah, Rasik V.; Kazachkov, Mikhail

doi:10.1002/ppul.24180

Cited by 10 publications

(3 citation statements)

References 23 publications

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“…Sputum neutrophils were higher in subjects with uncontrolled asthma, whereas eosinophils predominated in subjects with better‐controlled asthma, reinforcing the concept that neutrophil‐dominant inflammation may characterize an asthma phenotype of special concern . The second study by Ekman et al demonstrated that some children with severe persistent asthma have eosinophilic esophagitis (n = 3) or reflux esophagitis (n = 8). In these children, airway and esophageal eosinophils were correlated.…”

Section: Introductionmentioning

confidence: 86%

Pediatric Pulmonology year in review 2018: Asthma, physiology/pulmonary function testing, and respiratory infections

Loughlin

Muston

et al. 2019

Pediatric Pulmonology

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Pediatric Pulmonology publishes original research, reviews, and case reports related to a wide range of children's respiratory disorders. In our “Year in Review” series, we summarize publications in our major topic areas from 2018, in the context of selected literature in these areas from other journals relevant to our discipline. This review covers selected articles on asthma, physiology/lung function testing, and respiratory infections.

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Section: Introductionmentioning

confidence: 86%

Pediatric Pulmonology year in review 2018: Asthma, physiology/pulmonary function testing, and respiratory infections

Loughlin

Muston

et al. 2019

Pediatric Pulmonology

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“…Type 2 inflammation may be considered as an underlying immunopathological driver of atopic dermatitis. Hazard ratio: 1.7 and 40.0% (data from 2 studies) 102,103 Hazard ratio: 1.9 and 13.0% (data from 2 studies) 103,104 Children with atopic dermatitis 13.1-36.0% (data from 10 studies) 22,68,78,84,93,103,[105][106][107][108] 4.0-61.0% (data from 6 studies) 22,68,78,93,102,103 Hazard ratio: 3.2 (data from 1 study) 103 Children with chronic rhinitis 24.7-59.0% (data from 4 studies) 22,63,68,102 4.0-53% (data from 4 studies) 22,63,68,102 Hazard ratio: 2.8 (data from 1 study) 103 Children with eosinophilic esophagitis 45.4-59.8% (data from 3 studies)…”

Section: Respiratory Subgroupmentioning

confidence: 99%

Clinical relevance of type 2 inflammation as a driver of multi-organ disease: A Delphi consensus initiative

Björnsdóttir,

Deleuran,

Janson

et al. 2024

Preprint

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Background: This initiative aimed to elucidate the clinical relevance of type 2 (T2) inflammation as a driver of asthma, atopic dermatitis, chronic rhinitis, chronic rhinosinusitis with nasal polyps (CRSwNP) and eosinophilic esophagitis. Methods: A steering committee (SC) conducted a non-systematic literature search to inform the design of a Delphi questionnaire including 23 consensus statements, which was circulated to 30 experts including the SC. Experts rated their agreement with each statement on a 9-point Likert scale and provided optional feedback that was used to develop a second Delphi questionnaire. On 22 October 2020, a meeting was held to discuss the conclusions from the questionnaires and explore how this initiative may impact the management of patients with T2 inflammation-driven disease. Post meeting, a consensus statement on the role of T2 inflammation in eosinophilic esophagitis was circulated to the experts. Results: It was agreed that T2 inflammation may be an underlying driver of asthma, atopic dermatitis, chronic rhinitis, CRSwNP and eosinophilic esophagitis, and that the published evidence suggests that these diseases overlap. Some of this overlap may include related multimorbid conditions driven by T2 inflammation. Thus, in patients with multiple T2 inflammation-driven diseases, a cross-speciality approach is warranted to provide effective care. A question guide with input from relevant experts was proposed, to identify comorbidities and facilitate appropriate holistic patient management. Conclusions: These consensus recommendations should be used as a framework to further understand the extent of T2 inflammation-driven multi-organ disease and to improve the holistic management and care of these patients.

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“…Although most connective tissue diseases, such as eosinophilic granulomatosis with polyangiitis, lupus erythematodes, rheumatoid arthritis, systemic sclerosis, Sjögren syndrome, or scleromyositis may cause tissue eosinophilia in the GI tract, it occurs mostly in the small bowel, stomach, or colon [135, Peripheral blood eosinophils > 1500 cells/ml without secondary causes and evidence of an eosinophil-mediated end organ manifestation Atopic diseases (Asthma, aspirin-exacerbated respiratory disease, IgE mediated food allergy) [152,153] Extraintestinal manifestations Drug hypersensitivity and pill esophagitis Medical history Radiofrequency ablation for Barrett's esophagus [154][155][156] Typically without dysphagia Graft-versus-host disease [157] Eosinophil density correlates with GvHR Oral immunotherapy [158] Mostly transient and without symptoms Asymptomatic esophageal eosinophilia [159][160][161][162] Exclusive diagnosis 136]. An esophageal involvement is a rarity [136,137] and as opposed to EoE, most patients are female, have no atopy, and present with peripheral eosinophilia [136].…”

Section: Autoimmune Connective Tissue Diseasementioning

confidence: 99%

Eosinophilic esophagitis—established facts and new horizons

2021

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Despite dramatic advances in our understanding of the pathogenesis and course of disease in the relatively short timeframe since the discovery and first description of eosinophilic esophagitis (EoE) less than three decades ago, many open questions remain to be elucidated. For instance, we will need to better characterize atypical clinical presentations of EoE and other forms of esophageal inflammatory conditions with often similar clinical presentations, nut fulfilling current diagnostic criteria for EoE and to determine their significance and interrelationship with genuine EoE. In addition, the interrelationship of EoE with other immune-mediated diseases remains to be clarified. Hopefully, a closer look at the role of environmental factors and their interaction with genetic susceptibility often in context of atopic predisposition may enable identifying the candidate substances/agents/allergens and potentially earlier (childhood) events to trigger the condition. It appears plausible to assume that in the end—comparable to current concepts in other immune-mediated chronic diseases, such as for instance inflammatory bowel disease or asthma bronchiale—we will not be rewarded with the identification of a “one-and-only” underlying pathogenetic trigger factor, with causal responsibility for the disease in each and every EoE patient. Rather, the relative contribution and importance of intrinsic susceptibility, i.e., patient-driven factors (genetics, aberrant immune response) and external trigger factors, such as food (or aero-) allergens as well as early childhood events (e.g., infection and exposure to antibiotics and other drugs) may substantially differ among given individuals with EoE. Accordingly, selection and treatment duration of medical therapy, success rates and extent of required restriction in dietary treatment, and the need for mechanical treatment to address strictures and stenosis require an individualized approach, tailored to each patient. With the advances of emerging treatment options, the importance of such an individualized and patient-centered assessment will increase even further.

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Airway and esophageal eosinophils in children with severe uncontrolled asthma

Cited by 10 publications

References 23 publications

Pediatric Pulmonology year in review 2018: Asthma, physiology/pulmonary function testing, and respiratory infections

Pediatric Pulmonology year in review 2018: Asthma, physiology/pulmonary function testing, and respiratory infections

Clinical relevance of type 2 inflammation as a driver of multi-organ disease: A Delphi consensus initiative

Eosinophilic esophagitis—established facts and new horizons

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