Difficult-to-Treat Severe Asthma

Chung, K.F.; Bel, Elisabeth H.; Wenzel, S.E.

doi:10.1183/1025448x.erm5110

Cited by 12 publications

(3 citation statements)

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“…This is an important concept since severity genes may expose causal pathways that are more relevant targets for new therapies than those conferring asthma susceptibility. Traditional definitions of severe asthma include patients with asthma who are uncontrolled despite maximum standard treatments (4, 5). However, within this broad descriptor, there exist subpopulations each with different phenotypic characteristics (29, 30, 45).…”

Section: Genetics Of Lung Function and Asthma Severitymentioning

confidence: 99%

“…The varied clinical patterns found in severe asthma reflect individual genetic profiles combined with environmental exposures that initiate persistent bronchial inflammation and tissue injury which then lead to pathophysiological abnormalities and airway wall remodeling (3). One of the characteristics of severe asthma is resistance or reduced responsiveness to therapy (4, 5). Pharmacogenetic interactions may alter therapeutic responses reducing sensitivity to specific therapies facilitating more severe disease phenotypes.…”

Section: Introductionmentioning

confidence: 99%

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Asthma genetics and personalised medicine

Meyers¹,

Bleecker²,

Holloway³

et al. 2014

The Lancet Respiratory Medicine

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Nonbiased approaches, especially genome wide association studies (GWAS) have identified novel molecular targets in the pathogenesis of asthma, but so far only account for a small proportion of the heritability of asthma. Recognition of the importance of disease heterogeneity, the need for improved disease phenotyping and that genes involved in the inception of asthma are likely to be different from those involved in severity widens the impact of asthma genetics. Genes implicated in multiple causal pathways identifies the use of genetic scores to capture the impact of genetic variations on individuals. Gene-environmental interaction adds another layer of complexity which is being successfully explored by epigenetic approaches. Pharmacogenetics is one example of gene-environment interaction which is already having application in determining drug responders from non-responders and those most susceptible to adverse effects. Such applications represent one aspect of personalised medicine designed to help place the individual at the centre of healthcare.

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Section: Genetics Of Lung Function and Asthma Severitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Asthma genetics and personalised medicine

Meyers¹,

Bleecker²,

Holloway³

et al. 2014

The Lancet Respiratory Medicine

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“…В ряде исследований, посвященных определению клинических фенотипов ТБА, выявлены следующие фенотипы: аллергическая БА с ранним дебютом; поздняя БА, связанная с ожирением (преимущественно у женщин), и БА с выраженным персистирующим эозинофильным воспалением, характеризующаяся преимущественно поздним дебютом [5][6][7][8]. В европейском проекте U-BIOPRED, цель ко-торого -идентифицировать и охарактеризовать фенотипы тяжелой БА у детей и взрослых, отмечено доминирование эозинофильного воспаления у взрослых пациентов с ТБА, как некурящих, так и бывших или активных курильщиков, а у детей -преобладание аллергического воспаления [9,10].…”

Section: Introductionunclassified

The effectiveness of targeted therapy of various genetically engineered biological drugs in the treatment of bronchial asthma

Shogenova

2024

Terapevticheskii arkhiv

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This article presents the experience of successfully switching therapy from omalizumab 150 mg to benralizumab 30 mg/1 ml in a patient with a combined allergic and eosinophilic phenotype in the presence of hypersensitivity to nonsteroidal anti-inflammatory drugs. The effectiveness of biological therapy was evaluated when switching from omalizumab 150 mg subcutaneously at a dose of 600 mg for 36 weeks. Therapy for the drug benralizumab 30 mg/1 ml subcutaneously the first three injections monthly, the rest a month later for 52 weeks with bronchial asthma (BA), a severe uncontrolled course with a combined allergic and eosinophilic phenotype in the presence of hypersensitivity to nonsteroidal anti-inflammatory drugs in a patient Ch., born in 2004. Switching therapy from omalizumab 150 mg to benralizumab 30 mg/1 ml allowed to achieve complete control of asthma symptoms (AST = 23 points), to achieve the absence of asthma exacerbations during 52 weeks, restore respiratory function to normal values, as well as improve the quality of life. The study reflects the good tolerability, high efficacy and safety of biological therapy when switching from one genetically engineered biological drug (GIBP) omalizumab 150 mg to another GIBP benralizumab 30 mg/1 ml in severe uncontrolled asthma with a combined allergic and eosinophilic phenotype in the presence of hypersensitivity to nonsteroidal anti-inflammatory drugs. Therapy with benralizumab 30 mg/1 ml in severe BA has demonstrated a more effective clinically significant improvement in the course of the disease, control of symptoms of the disease. Reduction of exacerbations, normalization of respiratory function indicators, complete control of the disease has been achieved. Consequently, the use of different biological molecules for the therapy of BA with a combined allergic and eosinophilic phenotype contributes to achieving disease control, improving the patient's quality of life and reducing the dose of oral glucocorticosteroids. The targeted biological drug benralizumab 30 mg/1 ml has a targeted effect on the key links in the pathogenesis of severe uncontrolled asthma with a combined allergic and eosinophilic phenotype in the presence of hypersensitivity to nonsteroidal anti-inflammatory drugs and reduces the burden of severe disease.

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Application of ’omics technologies to biomarker discovery in inflammatory lung diseases

et al. 2013

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Inflammatory lung diseases are highly complex in respect of pathogenesis and relationships between inflammation, clinical disease and response to treatment. Sophisticated large-scale analytical methods to quantify gene expression (transcriptomics), proteins (proteomics), lipids (lipidomics) and metabolites (metabolomics) in the lungs, blood and urine are now available to identify biomarkers that define disease in terms of combined clinical, physiological and patho-biological abnormalities. The aspiration is that these approaches will improve diagnosis, i.e. define pathological phenotypes, and facilitate the monitoring of disease and therapy, and also, unravel underlying molecular pathways. Biomarker studies can either select predefined biomarker(s) measured by specific methods or apply an ''unbiased'' approach involving detection platforms that are indiscriminate in focus. This article reviews the technologies presently available to study biomarkers of lung disease within the 'omics field. The contributions of the individual 'omics analytical platforms to the field of respiratory diseases are summarised, with the goal of providing background on their respective abilities to contribute to systems medicine-based studies of lung disease. @ERSpublications Summary of the application of 'omics-based analytical platforms for biomarker discovery in inflammatory lung diseases

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Difficult-to-Treat Severe Asthma

Cited by 12 publications

References 0 publications

Asthma genetics and personalised medicine

Asthma genetics and personalised medicine

The effectiveness of targeted therapy of various genetically engineered biological drugs in the treatment of bronchial asthma

Application of ’omics technologies to biomarker discovery in inflammatory lung diseases

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